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Gravemonera t1_jaavr5t wrote

Many species of fish do this, in that the temperature will determine the sex of the eggs. Some fish species will also change sexes depending on environmental pressures. Unfortunately I don’t have sources on this for you at the moment.

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fletch44 t1_jaaxck5 wrote

Temperature affects the rate of chemical reactions.

Complex biological pathways result in more or less of particular hormones being produced at different temperatures. This is useful in cold-blooded organisms, because if the chemistry of some biological function tends to shut down beyond a particular temperature threshold, the organism can incorporate other biological systems that kick in to replace it.

The advantage of having offspring's sex affected in such a way is open to discussion.

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MrinkysAnimalSide t1_jab5vz6 wrote

Temperature dependent sex determination is fascinating! Just remember, mammals and birds use chromosomal sex determination (meaning sex is genetic) but other mechanisms are quite common across all organisms! Check out the cool graphs at tree of sex http://treeofsex.org/.

There is still a lot of work left to be done on mechanisms of how temperature during incubation leads to different sex ratios. This is a good scientific review on red-eared sliders https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695493/. The ultimate mechanisms, or why temperature sex determination occurs, is also an interesting evolutionary question. Here is a good starting point for further research: https://sites.utexas.edu/crewslab/files/2016/06/CrewsDVLGen.pdf.

Finally, it’s important to remember that sex is a complex phenotype with many components and is really a shorthand for biologists to describe a common suite of traits. But thanks to sweet, sweet variation there is no one size fits all! In fact, it’s not uncommon for sex to be broken down into at least 5 levels of animal sexuality but that’s just the beginning. Not to mention human-specific levels, such as gender. Just a fun aside, the genderbread person is a nice primer on gender https://www.genderbread.org/

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Ieatadapoopoo t1_jab9bkv wrote

Is it an advantage or just “this happened to work out slightly better than the alternatives present at the time”? It’s mostly randomness and a matter of “not so awful it’s untenable” which, over billions of iterations, tends to end up somewhat efficient. To assume that something happens purely because it’s advantageous in a general sense doesn’t really work though. I mean, look at human nasal passages. Horrible, but not so bad it’s untenable.

Edit: to be clear, I say this only to mean that it’s not inherently going to be a logical conclusion we can easily discern. I’m mostly supporting your point.

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PatrickKieliszek t1_jabbvo8 wrote

One thing about adaptations is that one mutation away from the parent needs to be at least as good if not better than other siblings.

If it's going to take three generations of mutations to get to an advantage, they probably won't make it.

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sir_jamez t1_jabcnhu wrote

Could have evolved to be an environmental variable?

Like when sea turtles lay a clutch of eggs in the sand, the ones closer to the surface sand might be warmer, the ones in the middle might be warmer, ones that hatch closer to dawn might be warmer, etc.

Might just allow for randomness in the sex mix of any individual batch of eggs, that gets smoothed out by the variation across any breeding season.

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MrinkysAnimalSide t1_jabfxzb wrote

It’s a great question and you’re exactly right! There are even some cases of fish having multiple sex chromosome systems interacting together to be XYZ. Cichlid fish in particular, well known for rapid speciation, show incredible evolution of sex chromosomes. In which case, you’re unlikely to find a single degenerate Y chromosome like you find in mammals.

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Tiny_Rat t1_jabhwuj wrote

>needs to be at least as good if not better than other siblings.

>If it's going to take three generations of mutations to get to an advantage, they probably won't make it.

This is largely up to chance, unless the mutation is both dominant and a significant disadvantage early in life. Many mutations that are recessive, neutral, or only slightly disadvantageous spread through populations just through chance. For example, just look at human traits like hair color or clinodactyly.

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frogjg2003 t1_jabitib wrote

As long as it's not so much worse that the individual dies before mating, the gene will spread through a population. Over a long enough period, if it is less productive at surviving, it may eventually die out, but that takes many generations.

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platoprime t1_jabkv8x wrote

Even neutral mutations are working against entropy if there isn't a pressure keeping it around. Sure you could have a three generation neutral->advantageous or even a twenty generation disadvantageous->advantageous. In the same sense you could phase through a wall if your electrons all randomly lined up.

