S2E07 - Genotype (Genetics) - Gaming with Science

Episode Transcript
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Jason (00:01):
Brian.

Brian (00:06):
Hello and welcome to the gaming with science podcast
where we talk about the sciencebehind some of your favorite
games.

Jason (00:13):
Today, we will be talking about Genotype by genius games.

Brian (00:19):
Hey, I'm Brian, and I am joined by a very special guest
today, an expert in plantgenetics. Jason Wallace, yay!

Jason (00:26):
Hey everyone. So I know you already know who I am, but
this is, like, today's topic iswhat I do for my bread and
butter. This is my researcharea. So we figured we'd run
with this. It's been a whilesince it's been just us for a
full episode. So

Brian (00:38):
yeah, it has. This is gonna be, this is gonna be
harder work than we normallyhave to do, but, you know, but
you are the expert today, so youare going to talk about it, and
I'm going to be here to ping youwith questions,

Unknown (00:47):
yeah, which means I probably should give a little
bit of background, because I'mnot sure I've ever done that. So
we're both researchers at theUniversity of Georgia, both
associate professors. Mybackground is in genetics and
molecular biology andinformatics, which basically
means studying very small thingsand how they get passed down
from organism to organism inbacteria and now plants. And my

(01:11):
specific area, which we may talkabout later, is quantitative
genetics, which is complextraits, but not actually the
very simple traits, like we'regoing to talk about with
Mendel's peas for today in thegame genotype, but traits that
are controlled by many, many,many genes and that have more
complex interactions.

Brian (01:28):
Cool, cool, cool, cool.

Jason (01:30):
Let's go ahead and start off with a fun science fact. And
Brian, I'm going to throw thisto you, because I'm going to be
talking a lot this episode

Brian (01:35):
Yeah. I mean, totally, totally fine. There was a paper
published recently in Nature,where they described and
identified the genes responsiblefor the last three of Mendel's
seven traits. So could not bemore appropriate for this game.
Four of the genes were known, soMendel studied seven different
traits.

Jason (01:54):
We'll talk about that later, and we'll probably talk
about this paper a lot later.Yeah,

Brian (01:59):
we probably will. Honestly, I'm hoping you can
explain it to me, because Istudy bacterial genetics, and
it's way easier than plantgenetics, but basically, the
four of the genes had beendescribed previously, three of
them had not. And this study wasa massive genome sequencing
effort across a huge diversityof domesticated and wild pea

(02:19):
species, and they were able todo something called a genome
wide association study. So theylooked to see which plants had a
particular phenotype, theylooked at their genotype, and
we're kind of able to say it'slike, well, if we look at this
sort of mathematically, we cansee that everything that has
this feature seems to be pointeddown to this region of the
genome. And we're able toidentify these last three genes

(02:41):
and and really it's interesting,right? Because we knew about
genetics way earlier than weunderstand how heredity actually
worked, how DNA worked, how anyof that stuff worked, because it
follows simple mathematicprinciples. And actually, what's
interesting is a lot of timesit's about how genes get broken.
And this study in particular wassort of understanding the for

(03:02):
the most part, the way thatthese traits were associated
with breaking these seven genesin very specific and very
different ways. It's a realsmorgasbord of different ways
that genes get busted, like lotslots of transposons interrupting
genes, lots of premature stopcodons interrupting protein
sequences. It's just everysingle one of them seems to tell

(03:22):
a unique story of all the waysthat you can break a gene.

Jason (03:25):
Brian, you just throw out so much vocabulary I have to
define for people now.

Brian (03:28):
Sorry, sorry.

Jason (03:28):
So we'll go over some of this later. So genotype,
phenotype, codon, transposon,like, if you don't know what
those mean, that's okay. Butbasically, the idea of the
studies, they looked at like 700different peas. And then they
did math, essentially to figureout, okay, we can see a bunch of
ways that these are differentfrom each other at the genetic
level, which of thesedifferences actually shows some

(03:51):
sort of association with thetraits we care about? And that's
how they were able to narrowdown on them. And they found a
bunch of different ways that,like Brian said, genes can be
broken basically, because mostof these are the original plant,
which biologists call the wildtype. It's something got broken
at some point, and humans said,Hey, I like that. And so we kept
it. It became more common insome of our varieties that we

(04:14):
cultivate. And so now it'scommon in, say, our domesticated
peas that people grow ingardens, or in some varieties of
them, but not in the wild ones.Usually, not always,

Brian (04:24):
yeah? So, like, and again, this is kind of a weird
science fact, because this isactually going to blend in with
our discussion of the game,right? But, like, yeah, okay, so
like, flower color, like,there's, there's a series of
gene. Have we talked about thatDNA really doesn't do very much.
Maybe, I feel like, maybe thisis the wrong story, because
honestly, discussing this paperis discussing this game, so
maybe we should just letourselves move ahead so we can

(04:44):
talk about it in more detail.

Unknown (04:46):
I think so probably yes, let's, let's let it go. All
right, so let's talk about thisgame then. So genotype by genius
games, basic stats, it's for oneto five players, obligatory
first player or single playermode takes about an hour to
play. Okay, ages 14 and up, butagain, depending on your kid, it
can be younger. I had a my nineyear old played it with me

(05:06):
several times, and she actuallyquite enjoyed it. So it is, it
is kind of complicated. Thereare a lot of moving parts to be
aware of. Suggested retail priceis about $60 which may be a bit
on the pricey side, but theyhave a bunch of custom
components. You get a bunch ofcustom dice, bunch of custom
punched out tokens, and sometrowel shaped meeples, which I
think are just lovely and such,because the whole point of this

(05:29):
game, the conceit of the game isthat you are playing assistants
to Gregor Mendel, who isessentially the father of modern
genetics. And we'll talk moreabout him in a bit. At Thomas
Abbey, way back in the 1800s andyou are essentially his field
assistants going out doing thework to try to get the data and
validate these traits he'sstudying in peas. And so you

(05:49):
have your little trowel meeples,which represent the work you're
putting in. You've got dice,which are the genes. And because
reproduction is a little bit ofa random process, you roll the
dice to figure out what types ofplants you get every generation.
The game is basically acombination of a worker
placement game and a draftinggame, because it goes into few
phases. In the first phase, youplace your little trowell

(06:11):
meeples to indicate what sort ofstuff you're doing. Most of this
is actually just set up for thesecond phase, where you roll
dice, and then you take turnspicking those dice to be able to
mark off your plants and scorepoints from them. And then there
is a third phase where you canbuy upgrades that will let you
do these things better in futurerounds. There's only five

(06:33):
rounds, so the game goes prettyfast, and the goal is to get as
many points as possible, whichmost of which happens from
marking off these pea plants,although there are a few other
things, partially competed.Plants are worth a few points.
You can pick up these littlecoin resources that are also
worth points, but generallythey're probably better spent
buying upgrades and otherthings, just because the pea

(06:54):
plants are really what give youthe most points.

