Ungrateful wretches

Today was a feeding day, and since I’m trying to include some variety in their diet, I gave the spiders mealworms. Nice plump mealworms, conveniently placed directly in their webs.

They all turned up their noses, or what passes for noses, at them. They didn’t exhibit the slightest interest, which was disappointing after their spectacular voraciousness when fed waxworms last week. I don’t know whether it’s that they’re still full, or they just don’t like mealworms, or they’re just being obstreperous. I told them, “If you don’t eat yer meat, you can’t have any pudding. How can you have any pudding if you don’t eat yer meat?” and even that left them cold and uncaring.

So no pudding today, ladies.

All right. One spider is nibbling on the delicious meal I prepared. Gilly gets pudding!

The pudding being served today is Jellied Beetle Grub Guts. I hear it’s very popular in England.

Focus stacking!

Some people mentioned I should try focus stacking on my spiders, so I fumbled around and found some inexpensive software to do it, and gave it a shot. Here are a couple of trial runs (including some spiders I photographed in a single plane yesterday.

I’m just going to say…nice. Also easy. I always take multiple shots anyway, so I just do what I always do, maybe being a little more careful about centering each shot as identically as I can, and then dumping 4-8 photos into the software. I especially like how the juvenile in the third image turned out, letting me see individual hairs on the legs while not compromising the sharpness of the abdominal pigment pattern.

A few words about how I’m doing this: this is my Spider Studio.

It’s nothing fancy, as you can see. I’ve got a Canon body and a speedlite; I’m using my lovely Tokina macro 100mm lens, with a couple of tube extenders for extra magnification, and there’s also a big white diffuser there. I’ve got a bright LED panel to the left and back, and a simple clamp light with a full spectrum light on a jointed arm.

There are some colored papers on the bench top that I can use for backgrounds, but they don’t matter much with the big adults, who are usually hunkered down in a corner of their cardboard frame. The camera is stationary on a tripod, and I’m doing everything manually, focusing by holding the spider’s container in one hand and moving it back and forth, while in the other hand I’m holding a remote trigger and clicking away madly. The juveniles are contained in these clear plastic boxes, about 5cm square — I just pop off the lid, and there’s plenty of light from all around to illuminate the animal.

Hey, if handheld focus stacking is good enough for Thomas Shahan, it’s good enough for me. I was worried that I was going to need a fancy optical bench and something that would allow me to do precisely calibrated advancement of the camera focus, but nah, it turns out to be far easier than I feared.

I was also concerned because I’d seen all these finicky tutorials about using Photoshop or some other software to prep and align each frame, which was going to be tedious. Nope, don’t need that either: I found a program called Focus Stacker that does automatic alignment and assembles all the images into a single sharp result. It’s totally mindless, which I need: shoot a bunch of images with changing focus, drop them into Focus Stacker, and a few minutes later it presents you with the stacked image. I’m going to do this with all my spider photos from now on!

Post-prandial #SpiderSunday

The spider colony wasn’t very lively today. Everyone is still bloated from that waxworm feast last week, and even when I threw flies right into their webs they wouldn’t move — they just sat there, at best they might waddle a bit and desultorily wave a claw at such mundane fare. They now expect more. I promised them mealworms for tomorrow, but no, this is not enough, they have acquired a taste for larger prey.

“Bring us man-flesh,” they whispered.

I countered by telling them that in their current state, they weren’t going to be able to run down a baby, let alone a college freshman. They waddled towards me and hissed, which wasn’t too scary. They look like barrage balloons with a couple of feebly waving legs underneath. Like this:

Look at that! She’s not in a state to scamper at all. She’s huge.

Also pretty. Parasteatoda has these mottled rings of pigment in shades of black and brown, not at all flashy, but subtle and elegant. With abdomens so distended, they’re easy to admire, too. (by the way, the white circle top right is scrap from a hole punch, so you can estimate the size.)

They’re also marvelously variable. Here’s another Parasteatoda with an abdomen that looks like it was made up as an abstract mosaic. If you stare at it long enough you’ll see patterns. I’ve got my eyes open for one with Jesus’s face.

Right now I’ve got a bunch of full-grown adult females that are mostly immobilized by their gluttony, and then a largeish collection of juveniles in the incubator. I’m hoping to upgrade some of them to the larger cages soon — probably over Christmas break — and then I’ve got to introduce males to these young virgins. The Parasteatoda babies really are babies, tiny little spiderlings, that will take a little longer. Meanwhile, the next generation of Steatotoda triangulosa are coming along.

