As anyone who has ever raised aquarium fish knows, they’re all different. Maybe you think a fish is just a fish, not very different from one another and all rather stupid, but I spent years sitting next to tanks of zebrafish, and I can tell you you’re wrong. I’d watch them gamboling about, and you’d quickly realize that oh, that one is aggressive, that one likes to hid, that one gets the zoomies and darts about the tank. You can learn to recognize individual fish by their behavior.

I always wondered about that. These were highly inbred animals, with only slight genetic differences between them, but could those little genetic variations account for strong differences in behavior? Then I acquired a new line of zebrafish, one that was the product of hybridization between our inbred lines and wild-caught native stocks, and oh boy, their behavior was radically different, instantly distinguishable. Maybe it is genetic. Maybe? I never did a formal, rigorous behavioral experiment, so I don’t know for sure.

But now a new study comes along that does what I would have been excited to know about 20 years ago (and I still am!). This is an analysis of The emergence and development of behavioral individuality in clonal fish, and it’s a bit surprising. Laskowski and others are working with the Amazon Molly, a small tropical fish that reproduces clonally, producing clutches of babies that are all genetically identical to each other — so even better than my old zebrafish — that can then be separated and raised apart from their mothers and siblings. This rules out the possibility of genetic differences causing individual differences, and leaves us to consider alternative sources of variation.

To determine the causes and mechanisms that can generate behavioral individuality in the absence of genetic and environmental differences, it is essential to first pinpoint when behavioral individuality emerges and how it continues to unfold after emergence. Birth marks a critical time point: if individuality is present at birth, this points to pre-birth influences––such as epigenetics, maternal effects, and/or pre-birth developmental stochasticity––as being key drivers of individuality. Alternatively, it could be that individuality primarily emerges after birth. This emergence could happen both gradually throughout early life, which would suggest that individuality is driven by positive feedbacks between behavior and the internal and/or external environment, or abruptly at particular points early in life, if it is linked to critical sensitive windows.

So if cloned fish are behaviorally identical to one another at Day One, but become different later on, that suggests the differences are generated by varying experiences over time. If, on the other hand, the genetically identical fish are different on Day One, that suggests that pre-birth factors (I’d lean towards favoring developmental stochasticity, just random variations at the cell and molecular level) generated the variation.

To cut to the conclusion, Amazon mollies differ on Day One, with all that implies.

I think their chosen behavior is a bit simple, they’re just looking at mean swimming speed — does a fish have the zoomies, or is it a calm quiet little guy? — which is fine, since they do get an early difference. They also used motion analysis software, so I presume they could go back and reanalyze the data for more subtle differences, but they got their answer with just one parameter. They also looked for other possible correlations.

Individuality is present at day one after birth and is not explained by differences in maternal identity or body size.

In panel A you can see that there was a huge amount of individual variation in swimming speed. In B, different mothers all produce progeny with a wide range of behaviors. That one has me wondering, though: Mama a’s babies were all a bit on the sluggish side. If they raise a second clutch from Mama a, does the second set exhibit a range of behaviors similar to that of the first set? Is there any genetic bias at all in this behavior?

Panel C shows that there was also variation in body length on Day One, which doesn’t surprise me at all — developmental stochasticity again. Body length is not a predictor of swimming speed, though, these seem to be unlinked variables.

Another feature of the study is that they observed the fish longitudinally, over 10 weeks of development. Variation increased, which would surprise no one, and it was correlated with Day One behavior. Zoomy fish stayed zoomy and became even more zoomy, while slow fish generally stayed slow for their life.

Individuality increases gradually throughout the first 70 days of development.

What have we learned?

Evidence is accumulating that even genetically identical animals reared under near identical conditions develop behavioral individuality, yet little is known about when exactly these differences emerge during ontogeny and how they continue to change during early life development. We show that genetically identical individuals already exhibit substantial behavioral individuality on their first day of life, highlighting pre-birth influences as being of critical importance to initializing durable behavioral differences among individuals. Epigenetic and maternal effects mediated through mechanisms such as changes to DNA methylation patterns or differential resource or hormone allocation, could influence the phenotype of offspring.