Brian (06:56):
One of the things that I've noticed because, you know,
there's an entire ecosystem ofof teaching people how to play
games on YouTube and everything,I had a really hard time finding
good videos teaching how to playGenotype because that first
round, that setup round, doesn'tmake a lot of sense if you don't
understand what you're doing inthe second part, where you're
actually planting and and whileI understand the desire and the

(07:19):
impulse to well, "you shouldstart at the beginning. It's a
very good place to start."Actually, you should not start
at the beginning. You shouldstart at the two things so that
you understand what you'redoing. And it took a very long
time for me to wait, what are weeven doing here? Why are, what
does any of this mean? You gotto explain what it means before
you can understand how thosesetup activities even do
anything.

Jason (07:39):
But yeah, when I was explaining this to my kids, I
would do with a high leveloverview, like, this is what
you're doing. Here are yourplants. You're going to be
taking these dice in order tomark these off and do the broad
scope of the entire game. Andthen I would zoom in, like,
Okay, here's round one. Here areyour options in round one.
Here's round two. Here's what wedo here. So I give that overview
first, and it sounds like that'swhat the videos may be missing.

Brian (08:01):
I think we could put out a good how to play genotype
video. Maybe we should do that.I don't know.

Jason (08:05):
I have now explained it to my children twice, so I've
got practice. So Okay, put thattogether if you want.

Brian (08:10):
I mean, let's do it. Why not? It'll be a bonus thing. Can
I tell an anecdote about thisgame?

Jason (08:15):
Sure

Brian (08:16):
When I first got introduced to genotype, it was
on Jason and I's list of thingsto play for a long time, and we
went to our public library. Alot of your public libraries
actually have pretty goodcollections of games. So it's
like, oh, this is so excited. Iwanted to play this anyway, and
now I don't have to buy it,right? So we we checked it out,
we brought it home. I read thebook, I watched the videos. It
was getting late, so what I didwas I got the entire board all

(08:39):
nicely set up, taught my wifehow to play, and then we just
put a blanket down over it. It'slike, okay, well, it's too late
to play this tonight. We'regoing to play it in the morning.
We put a blanket down to protectit from our very wonderful, very
over affectionate and very Cat,cat who does like to knock
things over. Some of you canprobably suspect where this is
going. The blanket did notdissuade him. We wake up in the

(08:59):
morning and every component hasbeen scattered to the four winds
in every corner of the room. Wehad to search the entire house
to figure out where Meatball,which is the cast I'm had put
everything we found, everymeeple, we found every little
cardboard token. We foundeverything except for three of
these custom dice that we stillhave not found. They are hiding

(09:20):
somewhere in the house.Remember, I checked this out
from the library, so I had tobuy a whole copy of genotype so
that I could return an intactcopy to the library. So the copy
that we played is ourreplacement copy with a couple
of like, generic, faceless dicethat I had to draw the little
symbols on. So anyway, thankyou, Meatball for that good

(09:41):
story. We did get meatball froma local animal rescue called odd
paws that specializes in specialneeds cats and neonates. So if
you happen to live in Georgia orthe Athens area and you would be
interested in having a trulywonderful animal who will
destroy your board gameexperience, check out odd paws.

Jason (09:58):
Yes, and we're not being paid for that. Like,

Brian (10:00):
absolutely not

Jason (10:01):
Brian had a good experience, and wanted to give
them a plug. Yeah. So before wego on to the science, I want to
talk a little bit about the gameand playing the games. Like the
game went pretty fast. I thoughtit was enjoyable because it
seemed to have a good mix oflike, control and randomness. So
there is some amount ofrandomness there, but within the
constraints of that, there aredecisions I can make to position

(10:22):
myself in better positions, andthat's kind of the mix I like,
is where it's not fully under mycontrol, because then things
tend to get kind of staid andthey get predictable, but it's
not too random for me to thinkthat I have no power.

Brian (10:36):
Yeah, that makes sense.

Jason (10:37):
And in the vein of all good work replacement games,
there's always more things youwant to do than you can

Brian (10:41):
so many more.

Jason (10:43):
It's like, you want to buy all the upgrades. You want
to place all the meeples and allthat sort of and of course, one
of the upgrade you can buy isadditional meeples, which is I
always went for. But, man, thoseupgrades are expensive, and the
more they get bought, the moreexpensive they get. So it's
hard. There are definitely somerounds. It's like, I want an
upgrade and I have no money,therefore I must look at them
sadly and pass

Brian (11:03):
we should play this with a higher player count, because
one of the things about workerplacement games that two, just
two players, is that you don'treally that sort of like
competing for sparse resources,doesn't come out as severely
like in some of these like everytime you buy a resource, there's
a little thing that makes thatmore expensive, a little abacus
that clicks up one die. So like,if you're not first, it really

(11:27):
puts more emphasis on there'ssomething that you can do to
make sure that you'll be thefirst player in a round, and
that becomes very important. Theother thing is that, like, you
get series of assistants thatcome out that have special
abilities, you have tools thatcome out that have special
abilities. Those will only bethere for that round. If there's
something cool out there and youdon't get it right away, you may

(11:50):
completely miss the opportunity.There's a huge FOMO associated
with playing this game.

Jason (11:55):
Oh yeah, this game is built around FOMO is, like,
every turn, all the pea plants,all the tools, all the
assistants, they get wiped andreset. And so, like, if you
don't grab it this turn, it'sgone, and depending on the deck
and how many players, it may notcome back.

Brian (12:09):
So lots of replay value. But man, you really feel
constrained with this one. Thisis a very, very worker
placement. Like, the idea ofworker placement, as you always
have to make hard decisionshere, and they always feel hard,

Jason (12:22):
yeah, but I'll say I had a lot of fun. Like I really
enjoy it. The game is beautiful.It's got very high quality art
and like tactile design. Thepieces the back of the game
board is this beautifulwatercolor of Thomas Abbey in
the Czech Republic. Theydefinitely put in their work to
make it a nice looking game, andin a game that is nice and
physically good to play, butalso has a lot of strategy and

(12:44):
tactics. Like I enjoyed thegame.

Brian (12:45):
They're sort of blending science and history in an
interesting way. I know some oftheir they have a game called
first in flight now, wherethey're talking about the Wright
brothers and the firstairplanes. And I can kind of see
they're sort of edging in thisdirection. This is a wonderful,
wonderful way of blending thesetwo things together.

Jason (13:00):
Plus, you probably figured there's only so many
scientific concepts thatconcepts that readily lend
themselves to a game,

Brian (13:04):
boo, no, that's not true. There's an infinite number of
scientific concepts that lendthemselves to games. We just, we
just reviewed a game that wascompletely based on a single
study. I think. No, no, no, no.

