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May 23, 2025 100 mins
What is in the This Week in Science Podcast? This Week: CRISPR, Government-Sanctioned Mass Extinction, Bugs in Space, Shrinking Clownfish, Bees Sleep, Dolphins Talk, Blocking Cell Death, Toothy Origins, and Much More Science! Become a Patron! Check out the full unedited episode of our podcast on YouTube or Twitch. Remember that you can find TWIS […] The post 21 May, 2025 – Episode 1016 – Do Dolphins Discuss Science? appeared first on This Week in Science - The Kickass Science Podcast.
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Episode Transcript

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Speaker 1 (00:00):
This is Twists. This Week in Science, episode number ten sixteen,
recorded on Wednesday, May twenty first, twenty twenty five, Do
Dolphins discuss Science? Hey everyone, I'm doctor Kikeean. Today on
the show we will fill your head with spacebugs, shrinking fish,

(00:21):
and some teeth. But first, thanks to our amazing Patreon
sponsors for their generous support of Twists. You can become
a part of the Patreon community at patreon dot com.
Slash This Week in Science Dizclimber disclaimer disclaimer. When lie
after lie makes you question the sky and wonder what

(00:43):
truth even is, remember to find the people who question
themselves and don't try to sell you oncertainty or their
life changing supplements. Snake oil is greasy and easily slips
past the lips of the charlatans and cheats. Remember to
think about the source of that length before clicking your
way past the brink. You hold the tools in your

(01:04):
head to parse the good from the bad, and when
you need more, remember this week in Science Coming up next.

Speaker 2 (01:16):
I've got the kind of mind I can't get enough.
I want to learn everything, I want to fill it
all up with new discoveries. It happened every day week.
There's only one place to go to find the knowledge
to seek.

Speaker 3 (01:30):
I want to know what's happened, What's happens happened this
week in sciences? Happens happenings happened this week in science.

Speaker 1 (01:49):
Good science to you, Kiki, and a good science to
you too, Blair and everyone out there, Welcome to another
episode of This Week in Science. We are back again
and to talk about science. And Justin is not here.
Hopefully he'll be able to be here next week, but
he's got some new responsibilities that are keeping him away

(02:10):
from Wednesdays for the time being. Fingers crossed, we will
see him soon. Well here we brought science right.

Speaker 4 (02:18):
Oh yeah, I'm very excited.

Speaker 1 (02:22):
Thank you all for joining us for this episode. We
do have tons of science news. I did measure it
out in the you know, using the metric measuring system.
I have new stories about a new and improved crisper,
some bugs in space, talking dolphins and toothy origins. What's
in the animal corner, Blair.

Speaker 4 (02:44):
Oh my goodness, I have endangered species. I have clownfish,
and I have b brains.

Speaker 1 (02:54):
At first I was like, this is a cool aquarium,
and then I was like those one of these things
is not like the other awesome.

Speaker 4 (03:02):
I mean you could submerge b brains and water. I suppose.

Speaker 1 (03:07):
Fish food not I mean I would feed the fish
with it. Okay, moving on forward everyone, I hope you're
excited about this show tonight. As we jump into the show,
I want to remind you that subscribing to the Twist
podcast on your favorite podcast platform, YouTube, Facebook, or Twitch
is the best way to keep up with this show

(03:29):
every week and whenever we publish it, because sometimes we
do it more often, sometimes less offn it's a very
interesting thing. We try to be every weekly. So we're
here Wednesday's eight pm ish specific time to do a
tight ninety show. And you can subscribe and be alerted
every time a new episode is published. It's really good.

(03:51):
You can get your friends to subscribe and then they
could be alerted every time a new episode is published.

Speaker 5 (03:55):
Whatever.

Speaker 1 (03:56):
If you need more information, go to Twist dot org.
You can find show notes linked to our Patreon community,
also to our saddle store Twist dot org. But now
it's time for the science.

Speaker 4 (04:08):
You ready, Blair, so ready?

Speaker 1 (04:11):
So you were born ready? I know, I know, I
see you there, So I'm going to start off the
show with just what everybody wanted, new and improved Crisper.

Speaker 4 (04:27):
Yeah.

Speaker 1 (04:30):
So we remembers crisper, right of course, right right, yes, yeah,
but Crisper it has caused a big not tumult hubbub.
I don't know, lots of movement in the traversy that too.

(04:56):
Exactly in the gene editing world, crisper that's called molecular scissors.
Crisper came from bacteria researchers a long long time ago.
They're like, oh, look at these cool tools the bacteria have.
They go snip, snip, and then they're able to add
new what is going on here? And on and on
and on, and eventually researchers were able to use this

(05:20):
crisper tool along with another enzyme called CAST nine, and
they've come up with other enzymes since then to create
more and more accurate methods with which to edit genes.
The hope is that we will be able to edit
our own genes to be able to get rid of disease.
And all sorts of issues are that crisper cast nine

(05:43):
tends to not be as accurate as we want, and
so in the scissor cutting, the DNA part of the
whole issue of the whole process. Sometimes they don't cut
the right place, and so you have what are called
off target edits. Sometimes once it's cut and a gene

(06:04):
is put in a place, sometimes there are errors in
the repair process. Because the body, the cells have its
own repair process that this Chrisper CAST nine takes advantage of.
So that as after a gene is newly edited into
or even single nucleotide nucleotide changes, after they're edited, they

(06:26):
might not be repaired correctly, and sometimes that messes up
how the resulting proteins or the resulting processes work. So
one of the researchers who was in a big who
was also involved in pushing Crisper cast nine forward at
Harvard University.

Speaker 6 (06:47):
His lab was also involved in a big patent fight
against the Berkeley Lab with Jennifer Daudner and EMMANUELA. Arpentier.
And so this David lou his lab at Harvard has
just come up with not CAST nine, but a new

(07:08):
little sidecar crisper and it's called cast in it.

Speaker 7 (07:13):
Can we pause, Sorry, you sound like you're underwater all
of a sudden, Yes, and now you sound fine, la
la la laa. Now you sound great Okay, good. Continue
for like three sentences you sounded.

Speaker 4 (07:31):
Like you were underwater.

Speaker 1 (07:33):
Weird was wrong?

Speaker 4 (07:35):
Sorry? Continue. So there's a new sidecar called CASS.

Speaker 1 (07:40):
There's a new side No, CASS is the old CAST nine,
CAST five, CAST eleven, like, that's the old sidecar. Now
they're using it for other things. But there's a new
sidecar that's been developed, just published in science this last week,
with an associated enzyme called a Crisper associated transposese CAST.

Speaker 7 (08:03):
So these casts that so I didn't hear you, so
it was like cast but that's what you said before.

Speaker 1 (08:08):
Cast C A s T.

Speaker 4 (08:11):
Wow.

Speaker 7 (08:12):
Okay, the branding. I take issue with the branding. It's
too similar.

Speaker 1 (08:17):
Yes, I must, I'm supposed to in radio. You're supposed
to mind your p's, q's and t's. Yeah, you don't
know pop for the popping the plosives. Anyway, This Crisper
associated transposese also comes from bacteria, and it is used

(08:38):
within bacteria for jumping genes. So these Crisper associated transpose
they're already in bacteria with crispers. They work with as
an enzyme with crispers to help these jumping genes move
around within a cell. Right, I don't want to be

(08:59):
here anymore. Are let's jump on out and across the
chromosome and go jump into another part of the genome.
And this CASTE system is what helps it do that.
And so they were like, that's great. What they discovered though,
is that human cells don't like cast and so they

(09:20):
used a a focused evolution process where they pushed the
cast enzyme to exist and survive and be able to
work with crisper within human cells. And so this this

(09:41):
approach they used is called PACE, and ah it is
I'm not even gonna go there. But basically, each each
round of evolution, each generation, there's little tiny you know, tweaks, mutations,
et cetera. And eventually what they've done, they say, over

(10:01):
two hundred hours with PACE, which is basically several hundred
evolutionary generations, say the researchers. And if they were doing
conventional methods and not using PACE, it would have taken
years and years and years. But this took just over
two hundred hours. Yeah, it's fine. So they have this
evolved cast they're now calling an evo cast, and it

(10:22):
has ten mutations that have come up. It can work
well in human cells. And they were like, let's try
it out. And so they tried to see how evocast
and Crisper would work to basically do some gene editing
in cells, and they found that it increased. So previously
when they tried to use cast in cells, it was

(10:44):
like one percent that actually worked, and this time it
was like twelve to fifteen percent. So they've one hundred
x two hundred. They've really amped up how well it works.
It still doesn't work really well well, but.

Speaker 4 (11:03):
It's better. Still, we're going to edit.

Speaker 1 (11:07):
Yeah, we're going to edit your genes, and you know,
it may or may not work. So it's still not
ready for prime time, is where they're at. But what
the methodology they're using has done is created a potential new,
not as scissor ish way for the UH for the

(11:30):
genetting to take place. So because of the way cast
works and the way it integrates genes or whatever they're
trying to put in with the Crisper system into the genome,
you don't have to rely on the same kind of
cutting and then repair, and so the accuracy is better.
There are fewer mutations or errors that occur in the

(11:50):
repair process, so they have lower accuracy in terms of
actually getting genes in or efficiency, I guess, but it's better.
So hopefully they'll be able to improve how well it
works to be able to get it to the right
cells in the body. Maybe they'll be using it to
edit like immune cells for Cartie cancer therapy. Yeah, so

(12:16):
researchers are pushing forward improving our ability to edit everything.