I’m still intrigued by the role of chance in development and evolution.

Another non-mutually exclusive hypothesis is that the behavioral variation we observed is the result of developmental stochasticity, that is, stochastic variation in any molecular, neurological or physiological markers that occur over ontogeny. An intriguing possibility is that the phenotypic variation we observed here––whether arising from epigenetic, maternal, and/or developmental stochasticity effects––might itself be adaptive, for example, as a potential bet-hedging strategy. Generating phenotypic variation among one’s offspring by such non-genetic means might be especially relevant in clonal organisms such as the Amazon molly. There is, for example, evidence in clonal fish, and poecilid fish specifically, that DNA methylation mechanisms and developmental plasticity more generally might be especially sensitive to environmental influences, offering a mechanism through which mothers can generate variation among their otherwise genetically identical offspring.

Developmental stochasticity as part of an evolutionary bet-hedging strategy sounds like an interesting model, and probably important in species like fish (and spiders!) that pump out huge numbers of offspring with concommitant high likelihood of death.

This kind of behavioral analysis of organisms with limited genetic variation is one motivation for what I’m doing in the lab — taking the offspring of one spider parent and then inbreeding them over multiple generations to reduce genetic variability in one lab population. A couple more generations, and then it’ll be time to work out some behavioral assays to identify differences that we can select for. Swimming speed won’t be one of our parameters, though. Not even speed in general, they tend to all be quiet lurkers. Web configuration, aggression, pigment patterns, though, those are all candidates for analysis down the line.

You want something more to fear? Try this on for size.

Across the world, there’s evidence that spider populations are in danger of collapse. A landmark 2019 study in Nature found that the number of spiders, insects, and other arthropods dropped precipitously in Germany from 2008 to 2017, with the total number of different species researchers counted declining by 33 percent and total biomass dropping by 40 percent. Remember the Australian trapdoor spiders I told you about? They’re disappearing, too. After a century of settlers clearing land for crops and raising livestock, they’re becoming harder and harder to find. It’s all but certain that entire species of spiders will go extinct before we even have a chance to discover them, falling victim to industrial agriculture, pesticides, and climate change.

Then there’s this:

Alaska canceled the snow crab fishing season for the first time on Monday, as crab populations mysteriously plummet.

An estimated 1 billion snow crabs suddenly disappeared from the Bering Sea, according to CBS News. The collapse deals a heavy blow to Alaska’s biggest crab industry, and could drive many fishers out of the business.

“Mysteriously.” What a useful word. We send out trawlers to shred the seafloor, we drop traps and snatch away millions of crabs, and we spew garbage and microplastics into the ocean, and then shrug and say it’s a mystery why populations abruptly and catastrophically crash.

Another example: we’re seeing fewer vehicles with dead bugs splattered all over them.

From 1996 to 2017, insect splatters fell by 80 percent on one of the routes Moller regularly travels. On the other, longer stretch, they plunged 97 percent. Conventional measures show similar trends, and more recent observations have seen even sharper declines, Moller told us.

This article takes the somewhat interesting approach of speculating about alternative causes — which is fine, they’re being thorough, but we’re eventually going to have to face the reality that something “mysterious” is also happening to insect populations.

So, given this uncertainty, isn’t it possible that our spookily clean windshields are caused by factors other than rapidly declining insect populations? After all, we still see bugs everywhere, we just don’t seem to mash them with our cars as much.

Many smart people we spoke with, including entomologists and wheat farmers, speculated that maybe the cars have changed, not the bugs. As vehicles become more aerodynamic, the thinking goes, their increasingly efficient airflow whisks the bugs away from the windshield instead of creating head-on splatters.