Jason (13:15):
Okay, fair. It does broaden their palate, though.
Yes, now they can. Now they canappeal to history buffs and not
just science buffs. Now, being agenius Games Game This, of
course, did half my work for me.It comes with a nice insert that
actually explains a lot of thebackground about Gregor Mendel
and genetics and all that stuff.I am not going to just

(13:35):
regurgitate that insert here,like if you want to read that,
buy the game, read the insert.They'll tell you stuff. We're
going to be talking about otherkind of broader picture things
here, but we will give somecontext. The core of this game
is about Mendel and genetics,and so we really need to give a
little bit of background aboutthat. Now, you probably learned
about Gregor Mendel in your likehigh school biology, because he

(13:57):
is the father of moderngenetics. He is arguably second
only to Charles Darwin in termsof the foundations of modern
biology. Mendel was a Christianmonk. He lived in the mid 1800s
he actually studied math andphysics at Vienna, which is
probably why he took thismathematical approach to
biology. And the thing he's mostfamous for is this work at

(14:18):
Thomas Abbey, which is in Brnoin the Czech Republic, where he
studied these seven differenttraits in pea plants over the
course of like, eight years. Andhe basically wanted to figure
out, Okay, how are theseinherited? Because this was an
active debate during his time,and it was actually an active
debate for like, 50 years afterhis time, maybe a bit more,
because Mendel's work wasunfortunately forgotten for

(14:39):
decades. He would publish it insort of like a mid tier journal.
Didn't get that much press, andapparently one of the issues was
that people didn't like reallythink it applied outside of
peas. It's like, okay, that'scute for pea plants, but what
does that mean for humans anddogs and all these other things?
And he got a little bit unlucky,because he did try to replicate

(15:03):
it with a different species, umhiratium. Common name is Hank
weed. I'd never heard of this.

Brian (15:10):
Hank weed interesting.

Jason (15:11):
Never heard of it. Don't know why it was picked.

Brian (15:13):
Is it pretty?

Jason (15:14):
It has a nice little orange flower that I saw. Okay,
but he there's a problem withHank weed in that. Now we know
that a lot of Hank weed and theones he studied are something
that are called apomictic, whichmeans that they make seeds
without going through sexualreproduction.

Brian (15:31):
That would be a problem.

Jason (15:32):
Yes, it is very problematic. It's basically the
plants do not really undergofertilization as normal, and so
a lot of the offspring arebasically clones of the parent.
Even though they're seeds, theyare clones, which completely
throws all of Mendel's work outthe window because he was
looking at inheritance throughnormal sexual reproduction, and

(15:53):
didn't realize that the secondplant he picked doesn't actually
do that.

Brian (15:57):
So he got really unlucky with his second pick, and
insanely lucky with his firstpick. I don't even know how to
explain. I'm trying to decidewhat level of detail we want to
go into here the seven traits,right? Yeah.

Jason (16:08):
So the luck with pea plants is they study these seven
traits, and the things that cameout of Mendel were called the
laws of segregation andindependence assortment. This
basically means, if you havevarieties for a trait, they go
independently of each other, andthat they can move off in a
different offspring. A very nontechnical definition there. But
the idea the independent one,especially, is that Mendel

(16:30):
thought every trait wasindependent of every other
trait. They did not care abouteach other. Now we know that's
incorrect, because all our genesare on the DNA. DNA is a long
string. It's in chromosomes.Genes that are close together on
a chromosome are actually notindependent. They tend to travel
together. And in fact, that'sthe basis of the genome wide
association study that wasmentioned in this in that paper

(16:53):
at the beginning is that you usethe fact that DNA that is close
to the gene you care about tendsto travel with it in order to
track it.

Brian (17:01):
What a wonderful modern paradox that the very study that
allowed us to identify thesegenes breaks the rules that
Mendel thought controlledgenetics.

Jason (17:09):
Yeah, basically. But the luck that Mendel got is that he
picked seven traits thathappened to either be all on
separate chromosomes, in whichcase they are independent or
very far apart on the samechromosome, far enough apart
that they act like they'reindependent, because within a
chromosome, there is a littlebit of breaking and shuffling
that happens between the genesyou got from your your

(17:30):
biological parents, and sothere's a little breaking and
reshuffling. So if you're farenough apart on a chromosome,
you are actually independent,and the ones he picked were far
enough apart. There is oneexception, there are two of his
traits that might be closeenough. And this gets into a
thing we don't actually knowwhich varieties of peas Mendel
was working with, so people havetried to figure this out based

(17:52):
off of what varieties wereavailable. What's out there in
the populations that big studyBrian mentioned, which we're
going to keep coming back to,found that for most of these
traits, there really is only onevariation out there. And so
that's what Mendel was workingwith. But some of them have a
few different ones. And so oneof the traits, I believe it, is
whether the pod is edible ornot.

Brian (18:12):
Yeah, the edible pod, they found, there are two genes
that control that, and theydon't know which one he had.

Jason (18:17):
They don't know which one he may have actually had both,
because they may have come fromdifferent ones. One of those is
actually close enough to theplant height gene that they are
linked. So if he worked withthose, and if he looked at that
particular combination, then hemight have seen that linkage
show up, that they are notindependent. But it seems like
either he didn't have thatversion, or he didn't look at

(18:37):
that combination very much, andso that his things about the
Independent Assortment hold forall the ones he worked out. They
hold in general, we've just nowknow that, as always, biology is
a lot more complicated than youthink at first, but in general,
that does pass, that does holdweight still.

Brian (18:54):
Can we talk about the seven traits and what they were?

Jason (18:56):
Yeah, sure. So seven traits, the game only includes
four of them. So the game hasthe round and wrinkled peas. So
whether your pee is round andplump or whether it's shriveled
and wrinkled when you dry itout, they have tall and short
plants, which is probably one ofthe most famous ones you get in
high school biology. It haswhether the pea pod is green or

(19:17):
yellow, and it has whether theflowers are purple or white. And
then the other three traits helooked at was whether the seed
is green or yellow, whether thepod is edible or the technical
one was like whether it'sinflated or constricted. So
inflated is kind of like thenormal pea pod you'd see, and

(19:38):
constricted or flat are like thesnow peas, where the pod is,
like a little flat thing, andyou could actually see the peas
poking out through it.

Brian (19:45):
Yeah, I think they're like, missing some kind of
papery parchment layer that isunpleasant to eat. So those are,
like, basically just thevegetable peas. You pull them
right off the plant and eatthem, and they're quite
delicious.

Jason (19:55):
And then the last one is about flower position.
Basically, do you have flowerskind of going all up the stem,
or are they all in one big groupat the top of the stem? And
those are his seven traits.