Speaker 4 (12:25):
Nice.

Speaker 1 (12:26):
That's interesting.

Speaker 4 (12:27):
I mean, Crisper.

Speaker 7 (12:29):
Crisper's been on the on the on the field, I
guess for a pretty long time.

Speaker 4 (12:36):
And I think a lot of promises were made very
early on.

Speaker 1 (12:41):
How often.

Speaker 7 (12:44):
Of course, of course, of course, but I think that
it happens a lot. But I think the difference is
that in this case they're like, oops, we over promised
and under delivered. And so there's other kind of company
group of researchers, whatever you wanna call it. It's like,
what can we take from this very lofty promise? What

(13:07):
can we tweak and what can we adapt to actually
try to get somewhere. It's honestly, it's surprising to me
it's taken this long that for somebody else to look
at Crisper Cast nine and go, okay, what's what can
I what can I tweak? Here, especially with you know,
what can I tweak here to have my own proprietary.

Speaker 4 (13:30):
Product. That's the other piece that I'm well, I mean
that has taken this long.

Speaker 1 (13:35):
That's I mean, that's the thing. The way that the
patent fight came out. This lab actually won most of
the patents again for the Crisper research, even though auDNA
and Charpentier were the first to publish. Anyway, there's a
whole thing.

Speaker 7 (13:53):
There's of course, there's lots of like sci fi dystopian
things that we could think about with with Crisper.

Speaker 4 (13:59):
Of course, you know you can always go there. But
I like to assume that because also just because if
I can still be jaded, there's so much money to
make in medicinal approach. Oh absolutely not, But there's optimism
in my jaded state right where, Yeah, there's a lot
of money to be made in the medical approach of

(14:21):
using gene editing. So sure, I'm optimistic that they will
find a way to make this work to help keep
people healthy longer, because there is money to make.

Speaker 1 (14:38):
I mean, right now, with the system we have, it's
a good reward, right like ye help, absolutely, it's good.
Do good have money? That's fine? Anyway. I don't think
they're getting all the money yet, but.

Speaker 4 (14:54):
They could, which is why they're scrambling for the pat.

Speaker 1 (14:58):
So on the line line of Crisper and this new
cast sidecar. There's also another story this week that I
thought was interesting and you're gonna love it because it's
the world's first gene edited spider.

Speaker 4 (15:14):
Ooh, okay, to make it more friendly. No, oh, to
make it extra fuzzy. No, okay, what four? Six more? Guesses?
I could do six more? No extra legs, less legs?

Speaker 1 (15:34):
Okay, what thing about spiders? Are we like? Hey, this
is cool, we could maybe use this for leg people
technology sometimes like, oh, yes, silk, of course, spider silk.
So what did they do to the spider silk? They
incorporated a gene into the young developing, well, actually not developing.

(16:01):
I think it was un uh, I don't. I think
it was before before there were actually eggs. I'm not
sure the eggs were there, but before anything happened to them,
the unfertilized eggs unfertilized. Thank you, I forgot words. Uh.

(16:22):
So the offspring got a gene to spin silk with
red fluorescent protein red silk. Yes, So the silk that
was made by these spiders is red fluorescent silk. Why well,

(16:50):
number one, spiders have been neglected in terms of gene editing. Okay,
we talked about Spider Man. What about Spider Spider.

Speaker 7 (17:00):
So you know there's Spiders Man. Did you know that
that is a man made of many many spiders. There's
also Man Spider, which is a man sized spider.

Speaker 4 (17:17):
So there's lots of variations in the Spider Man universe.

Speaker 7 (17:23):
And actually Spider Man turned into Man Spider because of
gene editing.

Speaker 4 (17:28):
I will tell you I do believe that is the story.
The chartroom can correct me if I'm wrong, but at
least in the cartoon.

Speaker 1 (17:35):
How often has it gone the other way where the
spider was gene edited and then turned into man Spider
or Spider Man. Right, spiders right or whatever?

Speaker 5 (17:45):
Right?

Speaker 4 (17:45):
Right?

Speaker 1 (17:46):
Spiders? Spiders have been neglected, and so these researchers, you know,
felt sad, I said let's do something cool, and so
they gene edited the spiders. But also because Spider's silk
is one of the interesting parts of spiders that we
pay attention to, and that if we can gene edit

(18:11):
the silk without messing up its formation, or construction while
it's being spun. Then that's actually kind of a neat thing,
like what could we put what other proteins can we
put in that don't destroy the tensile strength or the
potential uses for spider silk. So they used crisper Cast
nine to uh to do this.

Speaker 4 (18:35):
Interesting, So in what.

Speaker 1 (18:39):
In what.

Speaker 4 (18:41):
Scenario would we want to edit the nature of spider silk.

Speaker 1 (18:50):
When you want it to warning before you walk in?

Speaker 4 (18:58):
Yeah, so if you if you make it so you
can see it, then it defeeds the purpose of them
actually being able to catch things.

Speaker 1 (19:06):
Yeah. The other side of this story is they were
not just interested in the silk fiber engineering. They were
looking at other ways that they could not just knock
in a gene, but also knock out a gene. And
so with the crisper Cast nine they did a knockout
of the gene sinae oculus, which resulted in spiders without

(19:29):
any eyes. What No, Yeah, I don't like that part
of the study.

Speaker 4 (19:37):
It's not nice.

Speaker 1 (19:40):
Yeah, I mean I guess.

Speaker 4 (19:43):
Okay, So in thinking about all of the.

Speaker 7 (19:47):
All of the editing we do to mice, right, and
all of the knockouts that we do in mice to
test so I can see, Okay, we knocked out the
eyes in some spider to figure out how much they
use vibration in communication and navigation or something like that. Right,

(20:08):
like you could if I, if I, if I forget
about just the optics ha of this, sorry, and I
look at it in terms of how we use other
scientific models like fruitflies, like mice.

Speaker 4 (20:26):
Right, we do this kind of stuff all the time.
Just saying that you were you had them grow up
without eyes seem so wild, But yes, there is some
scientific precedence for doing things like this.

Speaker 1 (20:45):
So part of it is number one, Like I said,
the spiders have been neglected, so can this it's proof
of concept? Does this work and do how does it
impact the developing organism? And what they were able to
show is that they understand enough to successfully be able
to uh have spiders develop in live lives with red

(21:10):
spinning red fluorescent spider silk or not having eyes. And
as much as it's like right now, you go, what
what's going on the next question is, you know, if
we understand how these things work in spiders, you know
what more can that teach us? If we start looking
at it very specifically in terms of knocking genes in

(21:34):
or out to study evolution development, like to ask questions
related to comparative biology. How do the how do these
organisms which are the same genes that make these particular
traits happen? And spider's exactly the same as crabs or
humans or you know, how does it all work? So

(21:56):
there are specific questions that can be asked if this
process works properly. And now we know it does, and
we don't have to neglect spiders anymore.

Speaker 7 (22:06):
Now we have red fluorescent silk, and I will say
fada in the chat room. Ast haven't we brought stories
before about spider silk being used for all sorts of
new purposes? So occasionally, but the grand majority of stories
that I have seen related to spider silk is about
studying silk to be able to make similar substances artificially,

(22:28):
not about like farming spiders for silk for human use.

Speaker 4 (22:31):
I feel like that is not generally the narrative. It's
like we studied the silk to figure out about the
tensile strength and try to replicate it.

Speaker 1 (22:39):
And like as it's being formed in the spider, there
are very particular proteins that come together and there's a
very specific chemical process that leads to the silk that
comes out. And so for ages, it's been can we
create spider silk? And couldn't for a really long time,

(23:01):
And I think it was like a few years ago
when somebody actually was like, oh, I think I might
have figured it out. And nobody's wearing spider silk shirts
right now that I'm aware of. No, but maybe they
would if they were fluorescent red. Yeah, no, but anyway, Yeah,

(23:22):
Christopher cast nine, So fascinating. What do you want to
talk about there?

Speaker 4 (23:27):
Oh, I have bad news. Unfortunately it's.

Speaker 1 (23:34):
Right up front again.

Speaker 7 (23:35):
Yeah, I'm not gonna I'm not gonna mince words here.
The Trump administration is going to kill a bunch of
endangered species. That's ultimately what's happening here, because they are
gutting the.

Speaker 4 (23:48):
Endangered Species Act.

Speaker 7 (23:52):
And I wanted to bring it up because this is
where conservation science and politics do collide, happens, and we
do need to talk about it because there is going
to be some fallout. So the Endangered secies that passed
in nineteen seventy three, and it bans some of the
kind of legal eases the take of endangered species of

(24:12):
fish or wildlife, including harming protected species.

Speaker 4 (24:16):
And in nineteen seventy five they had to define harm
legally what is harm? So take is very clear, did
you remove that animal alive or dead from their space?
But what is harm of a protected species?

Speaker 7 (24:34):
And so they included the number one cause for animals
to be threatened or endangered, which is.

Speaker 1 (24:44):
People.

Speaker 4 (24:45):
Yes, but what what activity that people.