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rebbsitor t1_jabl3ma wrote

> Is it an advantage or just “this happened to work out slightly better than the alternatives present at the time”?

It doesn't even have to be better or provide and advantage, it just has to not be negative enough to cause them to go extinct. Fitter/better only applies to competitive situations where there's selective pressure. It's possible for a trait to have no impact on fitness and just be one way that works among others.

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platoprime t1_jabl4vs wrote

No all genes are working against the force of entropy to exist. If there isn't a pressure keeping something from mutating like it being adaptive or changing it being maladaptive then it will eventually be replaced.

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lqstuart t1_jabmph1 wrote

https://en.wikipedia.org/wiki/X_chromosome

Tldr - they noticed the X chromosome was weird, so they called it X. Then Y was the next letter. Then Z and W came about to distinguish between the ZW system and the XY system (also it's important to note that the X chromosome is the X chromosome, period, whether it's in a mouse or a human or whatever--it refers to a specific thing that plays a specific role).

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frogjg2003 t1_jabmzb7 wrote

Mutations are random. You can't make a gene mutate in the wild.

When a gene mutation does occur, it is still largely unrelated random factors that will determine if the individual with that mutation survives to pass on the gene. Only once that mutation has spread to a large enough portion of the population, will statistical tends become significant.

If an established gene is not harmful enough to survival and mating, then diffusion will sustain it in the population. Random mating means that any sufficiently established gene will reach an equilibrium between selective pressure reducing its prevalence and diffusion bringing all alleles into equality.

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Zachobomb t1_jabn82y wrote

Have you thought about the modality of disease vectors with this conversation? Maybe disease is a more efficient form of life. Maybe parasitism would be recursive and self contained in a computational mind frame. Other commenters have mentioned evolutions “discernment” of a modality and this is a flawed frame.

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aartadventure t1_jabnb5b wrote

Even recessive traits are selected for in the natural environment over time. However, they remain recessive for various reasons. This could include the recessive trait being advantageous in certain circumstances, but not others. Or that is only an advantage if other traits are also expressed at the same time. Many times a recessive trait can be an advantage but exacts a biological cost as well. If these traits remain recessive, evolutionary pressures cause them to become more common in the "required" circumstances, while allowing them to swiftly become less common when the environment is not suitable for that trait.

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aartadventure t1_jabnn6o wrote

Most mutations are not good, or downright lethal, leading to miscarriage, cancer and other awful outcomes. Especially in multicellular organisms, advantageous mutations occur quite rarely. That organism also has to be lucky enough to survive long enough to reproduce (you might have an incredibly advantageous mutation but just be unlucky and get struck by lightning before you reproduce for example). It may be something more akin to flipping 50 or 100 heads in a row.

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zakabog t1_jabpr91 wrote

> Most mutations are not good...

Based on what exactly? A single mutation isn't likely going to do much unless it happens in the correct place.

> It may be something more akin to flipping 50 or 100 heads in a row.

Which is rather easy if you've got millions of years to do it.

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TestTubeRagdoll t1_jabrave wrote

Not sure what you’re getting at here, can you clarify? What does this have to do with temperature-dependent sex determination?

Something like a virus could be considered “efficient” in that it has a small genome because it hijacks host machinery to replicate, but it can’t be “self-contained” due to this reliance on a host.

But genuinely, what are you trying to say here?

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mywan t1_jabvko2 wrote

You can also have a later mutation that randomly takes advantage of a past mutation that was neutral or even somewhat detrimental to confer a significant advantage that wouldn't happen alone.

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Faxon t1_jabwbf3 wrote

I cannot wait for the day I can replace my internal sinus structure with something more cyborg-y than the reconstruction I already had done once, which is gonna have to get done again (deviated septum due to allergies leading to infections, swelling, etc...) I feel so bad for brachiocephalic animals because I know how it feels having a smashed up nasal passageway that doesn't work properly, combined with asthma issues. I'd take a giant hook nose and my general skull structure elongating in that area by a half inch, if it'd mean no chronic dryness and other problems, but I know that any biological solution is still going to have the allergies pitfall. So cyborg it is! Maybe I'll get the upgraded model with higher sensitivity to certain smells (custom tuneable of course, nobody wants to smell themselves on the toilet)

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lazercheesecake t1_jabxhyl wrote

So you asked why/how temperature-dependent sex determinism works and a lot of people mentioned greater whys and whats but not a lot about the the how.