Um, no. That’s a very silly explanation, as the experts they consult state, but also for obvious reasons. Car grills have not become more aerodynamic, nor have radiators. Also, the cars…or rather trucks people are driving are not particularly sleek. In fact, the trends are for more aggressively blunt, large, flat front ends. A lot of column inches get wasted on this ridiculous hypothesis, which can also be dismissed experimentally.

But we also saw 60 percent declines in insects between 2004 and 2021 in a British study from the Kent Wildlife Trust, which built on a Royal Society for the Protection of Birds effort in which thousands of people used “splatometers” to measure bug splatters on license plates, which aren’t much affected by aerodynamic advances elsewhere.

So then we get another off-the-wall hypothesis. It’s not that insects are in decline, it’s that there are fewer insects splattered by individual cars because we’ve vastly increased the number of cars on the road. I’m losing patience with their efforts to find any explanation other than that we’re poisoning the environment, but OK…being thorough is good.

Americans now drive three times as many miles as they did in 1970, and the explosion of trucks and SUVS means many of us do it in cars with much, much larger windshields. Back-of-the-napkin math suggests acreage of windshields out on the American road has tripled. And that’s probably an underestimate in some places: A large majority of our increase in driving has come on a narrow set of major urban roads, according to our analysis of Bureau of Transportation Statistics data. And as Kenny Cornett of design-software giant Autodesk points out, more traffic means more vehicles riding in each other’s bug-free aerodynamic slipstreams.

So in our little thought experiment, which makes the depressingly accurate assumption that bugs are a finite resource, our bugs-per-windshield metric would have been cut by two-thirds even if the number of bugs had remained constant.

I…I don’t even. This would only work if, instead of sampling a tiny fraction of the extant population with our windshields, we were exhaustively extracting enough bugs with one car to deplete the population for the next car. If that were the case, then maybe tripling the number of cars would be responsible for the population crash. But that’s not the case. The column of insects wiped out by the passage of a car is minuscule compared to the population in the fields, over the lakes, around our homes.

Treating the excessive driving habits of Americans as a rationalization for insect extirpation rather than as part of the problem is troubling, too.

Weirdly, the article concludes that the problem may not be as big as we think because…we have so many cars?

So, simple math hints that the very real ecological disaster of the collapse of insect populations may look even more apocalyptic thanks to the parallel rise of another ecological time bomb: the world’s intensifying love affair with ever more and ever bigger automobiles.

No. This makes no sense. We’ve got other methods of sampling insect populations that are not bug-splatters on cars. When I first moved to the Midwest, a regular feature on the news was when vast clouds of mayflies and midges would hatch out and rise from our lakes to appear on weather radar. Nope, not so much anymore. I would go outside and marvel at the dense masses of flying insects that would cluster around streetlights — nowadays, all summer long, the lights are lonely and shining into an emptiness. I wanted to use spider populations as a proxy for insects, and spiders aren’t leaping in front of cars on the freeway…and see the first article cited, they’re in decline, too.

What’s going on? Oh, I know the answer: it’s something “mysterious”. Problem solved.

Don’t worry, though. We don’t even like bugs, so who cares if they disappear. Then, when they’re gone, the birds and fish and reptiles will fade away, but they’re not our pets, so who cares? Unexpected crop failures…well, we’ll come up with a technology to deal with that. And finally, when humans mysteriously go extinct, there will be no one left to worry about it, and all the windshields on the decaying cars we leave behind will be shiny and clean and their grills will gleam unspattered. No one will be standing around wondering what happened to all the people, and best of all, there will be no one standing around smugly to utter the non-answer, “It’s a mystery.”

Wait, no, I won’t. I’ll be long gone. I expect the human species will be extinct by then. This is entirely predictable, that thanks to ongoing plate tectonics, eventually the continents will collide into a super-continent, Amasia.

It won’t actually be named that, of course, since the hyper-intelligent spiders that evolve to replace us won’t be using English.

Biology will get interesting, though.

Surrounded by a new superocean, the newly formed supercontinent will also have decreased biodiversity.