I’ve also got a few S. borealis, but I’m not sure I want to expand their numbers, since the Parasteatoda and S. triangulosa ought to be enough to keep me busy. On the other hand, S. borealis is so goth, with their blackish-purple bodies and gray racing stripes.

They also grow to a larger size. I may have to keep a few around looking badass.

Can spiders die of over-eating? Asking for a friend

I found one of my Texas S. triangulosa, Jacinta, in her cage this morning, lying on the floor next to a completely drained and shriveled waxworm, unmoving. I nudged her, and she was lying bloated in a puddle of bodily fluids, dead.

This is not good.

So, like the title asks, can spiders lack self-control to the point that they’ll suck prey dry until they rupture? I may be treading new medical frontiers here.

Eye of newt, toe of frog, might as well fling some tardigrade genes into the cauldron

I have to love speculative science — it’s in my contract as a popularizer — but I also like solid, well-established science and the cautious determination of incremental advances in our knowledge. Looking at both ends of the continuum and everything in between sometimes exposes some very poorly thought-out leaps in people’s assumptions, though, and then it’s also in my contract that I have to be grumpy and point out the flaws. This morning I’m feeling my grumpy side.

Let’s start at the beginning, with some nice work in tardigrades. Tardigrades are cool, obviously, and have a reputation as being tough customers who can survive all kinds of stresses that the environment throws at them. Freeze them, dry them out, throw them in outer space, zap them with radiation, and they can cope…at least, they cope far better than we do. Part of this ability is that they’re small and relatively simple, and being tiny and compact in itself is an advantage, but in addition, their cells have a sophisticated battery of proteins evolved specifically to enable them to handle stressful cellular situations without giving up and dying. It’s a sensible approach to take apart the tardigrade genome and puzzle out the genetic strategies they use to optimize cellular protection from stress, as Kunieda and others have done.

They scanned through the tardigrade genome looking for differences with other, less resilient animals, and found that sometimes that change involved deleting pathways that triggered stress responses. For instance, the genes in purple below are present in us, but missing in tardigrades.

Gene networks involved in the regulation of mTORC1 activity. Magenta indicates genes absent in the tardigrade genome and green indicates retained genes. The interconnected eight genes mediating environmental stress stimuli to downregulate mTORC1 were selectively lost, whereas all components involved in sensing and mediating physiologic demands were present.

This absence makes sense. It is desirable for our cells to kick the bucket when hit hard by environmental stresses; one kind of instance where this could happen is in cancer, where cells are in a poor physiological state, and it’s better for them to die and be replaced by healthy cells. Tardigrades, on the other hand, are already in possession of only a few tens of thousands of cells, and may be trying to cope with a systemic stress that affects every cell in their body, so this approach is not such a good one for them.

They also identified unique genes found only in tardigrades, such as this one, called Dsup, short for damage suppressor. This gene makes a protein that is associated with the DNA, and which has a high affinity for DNA; it’s also expressed in tardigrades with a high resistance to radiation damage. So, the immediate question is…is this protein responsible for radiation protection, and how does it work?

Since tardigrade cells have a lot of mechanisms for dealing with stress, and they want to just look at this one protein, the authors extracted the tardigrade gene and transfected it into a human cell line in order to determine its effects on a cell lacking all the other stuff a tardigrade cell provides.

They chose to use HEK293 cells (HEK is short for human embryonic kidney). A word of caution: these are cancer cells, not normal human cells. They are a popular cell culture choice because they proliferate readily in a dish, and are easily transfected with foreign DNA. They are hypotriploid — having nearly 3 times the number of chromosomes of a normal human cell — and contain adenovirus DNA that has turned them into madly dividing cancer cells. That doesn’t matter for the Kunieda study, though, since they just want to add a tardigrade protein to see what new properties it confers on the cells.

So they hit untreated HEK293 cells and HEK293 cells incorporating the tardigrade Dsup gene with X-rays, and found that the Dsup gene protected the chromosomes — they saw 40% fewer single-strand DNA breaks. They also saw that Dsup reduced the number of double-strand DNA breaks in these cells. They also did good controls, for instance knocking down Dsup expression in transfected cells, and seeing the protection going away.

Distribution of the numbers of γ-H2AX foci per nucleus is shown. Each dot represents an individual nucleus of a HEK293 cell (Control) or a Dsup-expressing cell (Dsup) under non-irradiated and irradiated conditions. ***P<0.001; NS, not significant (Welch’s t-test).
[γ-H2AX looks for phosphorylated histones that form around double-stranded DNA breaks]

Good stuff. Good fundamental cell biology. There’s a lot of work here, but that’s what you have to do to tease out the role of various components of the stress response.