Brian (20:05):
Where did Mendel get his peas from? They had seed
catalogs in 18 in the 1800s andthese seven traits were listed
and being used by by peabreeders. Yeah,

Jason (20:16):
that's still a valid thing. I know the person who
works in the lab next to mestudies tomato fruit shape. And
when she was starting her lab,she just looked through the seed
catalog like, Oh, that was acool looking tomato. Let's order
that. The fascinating thing is,I say, we now know what every
one of these things does. We'veknown about the traits for 150
years. Breeders were using themfor decades before Mendel got a
hold of them. But it's only nowwe actually know the chemical

(20:39):
basis, the actual molecularchange that happened, because
every one of these is tied tosome sort of change in the DNA,
but the nature of that change isvery different, and actually
it's kind of cool with thatstudy, most of these have
different mechanisms forchanging, so almost all of these
are using a different way tobreak a gene. One or two of them
have a big chunk of DNA that gotinserted in the middle of it.

(21:02):
Some of them are these, what wecall selfish elements, or
transposons, jumping genes.Jumping genes, you may have
heard they're basically likeeven below a virus. They're just
a short stretch of DNA, maybeonly a few 100 or a few 1000
base pairs long. A base pair isone A, G, T or C, so very, very
short, that they basically onlycode for enough proteins to cut

(21:25):
themselves out or copythemselves out and stick them
somewhere else. They're not evena virus level, but they are
selfish, and they will jumparound your DNA and your body
thankfully has many, manysystems in place to stop them
from doing that, because it'sgenerally bad when a random
piece of DNA goes into someother part of your genome
because it usually breaks things

Brian (21:45):
well, they can't be doing too good of a job. I mean, a
huge percentage of our genomeand plant genomes are
transposons, right?

Jason (21:51):
Yeah. So if you've heard of how much of our genome is
junk DNA, a lot of that are theremnants of these, these selfish
elements, and they are doing avery good job. It's just when
you're talking over evolutionarytime, then you only have to let
one or two through pergeneration, and you get a lot. I
don't know what the rate is ofthose, suffice it, the mutation

(22:14):
rate in the game is way higherthan happens in normal life.

Brian (22:17):
I'm sensing a nitpick when we get to the end of the
episode

Jason (22:21):
The game designers pointed out. So it's not really
a nitpick anyway. So you've gotbig chunks of DNA that will sit
down in some of these genes andbreak them. The round, wrinkled
pea is due to one of those. Oneof these jumping genes went into
a, I think it's a gene thatcontrols starch, starch
production, and jumped intothat. Also the yellow versus

(22:41):
green seed one, I think there'sone there. It didn't jump into
the gene itself. It jumpednearby, and it broke how it's
regulated. So when it's turnedon and when it's turned off.

Brian (22:49):
Have we had a chance previously to talk about DNA and
how DNA works at all, or is thisour first time doing it on
gaming with science?

Jason (22:56):
I think it's our first time.

Brian (22:57):
Okay? I think we should just take a quick minute and
just talk about that, and atleast try to and try to make an
analogy. I'm sure we've allheard these analogies before.
What I think is interestingabout DNA is we talk about DNA a
lot. DNA, on its own, reallydoesn't do very much. It just
stores the information.

Jason (23:13):
It's kind of like the hard drive on your computer. If
you have just a hard drive, youcan't do all that much.

Brian (23:18):
So it codes that information in sort of like
Jason talked about base pairs,those As G, C's and T's, when
you're in a gene region, everythree bases codes for like a
letter corresponding to one ofthe 20 amino acids that make up
your proteins. So when the DNAgets read out, it's copied into
a strand of messenger, RNA, justa single stranded DNA-like copy

(23:41):
that then gets translated by theribosome into each of those
amino acids, which gets turnedinto little, a little chain of
these things that folds up intothe protein that actually does
the thing.

Jason (23:51):
If you want to hear more about that process, go see our
episode on cytosis, becausethat's basically the core of
that game. Is you have yourstart from your DNA, very true,
or your RNA, you go to proteinand all those sorts of other
stuff there. Yeah.

Brian (24:03):
So if you imagine that like your your little gene is
sort of a sentence or word,right? And then somebody takes a
whole nother sentence and jamsit into the middle of it. It the
sentence doesn't make any senseanymore. You've broken it,
right? So it's going to startjust fine. It's like a lorem
ipsum. And then it turns into,you know, absolute garbage. And
say, when you try to make theprotein from that gene, you

(24:26):
don't get a protein that works.You get a little busted up piece
of something that doesn't doanything.

Jason (24:30):
Yeah, it'd be like, if you have your, like, your book
library on the shelf and, like,you open it up to complete works
of William Shakespeare, you openup to a sonnet, and then you
paste in the middle of that,like

Brian (24:40):
Dr Seuss

Jason (24:40):
12 lines, yes, 12 lines from Dr Seuss, like, you've
broken the sonnet. It doesn'twork anymore, but this is the
basics of it stores information.That information gets moved out.
But because it's so complicated,there's various ways that can be
broken. So we talked about theselfish DNA coming in and either
breaking the gene itself orbreaking how. When it's turned
on and when it's turned off.

Brian (25:01):
Yeah, which kind of can do almost the same thing. It's
like, if the gene is there butnever gets turned on, then you
never get the protein, and itmight as well not be there.

Jason (25:10):
Yep, there's a few of these. So the tall, short
mutation for Mendel's peas isdue to a single letter change in
one gene that controls a plantgrowth hormone called
gibberellin. That's sort of thesmallest mutation you can have,
is you switch out one letter foranother. I think it's an A to a
G, but I could be wrong aboutthat.

Brian (25:29):
Yeah. So this is changing dear into bear, right? Big
change in meaning by changingthe one letter,

Jason (25:35):
wait, deer into bear? Those are two letters

Brian (25:36):
Like, Hi, my dear.

Jason (25:38):
Oh, okay. I was thinking two animals. I was like, there's
two letters difference. Therenot one. I thought you could
turn in Deer into beer.

Brian (25:46):
Yeah, we could do that too. Okay, definitely a bigger
change in meaning at that point.

Jason (25:52):
Anyway, you got those little individual letter
changes. There's one that isanother letter change. But
instead of changing the proteinthat comes out, it actually
changes the way that that theRNA, the secondary one that's
made, gets cut and pastedtogether. So it gets cut and
pasted together, wrong?
Oh, man, we are not going totalk about exons and introns,
are we?
No, we are not

Brian (26:11):
okay.

Jason (26:12):
Suffice to say, in us and most other complex organisms,
the DNA is not read directlyinto a protein. It goes to the
RNA. The RNA gets cut apart andthen re glued together. And if
something goes wrong there, itcan also mess up the protein.

Brian (26:26):
It's so unnecessarily complicated I don't understand.
Like bacteria really have thison lock. It's just the gene
looks just like the mRNA andgets made into protein. It's so
simple. I don't I don't knowwhat happened to you. Eukaryotes
drive me crazy. Humans,everything with a nucleus drives
me crazy.

Jason (26:46):
It's thought that cut and pasting is one reason why we can
get away with only like 20 or25,000 genes is because they can
be cut and pasted in differentways, and that's actually really
important for our braindevelopment. So don't knock it
too bad.