And to be honest, we don't really know the exact microbiological pathways. There are three main theories https://www.sciencedirect.com/science/article/abs/pii/S0306456518304170 as to how this happens. https://www.ncbi.nlm.nih.gov/books/NBK9989/ But the main thing that scientists agree on is that there is an organ(s) that measures/monitors the environmental temperature, and then that sends signaling molecules that allow the gonads to develop as male or female, and then the gonads will produce additional sex determining hormones that will influence how the rest of the body will develop. One such base hormone (or a critical hormone in the signaling path) is aromatase. When scientists injected aromatase inhibitor into developing lizards, those lizards became male.

So the following theories are as such.

  1. The yolk contains steroids (cholesterol based signaling hormones) that are released at certain temperatures.
  2. The brain releases neurotransmitters as a general signaling hormone that are released at certain temperatures.
  3. The gonads themselves react to the environment temperature epigenetically. This is the theory that is the biggest departure from the others as it doesn't specifically target a separate messenger hormone (even though one may or may not be present).

And while it's unknown specifically how these pathways form. The generic biomolecular pathway is pretty straightforward. Temperature can affect the shape of proteins directly. This is how some of your temperature receptors can figure out if things are cold or hot. A secondary method of temperature monitoring can happen by monitoring side effects of temperature. Chemical reactions vary based on temperature; generally reactions are faster the hotter it is. And by measuring the activity of certain chemical reactions (measuring the concentration of end/by-products, etc.) cells can determine the temperature. Then, that temperature protein can start a signal chain cascade to produce male hormones or female hormones depending on the environment.

And this is where the three theories take over. Scientists don't quite agree on where this temperature monitoring happens and which signaling cascades are involved.

But once those signals reach the gonads, they will influence the development into juvenile male or female gonads, which will then start to produce additional sex hormones that will further cement the development into male and female reptiles.

One thing that is important to note is that all fetuses start without sex differentiation. Embryos do not care about XY chromosomes, sex hormones, etc first. until a few weeks in. Male or female, all fetuses need lungs, heart, brains, intestines etc. This undifferentiated fetus stage is what allows fertilized reptile eggs to become either male or female based on these hormones. Fun fact, in humans, all babies start off development as females.

Hormone based sex determinism is actually very common and is one of many many many sex mechanism in even humans. One specific case is Androgen Insensitivity Syndrome. While it is a complex condition that affects many people, its base mechanism is that one of the sex determining hormones acts like the aromatase that I talked about in lizards. This hormone, androgen, is what allows human fetuses to halt development of female anatomy and promote male anatomy. Those affected by AIS are genetically male, but possess a lot of female anatomy and do not possess male anatomy because androgen could not act as a sex differentiating hormone. Due to mammalian XY genetics, however, their gonads are still proto-testicles and do not produce secondary sex hormones that promote the development of female anatomy. Nearly all people with AIS do not have uteruses or a fully formed vaginal cavity and are considered infertile. I hope I have not done the AIS community an injustice with my bullet overview of a complex topic.

The main point I want to get across is signal pathways, signal pathways, signal pathways. Complex multicellular organisms need a way to talk to itself and signal pathways is the method.

TLDR: Temperature -> temperature-sensitive protein -> signal hormone(s) -> sex differentiation -> additional signal hormones -> male or female.

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7LeagueBoots t1_jac0s19 wrote

No, it needs to be not worse than. Better is nice, but it's not necessary.

The selection process is often not about gaining an advantage, it's about not having a disadvantage. 'As good as' is usually just fine for evolution.

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owiseone23 t1_jac0w3l wrote

That's not quite true. I work on mathematical models of evolutionary processes and it's not uncommon for traits to evolve across "fitness valleys". That is, a trait with positive fitness that requires multiple generations to evolve with intermediate generations having negative fitness.