But then it gets weird as it percolates up into the popular press. This was a focused bit of research designed to assess how tardigrades defend themselves against radiation that used a human cell line as a tool, and suddenly, that’s the newsworthy part of the work. It starts with a Nature news article — they should know better, and it does start with a relevant discussion of the work, and then we get the section where it just has to be explained how it could affect humans.

This makes the new paper’s findings “highly interesting for medicine”, says Jönsson. It opens up the possibility of improving the stress resistance of human cells, which could one day benefit people undergoing radiation therapies.

Wait a moment. Just think it through. You, a doctor, have a patient with cancer that you’re going to treat with radiation therapy. Do you really want to make their cells more resistant to radiation? Sure, their healthy cells, but if you’ve got a way to transfect healthy cells with Dsup that does not similarly help cancer cells, you’ve probably got better molecular tools to target cancer cells selectively than radiation anyway.

Then, the line that’s going to spawn a lot of crap, from Kunieda himself.

Kunieda adds that these findings may one day protect workers from radiation in nuclear facilities or possibly help us to grow crops in extreme environments, such as the ones found on Mars.

Oh jeez. This is where Live Science steps in and builds a fantasy of genetically modified humans colonizing Mars.

Will we one day combine tardigrade DNA with our cells to go to Mars?

Chris Mason, a geneticist and associate professor of physiology and biophysics at Weill Cornell University in New York, has investigated the genetic effects of spaceflight and how humans might overcome these challenges to expand our species farther into the solar system. One of the (strangest) ways that we might protect future astronauts on missions to places like Mars, Mason said, might involve the DNA of tardigrades, tiny micro-animals that can survive the most extreme conditions, even the vacuum of space!

This is what prompted me to dig into this line of research. I read this hypothetical, and my cortex immediately sneezed “Bullshit!” in an acute skeptical reaction, and I had to read further. It’s the combination of an imaginary Mars colony and an imaginary radical re-engineering of the human genome to produce customized genetic humans to labor under conditions of extreme environmental hostility that set me off. None of this is realistic. None of the evidence so far is at all adequate to justify this kind of speculation. There is only the glimmering of consideration for the ethical consequences of such experimentation, if it were even feasible. Is genetically modifying your offspring so they can more efficiently farm potatoes on Mars likely to be something they desire? Hey, though, it’s an opportunity to bamboozle a gullible audience with buzzwords!

One way that scientists could alter future astronauts is through epigenetic engineering, which essentially means that they would “turn on or off” the expression of specific genes, Mason explained.

I detest the casual abuse of the word “epigenetic”. I’m doing “epigenetic engineering” right now — my metabolism undergoes the usual seasonal shifts as we move into winter. You’re doing it too. Cells are constantly going to “turn on or off” the expression of specific genes as an expected consequence of basic biology. It sure sounds sciencey though, doesn’t it?

Alternatively, and even more strangely, these researchers are exploring how to combine the DNA of other species, namely tardigrades, with human cells to make them more resistant to the harmful effects of spaceflight, like radiation.

This wild concept was explored in a 2016 paper, and Mason and his team aim to build upon that research to see if, by using the DNA of ultra-resilient tardigrades, they could protect astronauts from the harmful effects of spaceflight.

This is where I get really irritated. See that phrase, “explored in a 2016 paper“? The “2016 paper” is the Nature news article I cited above. The only “exploring” of the concept is that one line from Kunieda, almost certainly prompted by a journalist prompting him to say something about the relevance of his research to humans, because they don’t understand basic biology.

Then there’s that bizarre claim about building upon tardigrade research to use tardigrade DNA to protect astronauts from radiation. It’s not a quote, so I expect the Live Science journalist just invented it to say some random something to justify the article, but I would just ask a simple question of whoever made it up.

How?

What specifically is being experimented on to improve astronaut’s resistance to radiation?

I’m going to guess that the real answer would be nothing, at least not yet. Let’s keep on eye on those wacky basic biologists who are studying core processes in genetics and cell biology with work on weird organisms that aren’t humans at all, and hope that sometime in decades to come some methods will emerge that will be applicable to human medicine. But until then, nope, nobody is shooting up astronauts with magical tardigrade DNA.

I guess we have to kill all the superstar scientists now, too

A study of “star” scientists in biology discovers an unsurprising fact: their fields undergo a substantial change when they die.

