Check out Phil for the details. For us Minnesotans, the events start around 8pm, should reach totality around 9, and should be over around 11.
Here’s the good news: we’re supposed to have clear skies!
And now the bad news: it’s about -27°F outside right now, and while we’re supposed to warm up a little today, it’s still going to be about -15°F tonight. Don’t let your eyeballs freeze while you’re doing your moongazing.
It means “devil toad,” and it was a 10 pound monster that lived 70 million years ago, in what is now Madagascar. It’s huge, and judging by its living cousins, was a voracious predator. If it were alive today, it would probably be eating your cats and puppies.
In other words, this was an awesome toad, and I wish I had one for a pet.
Here’s what it looks like, with some very large extant toads for comparison.
There are some biogeographical puzzles associated with this beast. It’s found in Madagascar, but it’s closest extant relatives are South American…and since frogs and toads do a poor job of crossing salt water, that implies the existence of land bridges between those continents around the Cretaceous. It’s not a major puzzle, though, although some of the news reports I’ve seen play up the concern, as if it were a significant controversy. As the authors explain,
We suggest that extant ceratophryines are remnants
of a Gondwanan hyloid clade that once ranged from at least
South America to Indo-Madagascar. Whether this clade was
more broadly distributed and on which Gondwanan landmass it
originated cannot be determined on current evidence. However,
as the Late Cretaceous fauna of the Maevarano Fm,
including its ceratophryine anuran, bears little resemblance to
that of modern Madagascar, major biotic changes clearly occurred on the island in the intervening period. When and how the ancestors of the endemic mantellid and microhylid anurans arrived on Madagascar remains controversial,
but there is general agreement that these frogs did not diversify
significantly until the Paleogene. Their radiation
has been linked, at least in part, to the expansion of rainforests,
but may also have been facilitated by the extinction of archaic
faunal elements, including ceratophryines.
It was a diverse, widespread group once upon a time, and it’s not at all challenging to report that the continents have shifted in 70 million years. It’s just very cool that anurans achieved the status of charismatic megafauna*, once upon a time.
*For a generous definition of “mega”.
Evans SE, Jones MEH, Krause DW (2008) A giant frog with South American affinities from the Late Cretaceous of Madagascar. Proc Nat Acad Sci USA 105(8):2951-2956.
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.