Brian (26:57):
Okay, okay, well, I guess I needed exons and introns to
have a brain complicated enoughto almost sort of understand
exons and introns.

Jason (27:06):
Other things are some small deletions. So little
sections get removed. And likeBrian was saying, since you have
groups of three bases makeessentially one amino acid, if
you remove anything that's not amultiple of three, you mess up
everything from there on out,and it usually just completely
screws up the protein. So all ofthese different, these are all

(27:26):
the different ways you can messup your DNA. It's, it's actually
kind of like those Co Op gameswhere there's only one way to
win and so many different waysto lose. A little bit. There are
so many ways to mess up yourDNA.

Brian (27:37):
And peas seem to these seven traits seem to cover,
like, again, a huge spectrum ofthe opportunities to break a
gene. Yes,

Jason (27:43):
so like, they show not every way, but they show a lot
of ways you can break genes,which is really cool. Mendel was
studying these traits in peas,and he gathered a bunch of data,
and he published it, and it kindof got neglected and forgotten
for like, 50 years. But thenaround the beginning of the 20th
century, there were actuallythree different people who

(28:03):
rediscovered them at the sametime. It was Hugo de Vreis, Carl
Correns, and Erich von Tsermach,people who were all working in
genetics at the time. I guessthey were all looking for
similar stuff, results, and sothey all found it, and within,
like, a year, they'd all sharedit with people, and they
rediscovered Mendel's genetics.This did not actually solve the
problem of genetics, which iswhat you may have heard in

(28:25):
biology, because there was araging debate going on about the
nature of genetics, and itlasted for another like 10 to 20
years, which was how inheritanceactually worked. And this
actually goes into play withCharles Darwin and evolution,
because one of the big issueswith Darwin's publishing
evolution by natural selectionis that it was an explanation,

(28:47):
but had no mechanism.

Brian (28:48):
Yeah, Darwin didn't know how genetics worked. Nobody did

Jason (28:51):
yeah, and he had some speculation. It turns out his
speculation was wrong. He he wasa he was in favor what's called
the blending model. And thismakes sense when you look at
like how humans behave. If youhave a tall human and a short
human, and they have a childtogether, you don't end up with
only a tall human, only tallchildren, or only short
children, or only children thatcome in exactly two heights.

(29:14):
They tend to be somewhere in themiddle. And humans don't come in
exactly two heights. We have allsorts of different heights, and
The Offspring tend to be a blendof the characteristics of their
parents.

Brian (29:23):
So the blending model, if you had a plant with a red
flower and a plant with a whiteflower, you would get a pink
flower. That's what the blendingmodel would predict,

Jason (29:30):
yes, and that was Darwin's idea about how it
worked. But the problem is thatif you do a little bit of math,
you realize that completelyundermines evolution by natural
selection, because pretty sooneverything is average and you
have no variation for evolutionto act on. The reason why
Mendel's work is so important isbecause it brought back the idea
of discrete genetics. And Ibelieve this was floating around
beforehand, but it actually gavedata to support that. Yes, this

(29:53):
is true is that genes arediscrete units that get passed
down wholesale, and so the.There is still variation there,
and there was argument betweenthe people who did the blending
and the people who did thediscrete stuff for a while,
although some mathematiciansshowed relatively quickly that
all you need is a bunch of genesthat affect the same trait and

(30:13):
you can end up with somethingthat looks like blending, and
that is essentially where we aretoday. This is called the modern
synthesis of biology where wehave genes as the basic unit of
heredity and information,they're all discrete, although
some of them are sometimes youhave a single trait that is
controlled by many, many, manyof them, and that natural

(30:34):
selection is the dominant,although not the only, force
that changes which genes getpassed down which ones survive
in populations over time. Thatis the modern synthesis of
biology. It is essentially whatall modern biology is built off
of, and it is extraordinarilypowerful. It's what's behind
pretty much all, maybe not all.I'm sure there's some

(30:55):
exceptions, but it's betweenbehind the vast majority of
biology research being donetoday.

Brian (31:00):
You used one of the trigger words. You said
dominant. So I think we shouldtalk about Punnett squares.

Jason (31:04):
Yes. Oh, okay, all right. Well, let's back off from the
big picture. Then about largescale biology. Let's talk about
what Mendel actually found.Because what he found is he
found the pea plants he wereworking he was working with. He
had tall ones and he had shortones. And when he crossed a tall
one with a short one and a crossis basically he took pollen from
one and put it on the pistol,the female part of the other,

(31:27):
and made seeds. So basically hemade offspring from a tall
parent and a short parent. Allof them were tall 100%. the
short. It looked like this shorttrait had been erased, except
when he then took those, allthose tall parent, those tall
offspring, and he let them selfpollinate so they fertilized
themselves, which is what peasnormally do, the offs their

(31:48):
offspring. So the grandchildrenof the original cross actually
came in both tall and shortvarieties, and they had about
three times as many tall ones asshort ones.

Brian (31:57):
You ever heard the old adage about things skipping a
generation? Yeah,

Jason (32:01):
that's basically what's going on here. And the the term
that came out of this isdominant and recessive. So we
need to define some vocabularyright here. A gene is a section
of DNA that controls a trait andthat is good enough for us.

Brian (32:14):
I'm realizing that us both like this, having it be
specifically in our area ofexpertise is not helping us,
sort of like skip jargon,

Jason (32:23):
I know we're doing what the best we can bear with us,
please gentle listeners as wegeek out about our own fields.
So anyway, that is your gene, asection of DNA that controls a
trait, an allele, is a variationat that gene that has different
trait values. So we have theheight gene here in the peas,

(32:43):
and it can have a tall alleleand a short allele, so a tall
version and a short version. Andthen what Brian was getting at
is that you have a dom, you canhave a dominant or a recessive
one. So dominant means that itkind of overrules The other
option. So in this case, tall isdominant to short. If you have a
tall allele, then it will maskthe short allele, whereas short

(33:06):
is recessive, where essentiallyyou need to be pure short.
Because the math of this is thatall the peas had two copies,

Brian (33:14):
one from mom and one from dad.

Jason (33:16):
Yeah, the original parents were either pure tall or
pure short. The first generationoffspring were a mix. They were
50/50, tall, short, but becausetall is dominant, they were all
tall. The offspring from thatare a random mix of that you get
randomly, one from the paternalline, one from the maternal
line, one from mom, one fromdad. When you're self
fertilizing, like in peas, momand dad's the same thing, but

(33:38):
it's still random which one youget. It's basically a roll of
the dice, which is why they haveyou rolling dice here in the
game. And so you have a 50%chance of your first one being
tall and 50% of being short, andalso the second one tall and
short. You work out the math.Three quarters of the time
you'll have at least one tallgene and you'll be tall. One
quarter of the time you'll haveboth short genes, and you'll be

(34:00):
short and that math is reflectedin the game. They actually have
what's called a Punnett Square,named for Dr Punnett, who, I
guess, used or popularized thesethat shows the gene combinations
you have, and that shows theprobability based on the die
rolls of what you what sort oftrait you get out and it's part
of the game. You can actuallyadjust those squares by

(34:21):
essentially picking differentparents to go into your cross to
make the ones that you want morelikely and or to make the ones
that your opponents want lesslikely or even impossible.