In the first two years after a star’s death, publications in their subfields increased modestly. But as the years passed, breaking the numbers down by author showed a startling change: Papers by newcomers grew by 8.6 percent annually on average. At the same time, papers published by collaborators took a nosedive, decreasing by about 20 percent a year. After five years, growth from newcomers was so substantial, it made up for the deficit from the collaborators.

In other words, large swaths of these fields had essentially been turned over.

Strangely, the article doesn’t dwell much on the likely cause: funding. It doesn’t even have to be intentional, but reviewers and study sections at the funding agencies tend to be biased by the presence of those who have already been funded, and big labs will have an undue influence because they have so many former students cheerleading for their mentors. This stuff also affects hiring — if you come from a famous lab, you’re more likely to get interviews and jobs.

That’s always been my impression, nice to see the inertia of big-name biologists measured.

Today was supposed to be a feeding day…

But I don’t think my spiders would be able to move. Look at Texanne here; she’s so bloated she’s not going to step out of that corner, I don’t think.

A few others are purging themselves into egg sac construction.

Anyway, I’ll check on them tomorrow, and as soon as they get active again I’ll throw them some more bugs full of ichor. The menu for Monday is mealworms.

The Great Escape

Today was not a good day. My mission was to sort out the prisoners the newly emerged spiders into separate containers, and also to try to document the morphology of 4 day old Steatoda triangulosa. I started out well enough, using a small paintbrush to delicately pluck out the babies and move them, and then to snap their picture.

First problem: somehow, my scope had drifted out of whack, and the eyepieces were no longer parfocal with each other, or with the camera tube. This demanded immediate fixing, especially since the photos were coming out blurry and bad.

These were not acceptable. So I spent an hour fussing over the optics, tweaking the eyepieces, taking a bunch of photos of the tips of watchmaker forceps, etc., etc., etc., until I thought everything was nicely aligned. Then resume shifting spiders.

I was feeling pretty darned competent, deftly plucking up itty-bitty baby spiders, lifting them by their dragline to a new home, and then tossing them a few fruit flies. I got so confident that I deftly knocked over the source container, sending baby spiders flying all over the floor. Oops. Sorry, neighbors. Don’t worry, they won’t go far. I was down on my hands and knees trying to find them, but nope, they are very tiny and I’m pretty sure they made it to the Swiss border. I expect they’ll colonize the space under my benches quite nicely.

Well, that was about ten spiderlings lost in the architecture. So I decided I’d check out this large collection of egg sacs brought back from Texas. At a glance, though, I could tell they’d already all hatched out — after embryogenesis, they molt, and you can see the rumpled white sheet they’ve discarded inside, and then before they emerge, they molt again, leaving their spider-shaped cuticles behind. To be sure, I opened up the sacs and looked carefully, and nope, nothing but shed leg chitin everywhere.

No more spiderlings to deal with today. I do have some egg sacs in the adult cages that will probably hatch out in ten days or so.

Oh well. While I was down on my hands and knees, I did discover a previous escapee near the floor and baseboards. She was looking good!

I don’t know what she’s been living on, but she’s grown. I like to think my lab is a healthy, biologically rich environment, though, so it’s good news. I thought about scooping her up and putting her in the incubator, but instead decided to throw down some fruit flies. She snapped them up fast!

Don’t tell the custodian.

This has been a klutzy day, so I’m out of the lab for a bit, will focus on preparing for class tomorrow instead.

Bad science tries to drip its way into everything

You want to read a really good take-down of a bad science paper? Here you go. It’s a plea to Elsevier to retract a paper published in Personality and Individual Differences because…well, it’s racist garbage, frequently cited by racists who don’t understand the science but love the garbage interpretation. It really is a sign that we need better reviewers to catch this crap.

The paper is by Rushton, who polluted the scientific literature for decades, and Templer, published in 2012. It’s titled “Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals?”, and you can tell what it’s trying to do: it’s trying to claim there is a genetic linkage between skin color and sexual behavior and violence, justifying it with an appeal to biology. It fails, because the authors don’t understand biology or genetics.