Speaker 1 (24:48):
Do building these houses? Living?

Speaker 4 (24:51):
Yes?

Speaker 7 (24:52):
So usually, like when I used to teach our biodiversity
basics programs and the zoomobile, the kids would always say hunting.

Speaker 4 (25:00):
Hunting is the number one cause. Nope, like pollution, Nope,
it's not pollution, it's habitat destruction.

Speaker 7 (25:10):
Habitat destruction is responsible for eighty one percent of animals
being listed as threatened or endangered. Direct hunting or poaching
is only about seventeen percent. Sometimes it's less depending on
how you count things. And so habitat destruction is the
number one cause of threats to protect its species. And

(25:32):
so since nineteen seventy five it has been clear that
habitat destruction is included in the Endangered Species Act. Now,
in nineteen ninety five, there was a Supreme Court case
Babbitt versus Sweet Home Chapter of Communities for Great Organ, Oregon,
sorry which the Supreme Court ruled that the definition was

(25:54):
reasonable and allowed federal agencies to continue using it. But
now the Trump administration is planning on changing the definition
of the word harm to leave out habitat modification. And
so the plan is essentially to create free rein to

(26:15):
develop on protected animals' habitats. There's about one hundred and
seven million acres of land in the US designated as
critical habitat for endangered species. So they're not listed as
protected open space, they're not listed as a national park.
They are listed as designated critical habitat for endangered species.

(26:39):
The only reason that one hundred and seven million acres
of land is protected from development is because there is
a protected.

Speaker 4 (26:45):
Species in that space. And so the second you change
this definition of harm, that is when these lands are
open for drilling, development, any number of other things, logging
that different industries and stakeholders would have interest in using.

(27:08):
And so.

Speaker 7 (27:11):
This isn't in effect yet it was open for public comment.
The kind of the glimmer of hope I will give
you is that in the about month month and a
half that it was opened for public comment it close.
Two days ago, three hundred and forty five thousand people
left comments.

Speaker 4 (27:33):
Urging the government to not do this. Now, I don't
think that's.

Speaker 7 (27:36):
Necessarily going to do anything, but that means that the
general public is very much in support of the Endangered
Species Act. It is there is bipartisan support for the
Endangered Species Act. People generally all want to keep it
and think that it is a good thing.

Speaker 4 (27:54):
And so the general public have really spoken out about
this and demanded that this not occur.

Speaker 7 (28:02):
Unlikely that will cause anything. Likely, this change will still
go into effect. The other interesting pieces because of that
nineteen ninety five Supreme Court ruling. There will be legal
challenges if this does get changed, But the problem is
in the amount of time that it takes for that
legal challenge to be seen and heard. And even if
this change is overruled and returned to the original definition

(28:27):
of harm, there is no guarantee that land will not
get sold and developed in that period of time in between.

Speaker 4 (28:39):
So I tell you this.

Speaker 7 (28:41):
I know it's too late to do anything about it.
People have already left their public comments, but just so
you are aware what is going on and how there
are people working behind the scenes who actually are pretty
smart and know how to tweak specific language legally to
cause real harm to the positive progress we are made

(29:04):
towards the environment. Harm, real harm, yes, the actual meaning
of the word harm. Right, So, like, I just bring
it up so that we know what we're dealing with,
so we recognize that this is.

Speaker 4 (29:19):
An area of concern.

Speaker 7 (29:23):
If you have the ear of your local politician, go
ahead and call them and shout about this. Like Congress
wrote the Endangered Species Act. They wrote it, and I
have a where is it.

Speaker 1 (29:37):
A lot of help from scientists? Absolutely, yes, so it yeah,
go ahead, my partisan it was also my partisan.

Speaker 4 (29:46):
Yes.

Speaker 1 (29:46):
This is not just oh one side or the other.
This is not this is Congress.

Speaker 4 (29:51):
Yes.

Speaker 7 (29:51):
And so in nineteen seventy three, Congress wrote when they
enacted the Dangerousies Act, that it is to quote, provide
a means whereby the ecosystems upon which endangered species and
threatened species depend may be conserved, and to provide a
program for the conservation of such endangered species and threatened species.

(30:13):
So Congress wanted it, the general public wants it. The
Supreme Court ruled in favor of it. But there are
the powers that be that want to just unilaterally do
the right thing fiscally for themselves, and so I had
to daylight it. I don't really have a very high

(30:34):
bright side right now, other than to hope that it
either somebody steps up and recognizes how unpopular this is
and it does not go through, or that the legal
action resulting goes the right way and proceeds quickly so
we don't lose too much land. Those are the two
things that I can help for at this point. But
this is pretty bleak.

Speaker 1 (30:56):
And I want to come back and say it's this
is the the downside, right, This is the bleakness. This
is the are people. Are we going to be able
to do the right thing? Can we can we make
can we put up pressure against these movements? This is
not a said and done thing aside from the comments,

(31:18):
this is this is the part of the civic act,
part of science right where you're involved in the process
of how science is integrated into public policy, how everything
moves forward. It's talking to your representatives dot org. I.
I mean, there are lists of things that we could
be calling about every single day, but this is one

(31:41):
of those things where I think it's important too. Law
like science has its own definitions of words. And it's
only through those definitions that we have this very specific
way of focusing on information and being able to speak
to each other in a very accurate way. But when

(32:03):
you use that not as a tool to make things better,
but as a weapon, then it's it's something that it's
something that we all need to be aware of. And
this is the it's just a theory, right. We've been
talking about words in science for so long, and this

(32:25):
is where that is important. Where people need to know
how words matter, not just the way you understand them,
but the way that other people use them. So I
think even if change is made, it was one way once,

(32:45):
it can be one way and it can be another
way again. So even if something happens to change this
and it's a slow process, there's a whole bunch of
stuff that's going to need to be fixed. But this
is one of those things that I don't think people
will back down form.

Speaker 7 (33:00):
So no, the public will not allow this to go quietly.
I mean all of us will not allow this to
go quietly. The Endangered Species Actor, this is more than
fifty years of conservation work that has completely turned the
tide on species in this country.

Speaker 1 (33:19):
And so, but I think the thing for anyone out
anyone in the audience who wants to have a conversation
with people about why this matters. If we continue to
destroy diversity in ecosystems around our planet, our planet is

(33:40):
going to It's already moving certain ways. Species are dying anthropostine, YadA, YadA, YadA.
But if we prioritize our uses are wants to take things.
I'm going to use the word take things out of
the land for our own use is over being able

(34:02):
to exist on this planet in the long term. What
we're doing is we are going to shorten the ability
of humans to live on this planet. Might be great
short term, but it's certainly not going to go long term.
So preserving diversity, preserves ecosystems, preserves biosphere, preserves life on

(34:26):
Earth generally. And yeah, am I wrong, Blair? That's I mean,
it's like I mean, people are like, I need that
butterfly to move so I can build my condos. We
need housing. Housing's great, but we have to figure out
how to make things work in a more integrated way.

(34:50):
How can you do development in a way that maintains ecosystems,
habitats and doesn't destroy How can we have how can
we meet our thirty percent goal? Right?

Speaker 7 (35:00):
How can we We've found a lot of ways. I
think that's why I'm feeling so frustrated by all of
this is we've made great headway in the last fifty years.
We've brought animals back from the brink of extinction. We
outlawed DDT, We brought back the California condor, we brought
back the bald ego, we brought back the American alligator.

(35:21):
We did all of these things through the Endangered Species Inact.
And we built we built tunnels under road people.

Speaker 1 (35:30):
But you stopped people from mining and using land the
way they wanted to, so people couldn't do stuff with
the land that would make them money. So yeah, I mean,
come on, okay, but what about this.

Speaker 4 (35:47):
What about all of the people who work in environmental compliance.
What about all of the people who monitor in dangered
species around construction sites. Those are all going to be
people that have less.

Speaker 7 (35:59):
Jobs now, so that also impacts the economy. Economy, No,
because it is required because of the Endangered Species Act.

Speaker 4 (36:09):
So you still have to.

Speaker 7 (36:10):
Do environmental assessments, right, So the second you don't have
to do that there is an economic impact to that
as well. I think that's the piece that always gets
left out of this conversation is conservation does provide for
the economy one percent. There is a huge amount of
study around how biodiversity creates wealth for a community, and

(36:34):
when you remove biodiversity, wealth actually decreases in that space.
And I and this is where you're not measuring the
true cost of things. We're not measuring the impact of
these large boom and bust developments, and we're not measuring
the actual financial gain of conservation. And so it's put

(36:55):
as a cost benefit analysis, right.

Speaker 1 (36:57):
It's not the people there, it's not the priority they're
caring about.

Speaker 4 (37:02):
So it's right, it's lobbying.

Speaker 1 (37:05):
It's lobbying, and it's the way that people are misusing science.
It's cherry picking their information. They're not taking the full story.

Speaker 7 (37:14):
Yeah, yeah, absolutely, so there they're totally they're putting their
thumb on the scale, right because they're saying, oh, well,
if we build this development, that's feeding the economy. But
they're not looking at the fact that they're losing by
a diversity which costs money, and they're also eliminating conservation work.
So it's yes, it's totally unfair to why it is

(37:37):
a zero sum.