With a large population and a lot of time, random variation makes it possible to evolve across fitness valleys.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2711507/

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aartadventure t1_jac3zfp wrote

It could be that most mutations do nothing bad, or that they end up being harmful in time, such as cancer. Here is one paper on the topic:

https://www.sciencedaily.com/releases/2022/06/220608112504.htm

And yes, that was my point. Evolution tends to work slowly, over millions of years, due to the low chance of a beneficial mutation occurring, and then also being selected for in a given environment. And, since environments change, what was once beneficial, may end up becoming harmful over time.

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Dirty-Soul t1_jac6cw4 wrote

The way I understood it, crocodiles evolved before sex determining chromosomes like X and Y, or sex determining ploidy as seen in some plants and formics.

There's no reason for them to change the way that they do things, do they haven't.

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Richard_Thickens t1_jac6ya8 wrote

It doesn't have the intentionality of A/B testing, but it does allow for genetic divergence and drift, and it is subject to survivorship bias. Instead, it's survival by brute force calculation, with a high degree of casualty.

Edit: Changed a word to avoid redundancy.

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tayman12 t1_jac8kq8 wrote

Only thing I can think of off the top of my head is that the temperature is linked to food availability, when food is available its fine to make a bunch of females since their off spring wont have to compete for food, but if food is scarce then its better to make males, the ones best suited for survival will end up getting to mate, so its as if nature is using the food scarcity as a filter to get rid of bad genes

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viridiformica t1_jac8sa7 wrote

>in humans, all babies start off development as females.

I've seen this said a few times, and I'm always curious why the common early development pathway is considered female rather than ungendered?

It doesn't seem like enough to say that it requires activation of masculinising hormones to start being male, since presumably there are any number of hormonal triggers required on either path to spur development

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cjbest t1_jacdygl wrote

Related to this, researchers have found that higher temperatures cause more human males to survive gestation. They believe temperature acts as a stressor during pregnancy.

"The temperature coefficients (Table 1) suggest that a 1°C increase in annual temperature predicts one more male than expected for every 1,000 females born in a year. The median annual number of female births over the test period was 167,046. A rise of 1°C would, therefore, imply preservation of ≈167 males in the median year."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2538905/

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atred t1_jacj4vp wrote

> It may be something more akin to flipping 50 or 100 heads in a row.

50 heads in a row has a chance of 1 in a quintillion. Are you sure that's the chance to get an advantageous mutation?

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paroya t1_jacm0kh wrote

certain swordtail population can do a female to male change later in their life.

medaka (oryzias latipes) have about a 100% male exclusive hatch rate at 34°, starting from 27° and going up from there.

on topic of swordtails, there is a related species (amazon molly) which is unique in that it is the only known stable all-female species, reason so far unknown afaik.

in case anyone wanted to google papers.

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hananobira t1_jacni22 wrote

Other way around. Mothers are more likely to have daughters when the food supply is low. Females are hardier, are more resistant to famine and disease, and live longer. Mothers are more likely to have sons when they are living in plenty, because sons are less likely to survive childhood and require greater resources to grow taller and stronger.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2602810/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367790/

https://www.cambridge.org/core/journals/continuity-and-change/article/abs/famine-and-the-female-mortality-advantage-sex-gender-and-mortality-in-northwest-england-c-15901630/8D3B5297ABD8AFEAAFF9FA52923AE5F1

https://www.sciencedaily.com/releases/2011/09/110927192352.htm

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AMartin223 t1_jaco2pt wrote

I think the main reason for that mindset is that we have these various documented syndromes like described above where failures to emit certain hormones prevent the transition to male anatomy, so it feels more like the female path is the default rather than a different fork in the road. It seems though that describing the early stages either way can be a correct model.

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the__itis t1_jactczc wrote

It would seem to me that current climate conditions at the time of birth would change survivability rates dynamically.

Higher survivability rates should equate to a higher ratio of females as they would subsequently reproduce the overall population in higher numbers.

I believe mammals (Great apes specifically) have a similar “quirk” where older male age and higher average calorie diets lead to more female births.

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Alex_877 t1_jad7aag wrote

All of current life on earth is mediated through reactions by enzymes. Each enzyme has a most active temperature region based on its specific protein structure, length and folding etc.

In this case the difference in temperature is enough to produce a cascade of effects to make the enzymes responsible produce a difference in the offspring.

