Oh, joy! Carl Zimmer has published a profile of Roger Hanlon, the well-known cephalopod expert, and he is specifically discussing the work on camouflage that I previously summarized. I’ve also cited his work on sexual mimicry and nuptial dances — this is a fellow whose work all true worshipers of the cephalopod should be following.
Since I wrote about the wacky creationist who couldn’t wrap his mind around the idea that plants and animals are related, and since I generally do a poor job of discussing that important kingdom of the plants (I admit it, I’m a metazoan bigot…but I do try to overcome my biases), I thought I’d briefly mention an older review by Elliot Meyerowitz that compares developmental processes in plants and animals. The main message is that developmental processes, the mechanisms that assemble the multicellular whole, are very different in the two groups and are non-homologous, but don’t get confused: the basic cellular processes are homologous, and there’s no doubt that we are related. The emphasis in this paper, though, is the evidence that plants and animals independently evolved multicellular developmental strategies. There is some convergence, but the tools in the toolbox are different.
Now Shubin is on the Mindcast — have a listen.
Our little grievance with a certain paper in Proteomics has made it to the attention of the Chronicle of Higher Ed. Some of the new info (there isn’t a lot) is right here:
Michael J. Dunn, the editor of Proteomics and a professor at University College Dublin’s Conway Institute of Biomolecular and Biomedical Research, told The Chronicle that “it’s not our policy to promote creationism” and added that the journal might retract the article.
As was the case with a less-well-known journal that inadvertently published a creationist paper (The Chronicle, September 24, 2004), the paper in Proteomics had passed peer review. In fact, one of the reviewers for the mitochondria paper, said Mr. Dunn, “does a lot of reviewing for our journal.”
Maybe they ought to lighten that reviewer’s workload, because something slipped by him or her. Or maybe, as some have speculated, something got inserted after the review.
A dismaying update: the paper in question contains a significant amount of outright plagiarism, and large chunks of text are taken literally from Butterï¬eld et al. 2006, “Oxidative stress in
Alzheimer’s disease brain: New insights from
redox proteomics,” European Journal of
Pharmacology 545: 39-50. I hope we hear from Han and Warda sometime; they’ve got a lot of ‘splaining to do.
Mitochondria are fascinating organelles. They are the “powerhouses of the cell” (that phrase is required to be used in any discussion of their function) that generate small, energy rich molecules like ATP that are used in many cellular chemical reactions, but they also have important roles in cell signaling and cell death. They also have a peculiar evolutionary history, arising as endosymbionts; their ancestors were independent organisms that took up residence inside eukaryotic cells in a mutually happy and long-lasting relationship. They exhibit some interesting relics of that prior history, as mitochondria have their own private strand of DNA which encodes some of the genes needed for the chemical processes they execute. Other genes for those functions have migrated over evolutionary time into the nuclear genome, which means the mix of gene products operating in the organelle are from two sources, the mitochondrial and nuclear genome. It’s a good subject for studies in proteomics.
Right now, there is a paper that is available as an Epub ahead of print in the journal Proteomics. It is not promising. In fact, all you have to do is read the title to make you wonder what the authors, Warda and Han, were smoking: “Mitochondria, the missing link between body and soul: Proteomic prospective evidence.”
Attila Csordas asks, “Can you tell a good article from a bad based on the abstract and the title alone?”, and I’m inclined to say yes. Sometimes you get pleasant surprises in the full paper that were not well described in the abstract, but when the abstract and title contain hints that the bridge is out and that somebody has switched the train to the wrong tracks, you can predict that there will be a train wreck if you read further. Here’s the abstract. I’ve highlighted one provocative statement.
Mitochondria are the gatekeepers of the life and death of most cells that regulate signaling, metabolism, and energy production needed for cellular function. Therefore, unraveling of the genuine mitochondrial proteome, as the dynamic determinant of structural-functional integrity to the cellular framework, affords a better understanding of many still-hidden secrets of life behind the already known static genome. Given the critical mitochondrial role under different stress conditions, the aim of the current review is to merge the available scientific data related to mitochondrial proteomes and frame them into a reliable new agreement extending beyond the limited already accepted endosymbiotic hypothesis into broader fundamental mechanisms orchestrating cellular outcome on behalf of cell survival. The focus of this work is to cover first the mitochondrial proteome/genome interplay that is currently believed to be implicated in a range of human diseases. The mechanochemical coupling between mitochondria and different cytoskeleton proteins and the impact of the mitoskeleton on mitochondrial structure and function are then addressed. Further crosstalk between mitochondria and other cellular organelles, e.g., the ER and the nucleus is then discussed. Additionally, the role of mitochondria in apoptosis and the mitochondrial contribution in intercellular communication mediated by gap junctions are also described. These data are presented with other novel proteomics evidence to disprove the endosymbiotic hypothesis of mitochondrial evolution that is replaced in this work by a more realistic alternative. Furthermore, the role of mitochondria in development of oxidative stress-based diseases, e.g., neurodegenerative and cardiovascular diseases is pointed out together with the prospective proteomics view as an alternative prognostic and diagnostic tool for interpreting many mitochondria-related anomalies. The insights generated by recent proteomic research that provide a rational impact on possible mitochondrial-targeted therapeutic interventions are also discussed.