Speaker 1 (37:40):
And and why that location? Why? Why are maybe.

Speaker 7 (37:45):
Because there's already plenty of housing in the United States
for everyone to own a house, but it's all been
bought up by corporations. So you actually don't need to
build any more houses.

Speaker 4 (37:55):
What about that?

Speaker 1 (37:57):
I don't think that's actually true. Yeah, yeah, I mean
there's a lot. Yeah, there's a lot held.

Speaker 5 (38:03):
I know that.

Speaker 1 (38:04):
But yes, this is all that's a whole other game.
We're not going to get into that economics. That is
a debate, and I would need my list of facts
next to me to have it. It's getting hot in here.
Housing is the big thing right now. Like yeah, but
by moving backwards, by redefining the word harm for the

(38:29):
Indigous Species Act, we would be moving our society backwards.
That word being changed in that instance is also one
part of a landslide that changes the way that they're
able to get all sorts of things change. I don't

(38:51):
want to go backwards. No, I don't want to go
back That's we're doing a lot of that lately, I know,
but I think that sometimes you know, before we're going
back forward and back. You know, that's the whole two
steps for one step back two subs word, one step back.
But we have to make sure we keep working toward

(39:13):
that step forward, that next step forward, and not get
caught in the feeling of going backwards as this as
if that's where we're going to be forever, because this
is a moment, that's all. It's a moment. And I
mean we're not even talking about the Big Beautiful Bill

(39:39):
and the addition the poison pill within the Big beautiful
Bill to make sure that AI can never be regulated.
Have you heard about that one?

Speaker 4 (39:50):
No?

Speaker 5 (39:52):
Yeah?

Speaker 1 (39:52):
Yeah, So the Big Beautiful Bill that they're going all
night for recently has several poison pills, one to medicaid,
another that basically says AI no state can regulate any
AI technology whatever.

Speaker 4 (40:12):
I don't like that.

Speaker 1 (40:15):
They are a little the trojan it's a trojan horse bill.
There are things in there and it's God, take a look, everybody,
And that's the plans because you we need. It's a
trojan horse bill. I mean that happens with every bill.
Stuff gets shoved in and then you're like, what how
is that happening? But if they get it in and
then the methodology to fight it later is not there

(40:39):
because they've changed rules and various things. What's an issue?
So everybody pay attention. Do you want ai to rule
your life? Do you want harm to not really mean harm?
But what about bugs in space?

Speaker 4 (41:00):
They need really tiny helmets.

Speaker 1 (41:06):
That's really funny. Now I want to see that as
an animation or stop motion might be kind of funny.
Researchers have been looking at swabs from China's Changong space
station too, at look for bacteria. Like we've been talking
for years. This is usually a story that Justin would
talk about, talk about how there's so many bacteria in

(41:30):
clean rooms, how we have found bacteria on the International
Space Station previously. Well, now China's space station is part
of the club of having a new species of bacteria
they've discovered called Nealia Tiangong census. And this species is

(41:54):
related to an earth bound strain known as Niala circulands
And it's a usually rod shaped soil dwelling bacterium and
it's kind of thought of as pathogenic, a pathogetic form
of basilis. Anyway, these particular organisms and the others like

(42:16):
that we're found on the ISS. They the bacteria that evolved.
They are extremophiles, and one of the things that they
do is they form spores so that they can exist
and survive in the difficult radiation gravity, like all the

(42:36):
different strains not strain of bacteria, but the stresses of space.
And so this particular Niala Nealia tiangon zensis has it's
been published this last week. It's genes and functions, and
it's lost basically all sorts of genes that its relatives

(42:57):
normally have and others that have to to digest stuff
and get energy. The one thing it has is a
unique mutation that allows it to break down gelatine and
use gelatin as a source of nitrogen and carbon. And
that's really great because then it can use that to

(43:18):
create like a biofilm, which makes them makes the bacteria
stronger and more able to survive in space. The one
thing they don't know exactly they mutated to make their
own helmet. One of the things they don't know with
this yet because Nealia is related to Basilis, and basilisk

(43:43):
can call cause sepsis, and it's earthbound relative. Can we
kind of you know, can be toxic. They don't know
how bad it is or good it is for people
in space. So this is one of the interesting questions
and why they're doing these studies because you think you're

(44:05):
sending a clean ship to space, but basically you're sending
a ship to space with bacteria that have very survivalist
background And so the question is, in addition to their
new mutations for just existing, if they are related to

(44:28):
or come from pathogenic backgrounds, what does that mean for
these new evolved strains that exist in space? And what
does that mean about the pan spermia that are stations
are space stations, our space ship ships everything. What does

(44:49):
that mean about the for pam spermia of Earth organisms
into space and how they exist with humans?

Speaker 4 (45:02):
It just means it can't be avoided, which I think
we already knew, right, But are.

Speaker 1 (45:07):
They extra pathogenic? Like do any of the mutations? I mean,
so far realbody's been like, ah, I breathe and I
have sepsis, Like there's nothing like that.

Speaker 4 (45:14):
Right, Yes, Yeah.

Speaker 7 (45:16):
I feel like if that would have been a problem,
it would have happened already, right, Like we have people
living on the space station. We've sent people out to
space enough that I feel like people would keep coming
back with superbugs and be like, what the heck happened
to you?

Speaker 1 (45:31):
You didn't work out? You know? Oh yeah, I'm need
to compromise because I was in space and going to work. Yeah, Like,
do you know what I mean?

Speaker 7 (45:39):
It's the sample size isn't enormous, but it's also not
tiny of the number of people who've.

Speaker 4 (45:44):
Been to space.

Speaker 1 (45:46):
Not I mean any one sample set is pretty small,
but right time.

Speaker 4 (45:51):
But over time, I'm saying, the number of humans we've
shot into space is I.

Speaker 1 (45:56):
Think about it, It's like they're evolving and we just
heap sending different people. Yeah, that is very interesting.

Speaker 4 (46:07):
I don't know. I don't know. I mean, what's the
solution because our clean rooms can't handle it?

Speaker 1 (46:16):
Well, that's the question, right, how do you actually create
a really clean clean room because Bob and you, Oh no, guys, A.

Speaker 4 (46:31):
Teeny tiny one just in the room. It's insulated in
the room, right, I don't know. Yeah, that's the problem, right, like.

Speaker 1 (46:42):
Really long scrubbing bubbles. I don't know.

Speaker 7 (46:45):
So I guess this is identifying a need that now
more research has to go in how to make a
better clean room.

Speaker 4 (46:51):
That's really what what this story is about.

Speaker 1 (46:53):
Right, it is, but it's also it's either either or
how can you make a better clean room so that
we don't take more extremophiles to space? Or how do
we make sure we coexist with these new species in
a way that doesn't make humans sick? And can we

(47:15):
can we do it? And if we? I mean, I
think if we can't, we shouldn't be taking them with
us to other planets. That seems like I just.

Speaker 4 (47:24):
Take just take their helmet away.

Speaker 1 (47:26):
Are you draw were you drawing little space bugs? I know?

Speaker 4 (47:29):
Yeah? Here, let me turn off my blur.

Speaker 1 (47:33):
It doesn't want to it's gonna blur everything because even
though it's in the foreground, it's in the background. There
you go, gudy aw. We should make a sticker that's
really cute space bugs with helmets.

Speaker 4 (47:48):
I love that.

Speaker 1 (47:49):
It's really cute. I'm glad that I turned into like
a college lecture for you.

Speaker 4 (47:58):
Yeah, yeah, absolutely, I just I don't know. I started
thinking about germs wearing space helmets is funny.

Speaker 1 (48:11):
It is funny, and I'm really glad you went with it.
Had a pet paper and a pen next to you.
That that's amazing. All right, everybody, we're here and so
are you. Thank you for being here for this week
in science. Tell your friends about the fun times they
can have with Blair drawing little pictures of space bugs

(48:33):
and helmets if they were only here too. Oh my goodness.
Please tell your friends to subscribe. The more subscribers, the
more we can talk about using science, how science is
a part of our lives, how science is around us
every day, and we have more and more people to

(48:55):
talk about information and how we use it, how ye
analyze it, how we come across it in our lives,
and who we trust. So I'm really glad that you
trust us. I'm really really glad. Thank you for being here.
And oh, by the way, if you would like to
support us, we are listeners supported, so head over to

(49:16):
twist dot org, click on our Patreon link or the
Zazzle link and help us out. Thank you for your support.
We can't do it without you, all right, Blair? Are
you gonna draw through the animal corner?

Speaker 8 (49:31):
No?

Speaker 4 (49:32):
I can't possibly do that. I was just adding some
U is it gonna show you some planets and stars?
And I wrote space jure.

Speaker 1 (49:43):
I love it. I love that so much? Alrighty, well,
you all know coming back with more twists right now
for the second half, and it's time for Blaire's Animal Corner.

Speaker 4 (49:57):
With cry As.

Speaker 1 (50:02):
Five Pad Pad pad.

Speaker 5 (50:06):
You want to hear about animals.

Speaker 4 (50:10):
Except the more giant patterns.

Speaker 1 (50:19):
What you got, Blair?

Speaker 4 (50:20):
I have shrinking clownfish.

Speaker 1 (50:26):
What are they believes?

Speaker 4 (50:28):
Yes?