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-Metacelsus- t1_jad961c wrote

> The gonads themselves react to the environment temperature epigenetically. This is the theory that is the biggest departure from the others as it doesn't specifically target a separate messenger hormone (even though one may or may not be present).

This has been proven pretty well, at least in one species of turtle: https://pubmed.ncbi.nlm.nih.gov/29748283/

But other species might be different.

Also, you write, "in humans, all babies start off development as females." But this isn't correct. A better way to say it would be that they start off as undifferentiated, and trigger male or female development depending on whether the SRY gene is present.

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-Metacelsus- t1_jad9fo4 wrote

>Totally forgot about human fetuses starting as female.

This isn't actually correct, it's more like they start off as undifferentiated, and trigger male or female development depending on whether the SRY gene is present.

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platoprime t1_jadhh22 wrote

No I am saying the odds are lower than they stated which is true.

I am talking about the odds of any given mutation being advantageous not the odds of any member of a species eventually getting a beneficial mutation. I have no idea where you got that idea.

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Tiny_Rat t1_jadhudx wrote

>However, they remain recessive for various reasons. This could include the recessive trait being advantageous in certain circumstances, but not others. Or that is only an advantage if other traits are also expressed at the same time

This makes no sense. "Recessive" described how an allele intersects with other alleles, and this is largely determined by the molecular mechanisms the protein produced by that allele is part of. A trait cannot change from recessive to dominant, no matter how advantageous or disadvantageous that would be. And while recessive traits are acted upon by evolution, that only happens in homozygous individuals that have two copies of that gene and thus show that trait. A newly-arising recessive mutation could spread through quite a few generations of heterozygous individuals, being passed on but not expressed, until two heterozygous individuals met and bred to make a homozygote. In the meantime, that allele could pick up new mutations that would change it's function without significant selection pressure.

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The_Magic_Tortoise t1_jadphyt wrote

This may be ad hoc, but I could see warmer temps being a signal for environmental instability, therefore more males equals more genetic variability (more alligators), giving the population a better chance of adapting.

Cooler temps, creating more females, so as to "lock in" certain traits into the population.

IMO, systems seem to fluctuate between "searching" patterns and "chasing" patterns; robustness and efficiency, community and hierarchy, public square and tower, or as the alchemists said: solve et coagula.

You see this too in society: certain segments of society seem to follow either r or k patterns. Poorer people have more children, less neoteny shorter lives, etc.

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lazercheesecake t1_jadvkqt wrote

That there is an epigenetic component is not what was contentious. My point being it is unknown which mechanism in the temperature-signal pathway is the root of TSD. KDM6B is proven to be a vital component in the epigenetic expression of DMRT1 but what triggers KDM6B? That is unexplained.

Also, I do admit "in humans, all babies start off development as females." is a bit of an exaggeration, but it is not incorrect. As seen in AIS individuals, as I highlighted in my post, without male differentiating hormones, human bodies, for the most part, develop phenotypically into female presenting bodies. So much so that prior to modern times and ready genotyping, the most common diagnoses of AIS occurred in mid to late puberty when the individual did not start menses or develop other secondary sex characteristics.

Many male organs are direct descendants/adaptations of female organs, the differentiation of which occurs only in the presence of male differentiation hormones.

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silent_cat t1_jady8y2 wrote

Well, there are all sorts of genetic abnormalities that cause genetic males to appear female. But none that cause genetic females to appear as male.

Sure, there are any number of hormonal triggers, but if you miss all of them you appear female. Note, it's the appearance that relevant, because with these various syndromes they still tend to have testes rather than ovaries. It appears that the signal to produce a penis however requires an actual on signal.

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foolishle t1_jae88jc wrote

Well actually there have been cases where the SRY gene (the one that triggers masculine development) has been translocated onto the X chromosome which means that a XX person can develop male sex characteristics.

As usual with sex-development it doesn’t seem to matter how much we know, it turns out to be even more complicated than that!

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Excellent-Pattern119 t1_jaen3tv wrote

Not only temperature. Animals can even change sex. Each clownfish on an anemone is 25% bigger than the other and usually, the biggest is the only female. If one dies every other gets bigger to fill the gap and if the female dies the biggest of the male becomes a female.
The smaller ones don' reproduce and are undifferentiated. All clownfish have both reproductive organs.

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