Brian (34:32):
Would it be okay if we dig into that just a little bit?
Because I think we've talkedabout broken genes and not
broken genes and alleles, but Ithink the idea that the
inheritance the dominantrecessive is tied to that in an
interesting way, is somethingthat a lot of people sort of
don't get introduced to. It'svery common for people to learn
about a Punnett Square and adominant and recessive gene. But
let's talk about that, what thatmeans, and let's we can use

(34:53):
specifically the example of thetall and short to do so, right?
Jason already said that the tallplants are able to make, is it a
receptor for the plant growthhormone, gibberellin, or is it
the actual synthesis itself?

Jason (35:05):
I think it's the actual hormone gibberellin itself.

Brian (35:08):
Let's just, let's just assume that it is, because it's
easier to discuss it that way.So if you've got the functional,
wild type version of thegibberellin gene, you're making
this plant growth hormone, whichis why you're able to grow tall,
right? If you have the brokenversion of the gene, you're not
making that hormone, so you stayshort, right? So if you imagine
this, it's like if you'regetting a wild type copy of the

(35:29):
gene from one parent and abroken copy of the gene from the
other, you still have oneworking copy. You're still
making the gibberellin. So youlook like the wild type strain,
right? So that's why the onewith the mixture ends up being
tall because it has one copy ofthe working gene, and that's all
you really need.

Jason (35:45):
And important to point out, in this specific instance,
one copy is enough. There areother instances where it's not
where you would if you had onecopy, you would be medium height
because you had more than theshort one, but less than the
tall one.

Brian (35:56):
Another example of how Mendel got lucky, because all of
his traits were these traitswhere you had a clear one copy
is enough,

Jason (36:04):
yeah. And so that's how dominance and recessive genes
work. Most genes are notstrictly dominant or recessive.
Again, Mendel was a littlelucky, or maybe he was wise in
which traits he picked. A lot ofthem actually show independent
stuff. So there are definitelyexamples where you cross a red
flower and a white flower plant,you get a pink flower out, or
maybe you get like a light pinkone out, or a dark pink one out.

(36:28):
Like there's differentgradations here. And then, of
course, there's the traits thatare actually controlled by many,
many genes, the quantitativetraits, as we call them. Now
this is what my area, myresearch area, focuses on, which
can be controlled by hundreds or1000s of genes. I was just
looking at before this recordingwhat the current estimate is of
human height. So human height isvery quantitative, lots and lots

(36:51):
of genes there. The most recentstudy I found, found like 12,000
possible mutations that wereassociated with it in like 8000
spots on the genome. And thefact is, there's probably even
more than that, because each oneof these is controlling such a
minuscule amount of the ofwhat's going on. Like we're
talking one of these genes, abig effect from one of these

(37:12):
genes might be like a millimeterof height difference. That'd be
an enormous effect for most ofthese.

Brian (37:18):
Well, thank goodness. Mendel identified a good, simple
model system so that you coulddefine the rules that then your
area could go on to understandand break and understand the
true complexity.

Jason (37:30):
Yeah, that's the importance of model systems in
biology, we know that a lot ofour systems are not reflective
of the messy complexity of thereal world, but they let us
figure out fundamentalprinciples. And that's what
Mendel's peas did, is that theylet us figure out fundamental
principles. Real life is muchmore messy than this, with a lot
more complicated genes wethere's also the fact that, you

(37:51):
know, most traits are alsoinfluenced by environment. Going
back to human heights, we aretaller than people were 200
years ago, not because ourgenetics have changed, but
because we eat better, we havebetter nutrition. And so this is
nature versus nurture issue, andwe're not going to get into that
debate, because when talkingstrictly speaking about biology,
you can usually actually figureout what it is.

Brian (38:12):
Yeah, it's not a debate. It's just something you can
measure.

Jason (38:15):
Yeah, and we measure it, we calculate it out. And I do
that all the time for the workI'm on, and they range all over
the place. So some some traitsare nearly 100% genetic, some
traits are nearly 100%environmental, and a lot of them
are somewhere in the middle thiscore of looking at these peas
and these very simple traits isa good, a good way of

(38:36):
simplifying the system and beingable to make it tractable. I
actually looked up for this,what Mendelian traits, so traits
that follow this sort of simple,dominant, recessive pattern,
what sort of traits like thishumans have? And turns out most
of them are diseases, becausebasically something important
gets broken, and then thatdisease follows a a Mendelian

(39:02):
pattern, because you either havea broken gene or you don't.

Brian (39:05):
Oh, this is, this would be hemophilia in the royal
families of Europe,

Jason (39:09):
hemophilia, sickle cell, anemia, Tay sachs disease,
albinism. A lot of these arerecessive. So, like, if you have
one working copy, you'reprobably fine. Some of these may
be, like, partially dominant, sothat if you have one copy,
you're like, okay, but notgreat. Technically, sickle cell
is like this. So if you have onesickle cell and one not sickle

(39:30):
cell allele copy, technically,at the molecular level, you do
have traits, and that's whatgives resistance to malaria.
You've probably heard that thereason sickle cell sticks around
is because it does provideresistance to malaria. One copy
does that, but it's not enoughto actually cause disease
symptoms, but it is a singlegene trait, and we know exactly
the gene mutation that causedthat, an interesting one on this

(39:52):
list, lactase persistence, sothat's the fancy scientific way
of saying you can continue todrink milk as an adult. Hmm, for
people in the West, you may notrealize this, but the ability to
drink milk as an adult isactually really weird and
uncommon in biology

Brian (40:08):
and recent in human history, right?

Jason (40:10):
Yes, it's actually one of the best examples of human
evolution, like human evolutionof traits, because when you look
at at the ability to drink milkas an adult. What happens is,
everyone, unless something'sreally broken, can drink milk as
an infant, because that's howhuman infants are reared. You
drink milk, especiallyhistorically, before formulas

(40:32):
and stuff like that, was it. Youhad to drink mother's milk or
get a wet nurse or something, oryou died.

Brian (40:37):
Yep, you are a mammal, believe it or not.