Speaker 7 (50:29):
So, so this this headline caught my eye because normally
when we talk about animals shrinking, it's figurative and it
means that over time they're not growing as large. So
generationally the space is exactly absolutely, but in this case,

(50:58):
individual clown fish are shrinking. They are growing up large
and then they are ending up smaller, and then they
are growing large again.

Speaker 4 (51:11):
So they are like losing body mass and size. Why yes.

Speaker 7 (51:17):
So this is from universities of Newcastle, Leeds and Boston
and they were looking at clownfish. They had one hundred
and one hundred and thirty four fish. One hundred of
those shrank when exposed to heat stress. They looked at

(51:42):
them over a period of five months, and so they
found that this phenomenon was actually very common. The only
other example that I was able to see sighted in
the study was actually with marine iguanas, where it sounds
like during similar environmental stresses that marine iguanas will actually
reabsorb some of their bone structure, some of their bone matter,

(52:04):
and they will also shrink. So this actually has been
recorded in the animal kingdom before. I wasn't even aware
of that. But this is crazy because clownfish are already
crazy because they're sequential hermaphrodites.

Speaker 4 (52:20):
They start out male, you.

Speaker 1 (52:23):
Know, oh right, crazy because.

Speaker 4 (52:28):
Yeah, they're sequential hermaphrodites.

Speaker 7 (52:30):
So they start out male, they're tiny, and then there's, however,
many females, right, they're large, and then if a female
dies or leaves and there is space for a female
in the area, then the male will get larger and
larger and larger, develop female body parts, and transition to

(52:51):
become a female individual and then lay eggs. So the
age old kind of joke from peopleeople who know about
clownfish and their sequential hermaphrodism is that Marlin and Finding
Nemo should actually turn female throughout the course of the
film because the mom dies.

Speaker 4 (53:11):
At the beginning, so it actually progress and change.

Speaker 7 (53:16):
So the reason I bring that up it has nothing
to do with this study, but it's relevant because there
is proof of the plasticity of the body plan. In clownfish,
they have other mechanisms to completely change the shape and
function of their body throughout their lifetime. So I would say,

(53:37):
out of all the places to look for this weird
adaptation where you shrink because of environmental pressure, it makes
sense it would come from a clownfish.

Speaker 4 (53:49):
So I had to dig through the plasticity.

Speaker 1 (53:52):
But shrinking is different from.

Speaker 7 (53:55):
Yes, so okay, yes, So I looked through a couple
of different pressure releases, and I dug through the actual paper,
and I was trying to figure out the mechanism and
why heat stress would cause you to shrink, which generally speaking,
climate change is causing animals to shrink. But again on

(54:16):
the plant, on the on the scale of generations, they're
not growing as large just because they have environmental pressure
and so there's more demands on their metabolism. That could
be that they can't find as much food because the
climate is impacting plants, or it could be because the

(54:37):
heat is causing them to sweat and lose energy through sweat. Right,
if they're an animal.

Speaker 1 (54:42):
That could sweat physiologically like, body surface area is a
big deal when it comes to heat and heat transfer
and heat loss. So that would be one big thing,
but this is fish. So I'm like, there's this they live, right.

Speaker 7 (54:58):
So one thing that they called out in the paper
that I found very interesting is called gill oxygen limitation theory.
And so cold water carries oxygen, hot water carries less oxygen,
and so if the water is hot, there's less oxygen.
But this is where this is get this gets really interesting.

(55:19):
Gills are essentially two dimensional. They're flat, and when you
increase the size of a two dimensional object, the surface
area does not increase at the same rate as a
three dimensional object, and so the three dimensional body size

(55:42):
increases the overall Yeah, so the amount of body that
needs to be oxygenated o outpieces the size of the
gills increasing.

Speaker 4 (55:55):
It's very interesting.

Speaker 7 (55:56):
And so that is one of the main hypotheses of
this of this research group, is that that is kind
of the main stressor that they're feeling.

Speaker 4 (56:08):
Of course, there's other things.

Speaker 7 (56:10):
They could have changes and food availability, as I mentioned
that the content of the food could change, and the
effort to find food could change. There's lots of things
that could be impacted by climate. But this, I think this,
this oxygen, this gill oxygen limitation theory is a really

(56:32):
good one to to kind of explain why this might
be happening.

Speaker 4 (56:37):
Now, how they're losing body mass, They don't do not know.
This is totally weird. They think it might be a
hormonal trigger. But that still doesn't explain the mechanism by
watch by which the body shrinks.

Speaker 7 (56:57):
Is it eating itself, what part of the body is
getting reabsorbed.

Speaker 4 (57:04):
There's lots and lots of questions to be had.

Speaker 1 (57:07):
So and so this happens when there's like extreme heating
in the water.

Speaker 7 (57:13):
And so they measured the lengths of these fish for
about five months, and during that five month period they shrink.

Speaker 1 (57:24):
So yeah, but then so there's that, But then there's
the you know, like you said, where did their food go?
Was there enough food? Were they just not hungry? Like
they just wanted to drink cucumber spritzers?

Speaker 4 (57:37):
Right, So that it's not to prevent.

Speaker 7 (57:40):
Them from growing any larger. But see that's the thing.
Their length reduced. It wasn't just their they're lighter, They
didn't get skinny.

Speaker 4 (57:50):
They shrink.

Speaker 7 (57:52):
It's as if you lost an inch, and it's not
you didn't change your posture, you actually lost an inch.
How what is the mechanism there by which you lose height.

Speaker 1 (58:03):
Oh, I know, they're like shrinky dinks. Yeah, because it's hot,
You're right, yeah, it just got hot.

Speaker 4 (58:12):
They shrink in the dryer basically.

Speaker 7 (58:16):
But yeah, So I think I will be interested to
see if this research group continues to study and bring
some things into the lab to try to replicate this
or I don't know.

Speaker 1 (58:29):
Well, see now I'm curious from just the morphology perspective
of like a length changed, but what about like their
spinal column? What about what was the distance between vertebrae,
Like what happened?

Speaker 4 (58:42):
Yeah? Did they just lose cartilage? Right? Great? Yeah?

Speaker 1 (58:46):
Is there a limitation to what can be lost for
them to shrink?

Speaker 4 (58:52):
Like?

Speaker 1 (58:53):
Or are they like the incredible shrinking fish and they
just are like I get small, they're the hotter it
gets well.

Speaker 7 (59:00):
And the question that I have from a conservation standpoint
is how long did it take them to get back
to the size they started at, Like did they rebound
once temperatures regulated?

Speaker 4 (59:11):
And what was the.

Speaker 7 (59:13):
Long term impact on the population, Because again, the fish
that can grow up bigger become female, and so if
you have a size impact over time, does that impact
your sex ratios?

Speaker 4 (59:27):
In your fish.

Speaker 1 (59:29):
How does it change mating?

Speaker 4 (59:31):
Does it change how many eggs they lay because they
weren't female as long? Like, there's so many ways you
could extrapolate.

Speaker 1 (59:39):
This and they're interesting also, like you said, because of
the relationship between the male and the female and the
guarding the eggs and the way that they can switch.
How does it change the behavioral dynamics of the animals.
So if the population's changing you have fewer females, more

(59:59):
male because of limitations and sizes, not just number of eggs,
but then fewer females, is there more competition between males?
And then with that like, yeah, exactly how does it
change everything? Does it change the way that females accept males? Like,
I don't know. Yeah, this is fascinating, it's lair mm hmm.

Speaker 4 (01:00:22):
It's really interesting. They did a little bit of social
research with these groups and they did find that the
mating pairs didn't get disrupted, so it seems like they
stayed enough of the same size that it didn't impact
what sex they were or their sex organs or anything
like that. But it it was also short and it

(01:00:44):
was only five months, but that.

Speaker 1 (01:00:47):
In itself is interesting. So they're like maybe shrinking together.
Like was their correlation between the mated pairs, did they
shrink together? And like you said, there's hormone changes that
lead to the sex differentiation that lead to these things, and.

Speaker 7 (01:01:01):
Yes, so so one of my favorite things is they
have a better chance of surviving.

Speaker 4 (01:01:06):
Yeah, go ahead, I.

Speaker 1 (01:01:08):
Was just gonna say the heat stress doesn't impact. It's
it's not changing the hormone balance that would normally impact
or maybe it's even blocking the pathway that would impact
the sex transition, Like I think, I don't. Yeah, I
wonder how it works together.

Speaker 7 (01:01:27):
You're onto something because the they did a lot of
interesting social interactions studies alongside this too, and they found
that the survival rates were the highest when they shrank
alongside their breeding partner.

Speaker 4 (01:01:41):
So they both shrank, so they can have.

Speaker 1 (01:01:46):
It shrinks together, Yeah, stays together.

Speaker 7 (01:01:52):
So the other the other piece of this that I
think this this reminds all of us to look out
for in the future, is that what other animals are shrinking,
what other animals are changing their body plan in some
way to respond to environmental impacts in a way that
we haven't previously assumed they could.

Speaker 4 (01:02:11):
Like it felt like a one way Street. You grow up,
you don't grow down.

Speaker 1 (01:02:16):
So what I wonder is, like clownfish you said they
have this variable body form already, but like, what if
what we're seeing because we didn't see so much of
this sex transition at the same time, what if it
is other fish species like changing sizes and how common

(01:02:36):
is that across species.