“Earth as we know it will be drastically different when Amasia forms. The sea level is expected to be lower, and the vast interior of the supercontinent will be very arid with high daily temperature ranges,” Li said. “Currently, Earth consists of seven continents with widely different ecosystems and human cultures, so it would be fascinating to think what the world might look like in 200 million to 300 million years’ time.”

It’ll be a harsher world in many ways, but at least it won’t have Homo sapiens screwing it up further. Also, you might want to start getting on the good side of the hyper-intelligent spiders.

First up, look who won the 2022 Nobel in Physiology or Medicine: it’s human evolution! As represented by the paleogenomics work of Svante Pääbo, who has been recovering ancient genomes, digging up old Homo sapiens and Neandertals and Denisovans.

I do have one reservation, though: the Nobel announcement claims “the ultimate goal of explaining what makes us uniquely human.” I don’t think we can accomplish that by decoding genome sequences. Identifying the different ancestral groups that led to us is interesting and informative, but let’s not get hung up on just DNA.

Easy. Their harassing behavior affects the evolution of females. This isn’t sexual selection, it’s just that the juvenile females are disguising themselves with male plumage to escape harassment. These birds, white-necked jacobins, are typically sexually dimorphic, but juvenile females maintain a male-like coloration, because females with adult female coloration face more aggressive assaults from males. Adopting the male coloration allows them to feed uninterrupted, while putting on the sexy female green coat brings on a plague of annoying, obnoxious males.

Ornamentation is typically observed in sexually mature adults, is often dimorphic in expression, and is most apparent during breeding, supporting a role for sexual selection in its evolution. Yet, increasing evidence suggests that nonsexual social selection may also have a role in the evolution of ornamentation, especially in females. Distinguishing between these alternatives remains challenging because sexual and nonsexual factors may both play important and overlapping roles in trait evolution. Here, we show that female ornamentation in a dichromatic hummingbird, the white-necked jacobin (Florisuga mellivora), cannot be explained by sexual selection. Although all males are ornamented, nearly 30% of females have male-like plumage. Remarkably, all juveniles of both sexes express ornamented plumage similar to adult males (androchromatism), but 80% of females acquire non-ornamented plumage (heterochromatism) as they age. This unique ontogeny excludes competition for mates as an explanation for female ornamentation because non-reproductive juveniles are more likely to be ornamented than adults. Instead, avoidance of social harassment appears to underlie this female-limited polymorphism, as heterochrome taxidermy mounts received more aggressive and sexual attention than androchrome mounts from this and other hummingbird species. Monitoring electronically tagged birds at data-logging feeders showed that androchrome females accessed feeders more than heterochrome females, presumably because of reduced harassment. Our findings demonstrate that ornamentation can arise purely through nonsexual social selection, and this hypothesis must be considered in the evolution of not only female-limited polymorphism but also the spectacular ornamentation often assumed to result from sexual selection.

They’re evolving to be able to eat dinner in peace.

Boy birds should be ashamed of their behavior, is all I can say. They can’t even leave a taxidermy dummy alone!

---

Falk et al., 2021. Male-like ornamentation in female hummingbirds results from social harassment
rather than sexual selection. Current Biology 31, 4381–4387. https://doi.org/10.1016/j.cub.2021.07.043

I tell my intro biology students this on Day One:

Fantastic success, everyone! Two of the pairs of spiders featured in my spider porn video from last week have produced egg sacs! Stri7 & Stri4, and Stri2 & Stri5, to be precise. This is huge. It may be the start of, finally, a self-sustaining colony. I’ve been struggling with this for the past few years — I get a few thriving spiders, a few egg sacs, and then over the winter they die off and I need to replenish the stocks in the spring with wild-caught adults. This is no way to do genetics. Well, it is, but that’s a different kind of genetics than I want to do.