Jason (40:40):
Yes. So, but once the infant was weaned, there's no
reason to keep making all thethe proteins and enzyme needed
to keep drinking milk,especially lactose, which is the
sugar in it. And so your bodywould turn that off, because
that's just a waste of energy tomake that. There's no point
making all this protein that istrying to digest something

(41:00):
you're not drinking. However,once humans started keeping
animals for dairy, then itstarted becoming advantageous to
be able to keep drinking milk.The thought is that it started
with fermentation, so likecheeses and yogurts and stuff,
stuff where you let bacteriadigest the sugar first, so we
didn't have to deal with it. Butunder those conditions, if

(41:22):
someone had a mutation that letthem continue to drink milk into
adulthood, they could suddenlyaccess this entire other
nutrient resource that all oftheir peers couldn't, or at
least, they could access itbetter. They could get more out
of it, which I believe there wasa study a few years ago showed
that that meant they left likeeight times as many offspring as
people who didn't have it inthese cultures. Whoa, which is

(41:44):
insane.

Brian (41:45):
That is a huge that is a huge advantage.

Jason (41:49):
That is an enormous selective advantage, which is
why lactase, persistence, theability to continue to drink
milk as an adult, is so commonin cultures that have a long
history of dairy production,because it spread through the
population, because it was sobeneficial, and it is apparently
down to a single gene. And atleast according to this list I'm
looking at, it is dominant. Soif you have one copy of it,

(42:10):
you're fine. You can continue todrink milk into adulthood, just
fine.

Brian (42:14):
Very, very cool.

Jason (42:15):
I assume anyone listening to this already knows if you can
or not. So whether you have onecopy or two, I don't know, you'd
have to get gene tested forthat, but you, if you can, you
probably have at least one copy.Yeah,

Brian (42:25):
this is the problem with recessive genes. Is they like to
hide, right? You can't alwaystell that they're there. This is
why a lot of these, well, youmentioned a lot of these
diseases in humans, so a lot ofvery problematic ones are
genetically based, and a lot ofthem are recessive. So for
certain diseases, that's whygenetic screening can be
important to tell if your childwill have the risk of inheriting

(42:47):
one of these extremelydetrimental diseases.

Jason (42:49):
Yes, especially there are certain ethnic groups that have
that are known to have elevatedfrequencies of some of these
diseases, and so it'srecommended to get testing there
if, like you and your spouse areboth of that, or if you know
that you have a family historyof this, it's worth testing to
see, do I have this mutation,and especially, do I have it,
and does my spouse have it, sothat we can see, okay, what are

(43:11):
the odds that we will have achild who inherits it's both
broken copies and thus ends upwith some sort of genetic
disease? All right, so we reallyneed to start wrapping this up.
I'm sure we could keep talkingabout this for another for
another hour, because, again,this is our specialty. We suffer
the Curse of the specialist isthere's so much stuff we want to
talk about, we want to share,and we can only squeeze stuff in
one hour. So dear in the best wecan. Dear

Brian (43:33):
listener, please let us know. Did how did we do? Did we
actually talk this at a levelthat was appropriate, or did we,
like, forget ourselves, becausewe were too much of a specialist
in this.

Jason (43:44):
Anyway. The take home from this, though, is that genes
are the fundamental unit ofinformation in biology. They're
what pass information fromparent to offspring. They're the
raw material on which evolutionacts, and Mendel is the one who
found the first evidence ofthat. There's one little
interesting aside here is thatever since Mendel's stuff was

(44:04):
rediscovered, there's been anargument raging on whether he
cooks the books a little bit,because people have pointed out
the numbers he get are a littlelike, a little too close, or a
little closer to what his theorywould predict than you'd expect
by actual random chance. Butthey're not so close as like,
oh, okay, he definitely justfudged the numbers. And so
people have argued back andforth for a century now over

(44:27):
whether Mendel may have, like,fudged numbers just a little bit
to make them fit a little bitbetter. But suffice to say, the
theories that came out of themodels that came out are correct
and are the basis of modernbiology and genetics. So that's
the thing to take home.

Brian (44:40):
Also, if he was, if he was cooking the books, then his
Hank weed experiments, kind ofthrow that into some sort of
like what I mean, he did a wholecareful things, learned
something really important, andthen the second time he did it,
it all fell apart. Maybe hewould have picked something
different, or, I don't know,whatever. It just doesn't seem
like the act of someone who'sputting their thumb on the
scale. To me,

Jason (44:59):
I agree. Yeah. So, all right, let's get down here. So,
so nit pick corner, which Ialways feel bad calling the
nitpick corner. I just like the,let's call it the improvement
corner or something.

Brian (45:09):
I think nitpicks are fine. It's just, again, we're
very positive about these games,but I think it's, it's nice to
have an opportunity to complainabout things that are put I want
to be reviewer two.

Jason (45:17):
Okay, all right, Brian, reviewer number two, what would
you change about the game?

Brian (45:22):
No comments. It's perfect. Well, actually, no, I,
I'm just getting in terms ofcomments about the game. The
mutation die. The mutation rateis not only high, but the
problem is that it is. It is acompletely appropriate game
mechanic, and that is why itexists. The problem is, is, if
the real biology worked thatway, and you were randomly
mutating things that happen tolook like your phenotypic trait,

(45:42):
it wouldn't be the real Gene.And that whole idea of discrete
genetics, you'd actually breakthe entire game. If you were
really getting mutations thatway and generating your traits,
you would not be confirming it,because, again, we talked about
all the different ways to breaka gene. You're not going to
break it the same way twice.You're going to make a new
break, and maybe it's in thesame gene, and it would be fine,
but I don't know that that thisis my nitpick, is the way that

(46:05):
they're using mutation is realand completely inappropriate for
the specifics of this game.

Jason (46:12):
Yeah, and probably one of those decisions that was made
for the sake of gameplay, likethey wanted to represent
mutation somehow, I don't thinkthey wanted a one in 10 million
chance of actually having amutation. Because I don't think
that's like at that point. Whyeven have the mechanic?

Brian (46:26):
No, no, no, no. Yeah. I mean, you're right. Of course, I
understand, and there's alwaysthat compromise for the sake of
having an enjoyable game.

Jason (46:33):
Yep, mine is, it's almost more of a curiosity question. So
in genetics, when you have thesetraits and these alleles, you
usually represent them by aletter and on the game board, it
has the letters for thesedifferent traits, and it's
usually like a capital for thedominant one and a lowercase for
the recessive one. So like theround one is big R and little r,

(46:53):
the flower color is big F andlittle f. The thing is, these
aren't the symbols that are usedby scientists. No, they're not.
So R is the same for thewrinkled and round, but like the
flower colors at the A locus, isthat the A position? So these
big A and little a, or the tallis not big T, little T, it's Le.
For some reason, I don't knowwhy green and yellow pod is

(47:16):
actually Gp, instead of just g,so I would, I'd be interested
why. I assume this is anotherone of like, let's make it easy.
Because why on earth wouldflower color have A as a letter?
I suspect it was just to make iteasy for the people playing it.
I just they never mentioned thatin their little insert. And I'm
kind of curious about that,because I never saw them

(47:39):
referred to by the games onesanywhere, either.