Speaker 4 (01:02:38):
Yeah.

Speaker 1 (01:02:40):
Clownfish, though, are really interesting because they're coral reef species. Yes,
so they're important to the whole coral reef ecosystem, which
is impacted by high temperatures. Yeah, that's the next step
of it.

Speaker 4 (01:02:54):
Yeah, they keep those anemonees healthy. Yeah. Mmm mmmmm. Let's
end on some heartwarming b brains, shall we?

Speaker 1 (01:03:06):
Heartwarming b brains? Okay, go for us? I thought you.

Speaker 7 (01:03:12):
Or organ systems B brains, which are you know, they're
about the size of a grain of rice.

Speaker 4 (01:03:19):
They're pretty complex, but they're still also not a lot
of neurons. It's a very small group of neurons.

Speaker 1 (01:03:29):
It's actually not a brain. It's a gangly.

Speaker 4 (01:03:31):
Yeah, it's like a it's like a nerve ball.

Speaker 7 (01:03:33):
But also it's kind of a brain because it still
has certain structures. It has optic lobes, it has a
central body, so like there's there's brainy things about it.
So for for ease of discussion, I will call it
a brain for.

Speaker 1 (01:03:50):
This story, I will accept that great.

Speaker 4 (01:03:56):
A study from the University of Trento suggests that bees
have sleep similar to humans, and that in fact, we
could use bee brains to learn about human sleep. We
know bees sleep, we know bees will go into torpor
when it's really cold, but the mechanism and then the

(01:04:21):
individual brain activity that happens during.

Speaker 7 (01:04:25):
Bee sleep has not been well studied. And what researchers
found is that sleep appairs appear in a bee appears
to carry a similar signature at a neuronal level to humans.
Not too surprising. I feel like sleep is pretty.

Speaker 1 (01:04:47):
It's common as yeah. Rest cycles are common in every
living creature down like from vertebrates to yeast. Like there
is it, yeah, an active cycle and an inactive cycle
that can be identified as something quote unquote sleep.

Speaker 5 (01:05:07):
Yeah.

Speaker 4 (01:05:08):
Right.

Speaker 7 (01:05:09):
So the researchers combined optical brain imaging, They used imaging
on these little bee balls and nerves, machine learning analysis,
and computational neural neural modeling to study how sleep influences
the neural networks responsible for sensory perception, specifically in the

(01:05:29):
atennal lobes, which are the olfactory centers smell centers, and
so they had data collected during the night when bees
naturally sleep. Their body movements were monitored with a front
facing camera. Their brain activity was simultaneously recorded with a

(01:05:49):
two photon microscope. They analyzed, Yeah, they analyzed the calcium
concentration in neurons and by doing that able to detect
neuronal activity during sleep and wakefulness. Don't think too hard
about the mechanism of this research. I don't want to

(01:06:11):
talk about it. I kind of started thinking about it
and went.

Speaker 5 (01:06:18):
No.

Speaker 7 (01:06:20):
So we've they showed that in resting states, you know
what I'm talking about, Kiki. In resting states, the brain
networks of bees they switched to synchronize and reduced information processing,
which is like.

Speaker 4 (01:06:33):
What happens in US. So, for example, if you look
at a single parameter like smell, the synaptic coupling between
neurons caused the brain to no longer decode odor signals.

Speaker 7 (01:06:48):
So they reduced olfactory perception, just like it does for us.
So they saw that basically they.

Speaker 4 (01:06:54):
Went kind of numb to stimuli around them that they
would normally notice during sleep and.

Speaker 1 (01:07:00):
That yeah, like our deep sleep cycles right.

Speaker 4 (01:07:02):
Right right, that you can sleep through crazy things happening
around you, and it's because a lot of things are
shut off, or you'd wake up at every gosh darn thing.

Speaker 7 (01:07:13):
This this is cool to learn for b specific reasons.
Of course, they get to look at pollinator health, they
get to look at ecosystem stability, They look at potential
impacts on be sleep and how that might impact bee's
effectiveness to pollinate the YadA, YadA, YadA. But the other

(01:07:33):
thing that it seems like researchers are really stoked on
related to this is that this creates an opportunity to
study sleep at the level of individual neurons in a
sample species that has a much simpler brain than humans.

(01:07:54):
And because they're seeing a parallel between what happens in
our brain and what happens in a B brain during sleep,
they can study the individual neurons in the B brain
to learn more about sleep disorders in humans.

Speaker 1 (01:08:10):
Yeah, I get that. Like, basically, the B brain in
this scenario becomes a model system that can be tweaked
absolutely turn stuff down. YEA, what makes a bee an insomniac?
What makes them wake up multiple times in the night, like.

Speaker 4 (01:08:29):
Yeah, yeah, what yeah?

Speaker 7 (01:08:33):
What what makes every little sound or smell wake up
a bee when their friend bees don't do that? Or
what makes this be impossible to wake up.

Speaker 1 (01:08:46):
Like my child on a school day. Yeah, no, I
think this is uh, this is one of This is
one of those studies where you go, this is like
the spiders, like what why? And what they are discovering
is a simplistic model where you've got a million, one

(01:09:08):
hundred thousand neurons that are so much easier to be
able to parse and specifically identify and work with for electrophysiology.
It's totally what you want m because you can identify
very specific things. So do we think bees are indicative

(01:09:29):
of all sorts of invertebrates because I mean this is like, hey, invertebrate,
you sleep like people.

Speaker 7 (01:09:37):
So par bees are a little complicated compared to some
other invertebrates because they are able to do very extensive mapping.

Speaker 4 (01:09:49):
That they can then communicate with one another.

Speaker 7 (01:09:52):
And so that's the other thing that they learned through
this study was how the brain processes and stores data
while it sleeps, and that they it's very similar to
how our brain works. So the sleep is restorative, but
it also provides an opportunity for them to file away

(01:10:15):
the root that they learned that day to the really good,
beautiful nectar memory consolidation exactly.

Speaker 4 (01:10:23):
Yes, And so.

Speaker 7 (01:10:26):
They believe that there's a similar process happening in the
bees' brains that happens in our brain. That's unclear whether
that exists in other invertebrates or not, but I think
bees were a really good model species because they knew
that this very specific memory pattern had to exist in
their brains.

Speaker 1 (01:10:44):
And now I want to know because we know now
that they have the deep sleep. It's very much like
human brain. Do they have rem sleep like it's for
humans rapid eye music, music movement, rapid eye movement, But

(01:11:04):
is there an equivalent? And it's so, I mean, for
an organism that's consolidating memory the way our brains do,
it is kind of during that there's this rapid eye
movement portion where the stories our brain is parsing all
the metaphors. It's different. I wonder if bees dream.

Speaker 4 (01:11:25):
I bet they do.

Speaker 1 (01:11:27):
I wonder, yeah, I wonder if they're a little antenna
twitch like a little dog.

Speaker 4 (01:11:32):
Leg I bet I bet they do, and I bet
it's really cute.

Speaker 1 (01:11:39):
Yeah, thank you for this. Of course, you've brought some
dolphin stories in the research past, and I found this
particular study really interesting this week, and I thought you'd
love to hear it. The question the researchers were trying

(01:12:01):
to ask is what are dolphins saying? And so no,
nobody really wants to know, but the researchers in this
work developed a They're using methodologies that have been used
previously to record sounds of calls from individuals, and they

(01:12:26):
use they do a trapping technique that they're doing anyway
on a specific population or specific populations in an area
to tag and assess health. And during that process, there's
a a net collection period where they get a number
of dolphins together in a net and then go through them.

(01:12:46):
And what they do is they use like a section
cup on the top of their melon and record any
calls that are made while they are going through this
non invasive process.

Speaker 4 (01:12:58):
Mmm.

Speaker 1 (01:13:00):
So their question in this not just what are they saying?
But this is what they say. They've built a unique
library of sounds produced by known individual common bottlenose dolphins,
and so what they have are signature whistles, which are
the whistles of very specific individuals, like you going, I'm Blair.

(01:13:27):
I don't know, you run out into public all the time.
I'm Blair. I'm Blair. That's your signature whistle. I'm like,
I'm Kiki. I'm Kiki. That's my signature whistle. That dolphins
have a signature whistle, and then there are non signature
whistles that all dolphins have, and so they were looking
to see the responses after they recorded a whole bunch

(01:13:49):
of different whistles from these dolphins of basically, do the
different dolphins have whistles in common, and do the common
non signature whistles seem to seem to correlate with certain
behaviors that would be like a certain assessment prom us humans.

(01:14:10):
And so they have their signature whistles and non signature whistles.
They have resident community of one hundred and seven seventy
dolphins and they've been studying these non signature whistles for
a while and in this particular study, what they discovered
is that these bottle nosed dolphins they not only responded

(01:14:30):
there and other signature whistles, but the way in which
they respond to the non signature whistles is not always
the same. And there are certain non signature whistles that
they were saying that they were more like a novelty,
curious kind of approach, so that these these singles would

(01:14:54):
be called them like a query, so that this non
signature whistle whistle, it's not just sometimes it's an alarm,
Like dudes, people vets what alarm versus what, you know,
a query? What's going on? So there's the I heard
my name, you called my name kind of responses. But

(01:15:16):
then these non non signature whistles, they call them very
creatively non signature whistle A and non signature whistle B
negative is A that's the alarm and B is the query.
And so I'm really surprised that this is one of
the first times that researchers are putting these whistles together

(01:15:38):
in this kind of way because we've been talking about
dolphins as social, vocal, you know, interesting species for a
very long time.