Now I can start making plans. It will be about a month before spiderlings emerge, and then another month or two (depending on how well my fortified fruit fly diet works) to reach adulthood, which means I could have a Gen IV by Hallowe’en, or Thanksgiving at the outside. Exciting! I could be doing crosses by spring term!

Also, right now I’ve got so many spiders and spiderlings I have exceeded my lab’s capacity. In another first, while in previous years I have raided my garage for new spiders, today I took a container of about 50 Steatoda triangulosa spiderlings and released them into my garage. Sorry, babies, I can’t take care of you all, so you’re going to have to forage for yourself in the hard cruel world. Winter is coming, grow up fast.

I should look up from the spiders now and then. I did not know what was happening to forests.

Global trade and climate change are poised to make the spread and severity of arboreal plagues and pestilence worse. The hills around Syracuse are silhouetted with pale ash trees slain by emerald-colored borers. Ancient bristlecone pines out West are succumbing to bark beetle outbreaks triggered by rising temperatures. As many as 1 in 6 trees native to the Lower 48 states are at risk of extinction.

I should know. We bought a house 20 years ago that had a yard full of impressive trees, which we’ve watched steadily decline. Every few years it seems the city splashes another one with neon paint and we’re told it has to come down. But there’s hope! Science rides to the rescue, maybe! The article is about the American Chestnut, and how it’s been wiped out by a fungus.

All it takes is one gene.

The fungus infecting chestnut trees thrives by secreting a chemical called oxalic acid, which kills cells and allows the pathogen to feast on the dead tissue. But many other plants, including bananas, strawberries and wheat, avoid that fate by producing an enzyme called oxalate oxidase that breaks down the toxin.

By 2014, Powell and Maynard successfully added the wheat gene to chestnuts and were growing infection-resistant trees. The pair dubbed one line Darling 58, in honor of Herb.

Many plants use oxalate oxidase as a defense mechanism. It catalyzes the oxidation of oxalic acid into CO₂ and peroxides — reactive oxygen species. Is that going to have a side effect? I don’t know. Barley makes multiple forms of oxalate oxidase, and it doesn’t seem to harm beer production.

“Making a transgenic tree — I hate to say it like this, but it isn’t that hard,” Newhouse said. The most difficult hurdle for Darling 58, he said, is winning regulatory approval.

Well. This is sort of true. Making transgenic organisms is relatively easy nowadays, EXCEPT…the difficult part is figuring out what gene to use, and since most traits have complex origins, and since the expression of the gene is going to have multiple effects on the organism, it’s difficult to predict all of the consequences. There are good reasons regulatory approval is tough to get.

But in this case, they seem to have found a relatively simple way to confer fungus resistance on a tree, and it’s been tried experimentally, and they have successfully produced healthy, blight resistant chestnut trees. However, I think uncertainty about possible outcomes is a good reason to go slow, and regulatory agencies are doing the right thing by putting the brakes on the process.

There are also bad reasons for resisting the transgenic trees, and there seem to be a lot of people blocking it. Their primary argument is this weird idea that “natural” mechanisms like breeding hybrid trees are somehow “better” than transgenic methods — this is the same reasoning that has led to GMO labeling in our grocery stores, as if somehow the fact that an agricultural scientist has intentionally tweaked a plant is bad, while wholesale, random interbreeding of varieties is more pure. I don’t get it. Don’t people realize that all of the crop plants producing your food have been extensively modified by centuries or millennia of intentional manipulation of their genomes? Everything in the supermarket is a mutant, GMO or non-GMO. I’d argue that the genetically modified plants have undergone less drastic changes than those produced the old-fashioned way.

…Powell countered that crossbreeding transfers far more genes between species. “Genetic engineering is actually a less-risky procedure than a lot of things that we’ve done in the past,” he said. “We are very precise. We’re only moving one, two — just a small number of genes into the tree.”

That the changes are small are not a reason to dismiss regulatory oversight, of course. The reason they can use only one or two genes is that they have specifically selected target genes of very large effect.

Of course, re-creating vast chestnut forests would also be a huge effect.