They’re advocating something called the pleiotropy hypothesis, which is the idea that every gene has multiple effects (this is true!), and that therefore every phenotype has effects that ripple across to every other phenotype (partially, probably mostly true), so that seeing one aspect of a phenotype means you can make valid predictions about other aspects of the phenotype (mostly not at all true). This allows them to abuse a study in other mammals to claim that human outcomes are identical. Here’s the key graf:

The basis of the pleiotropy hypothesis presented by Rushton and Templer hinges on a citation from Ducrest et al. (2008), which posits ‘pleiotropic effects of the melanocortins might account for the widespread covariance between melanin-based coloration and other phenotypic traits in vertebrates.’ However, Rushton and Templer misrepresent this work by extending it to humans, even though Ducrest et al. (2008) explicitly state, ‘these predictions hold only when variation in melanin-based coloration is mediated by variation in the level of the agonists at MC1R… [conversely] there should be no consistent association between melanin-based coloration and other phenotypic traits when variation in coloration is due to mutations at effectors of melanogenesis such as MC1R [as is the case in humans].’ Ducrest et al. continue, ‘variation in melanin-based coloration between human populations is primarily due to mutations at, for example, MC1R, TYR, MATP and SLC24A5 [29,30] and that human populations are therefore not expected to consistently exhibit the associations between melanin-based coloration and the physiological and behavioural traits reported in our study’ [emphasis mine]. Rushton and Templer ignore this critical passage, saying only ‘Ducrest et al. (2008) [caution that], because of genetic mutations, melanin-based coloration may not exhibit these traits consistently across human populations.’ This is misleading. The issue is not that genetic mutations will make melanin-based pleiotropy inconsistent across human populations, but that the genes responsible for skin pigmentation in humans are completely different to the genes Ducrest et al. describe.

To translate…developmental biologists and geneticists are familiar with the concept of an epistatic pathway, that is, of genes affecting the expression of other genes. So, for instance, Gene A might switch on Gene B which switches on Gene C, in an oversimplified pattern of regulation.

Nothing is ever that simple, we know. Gene A might also switch on Gene Delta and Gene Gamma — this is called pleiotropy, where one gene has multiple effects. And Gene Gamma might also activate Gene B, and Gene B might feed back on Gene A, and B might have pleiotropic effects on Gene Beta and Gene E and Gene C.

This stuff gets delightfully tangled, and is one of the reasons I love developmental biology. Everything is one big complex network of interactions.

What does this have to do with Rushton & Templer’s faulty interpretation? They looked at a study that identified mutations in a highly pleiotropic component of the pigmentation pathway — basically, they’re discussing Gene A in my cartoon — and equating that to a terminal gene in humans, equivalent to Gene C in my diagram. Human variations in skin color are mostly due to mutations in effector genes at the end of the pathway, like MC1R. It will have limited pleiotropic effects compared to genes higher up in the epistatic hierarchy, like the ones Ducrest et al. described. Worst of all, Ducrest et al. explicitly discussed how the kind of comparison Rushton & Templer would make is invalid! They had to willfully edit the conclusions to make their argument, which is more than a little dishonest.

It reminds me of another recent disclosure of a creationist paper that also misrepresented its results. This paper, published in the International Journal of Neuroscience, openly declared that it had evidence for creationism.

In the paper, Kuznetsov reportedly identified an mRNA from one vole species that blocked protein synthesis in a related vole species. That same mRNA, however, did not block translation in the original vole species or another species that was more distantly related. The finding, Kuznetsov wrote in his report, supported “the general creationist concept on the problems of the origin of boundless multitudes of different and harmonically functioning forms of life.”

I vaguely remember reading that paper and rolling my eyes at how weak and sloppy the data was — it was never taken seriously by anyone but creationists. I don’t recall the details, though, because it was published 30 years ago, and is only now being retracted, after decades of the author fabricating data and being so obvious about it that he was fired as editor of two journals in 2013. The guy had a reputation, shall we say. Yet he managed to maintain this academic facade for years.

Phillipe Rushton had similarly managed to keep up the pretense of being a serious academic for an awfully long time, right up until his death in 2012. He used his reputation to spray all kinds of fecal nonsense into the scientific literature, and that’s why you have to maintain a skeptical perspective even when reading prestigious journals.

Yeth, Mithtrethth, I live to therve.

Yesterday, I fed my spiders waxworms, and they went mad for them. Their cages were festooned with dead or paralyzed grubs, and the spiders were sucking out their guts. It was all very charming. Today, though, I come in to find cages littered with blackened corpses, the effects of all that necrotic venom and digestive enzymes. Yuck. All of the spiders were bloated and engorged and had retreated to shadowy corners to digest. Except one, that was eager to use all her energy for a new purpose: Trillian made an egg sac! I just had to record her proud moment.

They’re such sweet little monsters.

Tomorrow, I get to clean out the decaying corpses. I’m feeling a bit like an Igor now.