Speaker 4 (01:15:51):
I swear we've had studies like this before. We've talked
about how dolphins have been assigned.

Speaker 1 (01:15:57):
Names to each other, right, so that's the signature whistle, and.

Speaker 4 (01:16:01):
We've talked about vocabulary and syntax amongst different groups.

Speaker 1 (01:16:08):
Which is that's what I thought. I thought we've done that, Yeah,
which is why I wanted to talk about this, and like,
how is this study saying this is like the first evidence?

Speaker 4 (01:16:16):
Right, there's also an I think it's a different, distinct
study that's all about using AI to categorize different dolphin
sounds and use it to communicate with them.

Speaker 1 (01:16:30):
Yeah, you brought that story.

Speaker 4 (01:16:31):
That's going on right now.

Speaker 1 (01:16:33):
Yeah, So I found this one really interesting also because
they're like capturing the dolphins and using this uh suction
cup hydrophone to record them, and so they're going to
get a very limited sample set of calls, right, Like
it's going to.

Speaker 4 (01:16:51):
Be what, get this thing off my head.

Speaker 1 (01:16:55):
Get this thing off me, go away, you know, like
don't come over here, guys. So the sounds that you're
going to get from that, and they do acknowledge, oh well,
maybe you know the next we got to do a
more open wild animal sampling. But I just I thought
it was really interesting. I think what they were trying
to do with the suction cup hydrophones is get like

(01:17:15):
really direct and not underwater transferred recorded vocalizations, but like
the the actual all the frequencies and everything involved in
the calls that they're doing directly from their melon, which
it is their melon.

Speaker 4 (01:17:34):
Yeah, I'm seeing that there have been previous kind of
explanations of what different sounds mean.

Speaker 5 (01:17:43):
Yeah, and even looking at the spectrograms and the way
that they've put this whole study together, which is interesting.

Speaker 4 (01:17:55):
You know.

Speaker 1 (01:17:55):
So they've done the recording and then they did playback experiments,
but they didn't, like, I don't understand how they can
say in their title, this is the first evidence of
this work, you know, they had they looked at things like, oh,

(01:18:17):
we played music played, they played their songs back at them,
and they were ambivalent, you know that, but that means something,
you know, they're ignoring you. I don't know. I I
thought this was an interesting one from the way it
was hyped in the title and how it was being
put forward that.

Speaker 4 (01:18:37):
Yeah, I feel like you have to be really careful. Yeah,
go ahead.

Speaker 1 (01:18:41):
I would just say that they're not just saying, you know,
they're saying that this is the first evidence of language
possible language like communication and dolphins, And I am really wondering, abs, Oh,
that's true.

Speaker 7 (01:18:58):
I feel like whenever I see this is the first
time x y z or is recently discovered, the first evidence.

Speaker 4 (01:19:09):
Of x y z or.

Speaker 7 (01:19:11):
Anytime it's like the the very first or a new thing,
I always try to look really carefully to see if
there's a specific qualifier on it.

Speaker 4 (01:19:20):
So it's like, this is the first time we've studied
dolphin language on a Tuesday, Like you know what I mean,
Like just say some weird variable that makes it a first.
But this sounds like they're just claiming that it's a first,
And I really feel like we have we have talked

(01:19:41):
about this several times over many years.

Speaker 1 (01:19:46):
We have and I've always like we've talked about like
don't and some of guys they're talking to tail what's
going on? And of course they're calling it signature whistles,
I'm lair, I'm kiky. Then they're the other thing that's.

Speaker 9 (01:19:58):
Most animal communication is hello, But this is also you know,
beyond that, it's like does it go further?

Speaker 1 (01:20:09):
Do these vocalizations mean more? Is it not just alert
or query?

Speaker 4 (01:20:18):
Definitely?

Speaker 1 (01:20:19):
If they play, where does it go?

Speaker 4 (01:20:22):
They play? They have culture, They're like I want to
use this sponge, Well, I want to use this sponge.
They're communicating there's a very intense communication happening. There's also,
you know, beyond all the things that you mentioned, there's
the clicks and the squeaks and all the other things
that people who work directly with dolphins know what those

(01:20:42):
things mean, which means it is language.

Speaker 1 (01:20:46):
All of it inclusively together is part of it's part
in parcel. Right. So anyway, final point on this if
you see it in the news, this is a bio
arc study has not been peer reviewed, so hopefully it
will be peer reviewed and there will be I don't know,

(01:21:07):
maybe some adjustments before it's really published. But yeah, there's
a whole lot of issues with that study. But have
we talked about programs cell death a lot. We've talked
I love programs sell death apoptosis. When things go to

(01:21:29):
a certain state in your cells, calcium channels open and
they and then it's like, oh no, the calcium meter
is too high, and so the cell goes well that's
it for me, and a whole process of mechanisms take
place and then the cell dies. And this is it.

Speaker 7 (01:21:49):
Reminds me of just because it's easier for me to
picture big things and then scale them down. How like
octopuses go into senescence after they reproduce. It's basically program
cell death system wide.

Speaker 1 (01:22:06):
Right, yeah, and so like program sell death and little
scales or even sometimes on organ level scales, like sometimes
it works. It's right, and you need to have it
as part of development, not just death. It's part of life.
And this programmed cell death is an important process for

(01:22:26):
keeping an organism healthy. However, sometimes it's involved in things
like Alzheimer's disease or Parkinson's or you know, other neurodegenerative diseases.
And so researchers at Melbourne at Walter and Eliza Hall
Institute in Melbourne, Australia just published in Science Advances their
work trying to stop it, because hey, why stop the

(01:22:56):
cause when you can stop the process. So, if you
see lots of cell death, the cell death potentially is
part of in neurodigeneration, your brain, parts of your brain
dying off. And when they when your neurons die off,
then you lose the things that those neurons did. And

(01:23:17):
so if you could block it, maybe maybe that would
be good. I don't know. I am actually I question
this methodology because I don't know that it would be
better to block cell death if the processes that are
leading to cell death would negatively impact those neurons in

(01:23:39):
other ways that would be bad, Like is cell death
is yeah, this is this is an interesting question. But anyway,
the researchers have found a target, a protein called backs
that uh, there's a killer protein called backs, and it
kills cells by damaging mitochondria. But it's part of the

(01:24:03):
apoptosis programmed cell death process. And so these researchers were like, ooh, this,
look at a whole bunch of molecules, chemicals, et cetera.
And they found one that is specific to hitting backs,
and when it hits backs, it makes backs stop, and
so backs can't turn off mitochondria. And so I think

(01:24:26):
this is really interesting in the large scale conversation that
we've had over the last few years about the importance
of mitochondria and mitochondrial health to aging. Right, And so
there's this whole systemic question right where it's like, Okay,
there's something wrong with maybe the garbage disposal system in

(01:24:48):
the brain, maybe something wrong with mitchondria. I don't know,
but they are broken. And so because they're broken, apoptosis
starts and backs comes in and goes Okay, you're done
now and the cell needs to die. But if you
just stop backs from working, the broken stuff keeps going.

Speaker 4 (01:25:07):
Mm hmmm.

Speaker 1 (01:25:08):
Yeah, this is you don't have You you don't have neurodegeneration.

Speaker 5 (01:25:14):
You just have.

Speaker 1 (01:25:16):
I don't, and you guys have less functional neurons.

Speaker 7 (01:25:21):
You're treating the symptom and not the cause. Basically, right,
you're yep.

Speaker 4 (01:25:26):
So you're.

Speaker 7 (01:25:31):
You're putting a band aid on your cut, but your
blood won't clot, you know what I mean? Like you're like, oh,
I'm fixing the problem. No, you're fixing the symptom, not
the problem. Similarly, it feels too broad because some cells
need to go. There are conditions where too many cells

(01:25:53):
are going. But if you stop all of it, you're
gonna have huge problems.

Speaker 1 (01:26:00):
Yeah, yep.

Speaker 7 (01:26:02):
Yeah, So I keep vacuuming up legos, So I stopped
vacuuming the house entirely.

Speaker 4 (01:26:08):
Instead of picking up the legos.

Speaker 1 (01:26:12):
As, I'm having my child pick them up.

Speaker 4 (01:26:15):
Yeah.

Speaker 1 (01:26:17):
Yeah, So, I mean what I'm wondering it's I think
it's good to understand potential targets and places to act,
but I'm wondering if this, if they get it past
this just general understanding phase. Is this a worthy target
for therapeutics? And it would would it work with other

(01:26:38):
you know drugs that people are taking for their you
know symptoms.

Speaker 7 (01:26:44):
And I guess ultimately, if you're going to die from
Parkinson's or Alzheimer's, you could do with some junk cells
if you're not going to die, right, Like, like it's
a trade off in this case.