My blog makes a career out of describing train wrecks, so how could I not continue on and read the paper?
Many of you have already seen the gorgeous video below: it’s a spectacularly beautiful animation of the activity in a cell.
I like it, and it’s a useful illustration, but … there’s something fundamental that it gets completely wrong. So today I’m not going to praise it, I’m going to criticize it. It’s a substantial criticism, too, one that means I wouldn’t show this video in my classes without spending more time explaining the error than it takes to show it.
Come on out to Morris this evening — at 6:00, at the Common Cup Coffeehouse, Van Gooch of the biology discipline will be talking about bioluminescence and other phenomena in our Cafe Scientifique. The title of his talk is “Light Giving Life: Real and Artificial,” and I know he’s planning to bring sample organisms to hand out to the attendees.
… you should check out their recent appearance together on Bloggingheads.
We had Neil Shubin here last week, and now Jerry Coyne is guest-blogging at The Loom. I look forward to the day that I can just sit back and invite prominent scientists to do my work for me here.
Although, I have to say that while Coyne is largely correct, he’s being a bit unfair. He’s addressing Olivia Judson’s recent article on “hopeful monsters”, a concept Coyne and the majority of the biological community reject. I reject it, too, but I think there are some legitimate issues that are associated with the idea that are also all too often and unfortunately discarded.
One point that Coyne handles well: there is a disconnect between the magnitude of genotypic changes and phenotypic effects — a single point mutation can cause amazing morphological changes. As Coyne points out, though, although this can happen, it’s not likely to be a major force in evolutionary change. Dramatic, single-step phenotypic effects are the kinds of things that geneticists select for, but they are also exactly the kinds of things that nature selects against. Evolution is much more likely to sidle up towards a major change by successive smaller steps, since those small changes are less likely to be accompanied by major deleterious side effects. Also, phenotypic outcomes of development should be robust to be advantageous, which typically means that there are many regulatory events cooperating to produce them — and they are therefore buffered by multiple controls.
But please, let’s not always dismiss Richard Goldschmidt when discussing “hopeful monsters”. It really wasn’t that awful an idea. Goldschmidt worked on stable variations in organisms: he studied sex differences (ever noticed that males and females have pretty much the same genes, but different phenotypes?) and metamorphosis (similarly, an organism builds two or more very different morphologies with exactly the same genome). He postulated that there could be specific, well-structured, stable nodes of patterns of gene expression — genes weren’t generally fluid, but tended to lock in to particular states. If he were writing today, he’d probably be bringing up the notion of attractors in chaos theory; the ideas are very similar. In that context, he was proposing a worthy concept that should have been taken more seriously than it was — Mayr’s hatchet job was particularly awful.
The “hopeful monster” concept was not shot down by the synthesis — it was ignored. I think it’s been dismantled by developmental biology, though; what we’ve learned is that the stable morphological types we see in a single species are not simply fortunate stable nodes in a nucleus that can be tuned in different ways, but that each are the product of many generations of slow sculpting by the processes of evolution, and that they are riddled with clumsy kluges that aren’t the outcome of some elegant global pattern switching mechanism, but of a long history of small tweaks.
Now also, Coyne is no fan of evo-devo, and he briefly voices the suggestion that the evolutionary developmental biologists are among the sources of this idea that saltational changes lead to sudden, drastic changes in body plans … but I’m just not seeing that. I am seeing work, for instance, that suggests that Hox duplications have been part of the process of producing additions to body plans, but it’s not a case of “poof, arthropods gain a metathorax in one change” — it’s been quite conventional. It’s more like “poof, arthropods gain an extra Hox gene, which initially adds redundancy and is later shaped by evolutionary processes that confer additional specializations on a segment,” quite ordinary stuff that shouldn’t be at all objectionable to Coyne.
It’s especially peculiar to pin the “hopeful monster” concept on evo-devo, when the one evo-devo expert he quotes, the biologist Sean Carroll, explicitly points out that evo-devo doesn’t support it.
Coyne is also going to be speaking at an evo-devo symposium I’ll be attending in April — I’m going to be very interested to hear what he has to say.