Brian (47:42):
No. I mean, you're right, it is, it is A and I guess, I
mean, there is an answer. I justdon't know it. I mean, I would
guess anthocyanin perhaps, yeah,because anthocyanins

Jason (47:51):
are one of the common pigments in plants, they're
usually the ones that are kindof your purples and pinks and
bluish ones.

Brian (47:57):
So they, they use the same type of way that we would
represent a dominant andrecessive, which is the
uppercase versus lowercase, butthey didn't use the real gene
names because or genedesignations because it's
confusing.

Jason (48:10):
That's what I'm guessing. Yeah,

Brian (48:12):
but would it have really been that confusing, though,
because it's on all the cards.They could have just done it
right.

Jason (48:17):
They could have, but thinking with my game designer
hat on that could be a frictionpoint, and at least as a
designer, unless it's importantfor the game, my goal is to
remove as many friction pointsas possible, okay? And I think
that particular one does notaffect the game. It doesn't
affect the science they'retrying to portray. So I can
agree with them changing

Brian (48:36):
that, okay, all right, fair enough. Well, I mean, hey,
oh, I guess we got to do ourgrades then, huh?

Jason (48:41):
Yep, final grade. So how about you for gameplay? What do
you think about gameplay here?

Brian (48:46):
Gameplay? Um, I think I it's gonna get docked just a
little bit as a game. That'sactually kind of hard to learn.
And I don't really, I don'treally know how to get around
that. I mean, everybody has ahard time learning just from the
book. Do you primarily learn howto play games by reading the
rule book? Is that yourapproach?

Jason (49:03):
That's the first pass Yes, I'll either read. I'll read
the rule book. I will watch howto plays. Sometimes the order of
those, which one I do do first,which one I do second changes.
But yeah, I will usually readthrough the rule book.

Brian (49:14):
Okay? I usually watch the videos first, then read the rule
book, and then kind of layeverything out to try to
understand how it's going thisone's way harder to learn than
you'd expect for a game thatonce you've got it plays very
quick and easily. I think I'mgoing to dock it just a bit for
that, because the teach isdifficult. I'm just going to
give it a, B. They can arguewith me if they feel like that's
an undergrad. What about you?

Jason (49:34):
Well, I'll argue with you. I was going to think about
an A, but I think you bring up avalid point, that it is a little
challenging to teach because ofthe moving parts and the way the
order that the game happens isnot the best order to actually
teach it in. So I'm going tojust say A minus, because I
thought this was really fun toplay. I enjoyed it. I managed to
get my nine year old to play itmultiple times, so she enjoyed

(49:55):
it. So like, the game's fun. Ilike, once I get past that, once
I get past. Has to learn. Once Iunderstand what's going on, it
plays relatively fast and fun.

Brian (50:04):
I think if we're grading for the Wallace girls, we're
really grading the rest ofsociety on our curve, though
you've been training them fromlike, you know, for as soon as
they could talk how to playgames. I think maybe, maybe
they're not exactly at the meanon that particular bell curve?

Jason (50:22):
I don't know, but I am very proud when I hear my 14
year old talking about, like,choosing the optimal play for
the games we're playing. It'slike, there you go.

Brian (50:30):
Yeah. Well, she is your clone, let's be honest. She
definitely got that trait fromyou.

Jason (50:34):
Okay, all right, science, so give me a moment to think
about this science grade forwhat it's trying to portray
here. I think I'm going to gowith an A minus again for the
science grade. I think the coreof it like, Oh, here's genetics
and your Punnett squares androlling the dice. I think that's
fine. The place I'm going todock it is actually in some of
the ancillary stuff, some of thelike, the tools you can use to

(50:57):
accomplish certain things, andthe like, some of the
assistants, where, mechanically,they make perfect sense, they're
giving you some access to anadditional resource, or an
additional thing to do thathelps make your moves more
powerful. But logically, itdoesn't necessarily make sense.
Like, why does the rake do thisparticular effect? I'd

(51:17):
understand. Why does a pruningshear let me take another die,
or something like that. I forgetwhat all the tools do. The one
that makes sense is the pollenbrush, where you basically pick
up the pollen and you brush italong all your different plants
like that. One actually makessense, yeah. And so that's it's
like, it's that there's a littlebit of a disconnect of the
metaphor for me in thosepositions that said I do like

(51:38):
the fact that one of the spotson the board is basically you
paying the university money todo your research for you. So,
yeah, I'll give it another Aminus there.

Brian (51:49):
Yeah, I think I'm actually comfortable with an A,
and I'm gonna give it an A forthe use of the Punnett Square
and setting the parentalgenotypes to create the dice
drafting system. I've seen othergames do genetics in different
ways. This is the only one I'veseen where they're actually
trying to replicate that processof genetic inheritance in a way

(52:11):
that mimics how it happens innature. Usually, there's just
sort of a very, sort of a vagueapproach to it, but this is much
more specific, and that practicewith the Punnett Square is
really useful. It's kind of inthe same way that, like if you
play cytosis and then go takecell biology, oh, well, you
already know all the principleshere. If you play genotype,
you're going to understand howto do a Punnett square, because
that you're just going to bedoing it a bunch of times.

(52:32):
You're going to be getting a tonof practice using Punnett
squares and manipulating Punnettsquares in a fun way.

Jason (52:37):
Yeah, I'll agree with that. So I definitely think it
would give a good foundationthere. I wonder, because of the
age range, this is ages 14 plus.So you're talking middle school
already. I think many of thosestudents have already been
exposed to Punnett squares bythat point, which may make the
game easier to pick up. Whoknows?

Brian (52:51):
But, yeah, probably. But, I mean, like, again turning
Well, that's not a bad thing. Ifthey know how to use a Punnett
square, it's just helping toreinforce it, right? Yeah,
probably.

Jason (52:59):
And, I mean, let's, let's face it, I mean, how much stuff
does your average sixth graderremember by the time they get to
eighth grade? So it's like arefresher, like this would be
helpful. All right, I thinkwe're going to wrap it up there.
Keep an eye out. We may do a howto play genotype if you want to
see more of that. If you'reinterested in the game, go pick
it up from genius games or yourfriendly local game store. And
with that, have a great monthand have great games.

Brian (53:21):
Have fun playing dice with the universe. See ya.

Jason (53:25):
This has been the game of the Science Podcast, copyright
2025. listeners are free toreuse this recording for any non
commercial purpose, as long ascredit is given to Game of the
science. This podcast isproduced with support from the
University of Georgia. Allopinions are those of the hosts,
and do not imply endorsement bythe sponsors. If you wish to
purchase any of the games wetalked about, we encourage you
to do so through your friendlylocal game store. Thank you and
have fun playing dice with theuniverse. You.

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S2E07 - Genotype (Genetics)

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.css-14f5ked{margin:0;word-break:break-word;display:-webkit-box;-webkit-box-orient:vertical;box-orient:vertical;-webkit-line-clamp:2;overflow:hidden;}S2E07 - Genotype (Genetics)