Speaker 1 (01:27:02):
I mean, and that's the question, Like we don't know.
All we know right now is they found this, like ooh,
we could block apoptosis. We could stop this molecule from
destroying mitochondria that are probably if they don't die, going
to impact the cell in other negative ways, because like
the reason you have apoptosis is so that this cell

(01:27:23):
doesn't go out of control, like it's a control factor.
But I know this is one of those things where
it's like, oh, let's just put like rabbits in Australia
and see what happens.

Speaker 4 (01:27:38):
So if you stop cell death, do you stop making
new cells?

Speaker 1 (01:27:43):
No?

Speaker 4 (01:27:44):
So that's bad too, right.

Speaker 1 (01:27:49):
Yeah, as you age, you have an increase in cell death,
not necessarily it depends on what stage of development, but
you also have a slowing of cell birth as well.
As you're aging but not stopping. It doesn't stop. And
so yeah, all of this is like when you have

(01:28:09):
the disease states. I mean, the ideal would be to
figure out exactly what's happening with the diseased disease state
and try and figure out how to target the costs.
Is it the mitochondria, is it, you know, the energy function?
Is it the garbage? You know? Is it your glial
cells not working? Or you know what else is going

(01:28:33):
on as opposed to, Hey, let's just let the broken
system keep working and see if that works so you
can limp along. But yeah, I nobody knows anything yet.
This is simply a study that has figured out this

(01:28:53):
mechanism with the idea that they're selling behind it, of
like maybe we could use this to stop a pup.
And I'm sitting here going please don't, please, please don't.
Oh my gosh, why would you do that? Ah? But
I'm not in charge.

Speaker 4 (01:29:10):
Well, rat studies coming next. Let's see, we'll see what happens.

Speaker 1 (01:29:16):
What about teeth?

Speaker 4 (01:29:19):
Yeah, you like them? I love having teeth.

Speaker 1 (01:29:25):
You know that they probably came from armored exoskeletons. Yes,
I did know that. That's really cool. All right, great,
we're done.

Speaker 7 (01:29:40):
No, actually I think that I thought what I was
taught in evolutionary biology was that they were most likely scales.

Speaker 1 (01:29:50):
Yes, so skates, rays they have, and sharks they have.

Speaker 4 (01:29:56):
These tooth like dermal dentical denticles.

Speaker 1 (01:30:01):
I love that word. Yes, so this is something that
we know. However, researchers just publishing in Nature. A researcher
at the University of Chicago and Neil Shubin's lab was like, Hey,
I want to see where I'm looking for. Actually, what

(01:30:24):
is the earliest vertebrate in the fossil record. And so
this researcher, yar A Heredy, took a whole bunch of
fossil specimens that she could identify as vertebrates because they
had these bumps, these denticles on the outside of them.

(01:30:45):
They're called odon toads. There's this sign is the presence
of dentin in these bumps in their external armor. Odon toads.
She got a bunch of bunch of specimens. She took
them to Argone National Laboratory Advanced Photon Source and stayed
up all night. She says, it was a night at

(01:31:06):
the particle accelerator that was fun. And they did high
resolution CT scans of all of these fossils, and what
she found was not the earliest evidence of a vertebrate
in the fossil record. What she found is evidence of

(01:31:27):
where the very first tooth like structure invertebrate tissues came from.
So they were looking at all of these and they
found one sample from the Cambrian fossil called anatolepsis, and
it looked like it had the ooton toads and everything.
Then they looked at it, they're like, oh my god.

(01:31:49):
And so they're looking at things. They found some that
had the dentin and others that didn't. There's one fossil
that they thought was a vertebrate, and everybody thinks it's
a vertebrate, but then they found it didn't have dentin
in it, and they're like, oh my gosh, it's an invertebrate.
So they completely moved a fossil to another part of
the taxa. But anyway, these dentin like tubules that's where

(01:32:15):
it all came from. And teeth. They say, this shows
us that teeth can also be sensory even when they're
not in the mouth. That's what Harden Parody says. So
there's sensitive armor in these fish, there's sensitive armor in
these arthropods. And it explains the confusion with these early
Cambrian animals. People thought it was the earliest vertebrate. Actually

(01:32:38):
it was an arthropod.

Speaker 4 (01:32:41):
Yeah.

Speaker 1 (01:32:42):
Sometimes sometimes we all need to spend the night at
Argone National Laboratory the t scans of ancient fossils to
look for evidence of things that we did, you know,
asking one question, but instead follow the evidence and answer another.

(01:33:02):
So it is Yeah, Pepticola in the chat is saying
lucky find and that is I think one of the
one of the things about the study that I think
is great is the researcher Harody didn't focus on what
they wanted out of the fossils. They followed what they got.
And so yeah, so we all get these denticles, odon, toads,

(01:33:30):
and denticles. I love these words too, right, they're great.
But the teeth in your mouth, as sensitive as they are,
at one point, maybe there were similar cells and instructions
on the outside of your ancestors body saying we're gonna
have sensitive teeth on the outside.

Speaker 4 (01:33:51):
So just imagine next time you're running your tongue across
your teeth. What if your teeth were made of skin,
But it's not skin, it's the equal because it's it's
on the outside of the body, right, So yeah, exactly,
it's sensitive like our skin is.

Speaker 1 (01:34:14):
The creepy direction, which is what if we were covered
in teeth?

Speaker 4 (01:34:20):
I think that looked cool. They just look like white scales,
kind of like a like a deco page. Is that
the right word?

Speaker 1 (01:34:30):
Do you like my teeth coat? What do you think?
What do you think of my teeth today?

Speaker 4 (01:34:37):
Mm hmm, yeah, deco page. I think that was right.

Speaker 1 (01:34:44):
But what if we had our whole bodies covered in
teeth and then like everyone's like, oh, I gotta go
to the store, and I like those bleach strips teeth.

Speaker 4 (01:34:56):
Oh man, never a dull moment.

Speaker 1 (01:35:02):
Have we done it? Blair?

Speaker 4 (01:35:03):
Oh yeah?

Speaker 7 (01:35:04):
Can you imagine getting getting a cavity on your skin?

Speaker 4 (01:35:09):
All right? Yes, now we're done.

Speaker 1 (01:35:12):
I love of toothpaste. You don't need soap in the shower,
you just need toothpaste.

Speaker 4 (01:35:23):
Yeah, we've done it.

Speaker 1 (01:35:25):
I wanted to make jokes about teeth coats all day, everybody. Blaire,
thank you for tonight, of.

Speaker 4 (01:35:33):
Course, thank you. What a fun night. Yeah, it was good.

Speaker 1 (01:35:37):
Everybody. Thank you for joining us for this episode of Twist.
We're so glad that you're here. I hope you had
a wonderful night. And now I want to thank especially
certain people, those of you in the chat room, Oh
my gosh, thank you for being here and chatting and
being just wonderful, wonderful people. Thank you for being real

(01:35:58):
and compassionate and respectful. I really love that. Gord Ur
and lare others who help with making sure everyone is
being being respectful and it's a good place to be.
Thank you. Thank you for being here for so long, too,
Identity for it. Thank you for recording the show. Fouda,
thank you for help with show notes and with social media.
I really appreciate it. And Rachel Rachel, thank you for

(01:36:21):
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(01:37:48):
click on that Patreon link. On next week's show, we.

Speaker 7 (01:37:52):
Will be back on Wednesday at eight pm Pacific time,
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Speaker 4 (01:38:13):
Sure sure yeah.

Speaker 7 (01:38:15):
For more information on anything you've heard here today, show
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Speaker 4 (01:38:23):
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you can also sign up for a newsletter. When that
pops up, it'll arrive somewhe somewhere, somehow. It'll be a surprise.
We love your feedback.

Speaker 7 (01:38:36):
If there's a topic you would like us to cover
address or a suggestion for an interview, please let us
know on one of our social media accounts or better yet,
send us an email. Just be sure to put twists
t wis and the cerdic line, or your email will
be spam filtered into a red fluorescent spider web. We
look forward to discussing science with you again next week,

(01:38:59):
and if you anything from the show, remember.

Speaker 1 (01:39:04):
It's all in your head.

Speaker 8 (01:39:07):
This week in Science, This week in Science, This week
in Science, This week in Science, it's the end of
the world. So I'm setting up shop. Got my banner unfurled,
it says the scientist is in. I'm gonna sell my advice,

(01:39:28):
show them how.

Speaker 4 (01:39:29):
To stop the robots with a simple device.

Speaker 10 (01:39:32):
I'll reverse all the warming with a wave of my hand,
and oh it'll coffee is a couple of grass.

Speaker 3 (01:39:41):
Because this week science is.

Speaker 2 (01:39:43):
Coming your way, So everybody listens to what I say.

Speaker 8 (01:39:47):
I use the scientific.

Speaker 10 (01:39:49):
Method for all that it's worth, and I'll broadcast my.

Speaker 4 (01:39:52):
Opinion all over the.

Speaker 1 (01:39:56):
Well.

Speaker 10 (01:39:57):
It's this week of science.

Speaker 4 (01:39:59):
This weekend's science.

Speaker 2 (01:40:01):
This week in science, Science Science, Science, Science.

Speaker 10 (01:40:04):
This week in science, This weekend Science, This week in science,
This week in Science, This week in Science, This week
in Science, This week in Science

Speaker 3 (01:40:16):
This week in Science,
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