This is a nicely done periodic table on the web — I particularly liked the little slider that would let me change the temperature and see which ones would melt and boil.
Early Cambrian shrimp! I just had to share this pretty little fellow, a newly described eucrustacean from the lower Cambrian, about 525 million years ago. It’s small — the larva here is about 1.8mm long, and the adults are thought to have been 3mm long — but it was probably numerous, and I like to imagine clouds of these small arthropods swarming in ancient seas.
I have some thoughts on the topic of male and female dominance brought up by Blue_Expo.
In fact, it was the topic of a paper for my Evolution of Human Aggression class…
Females are under some different sexual selection pressures than males stemming from the fact that they are the limited sex. They can only produce a finite number of offspring and are heavily invested in their progeny. Perhaps this is the basis for the female dominance social hierarchies observed in bonobos (Parish et al., 1994) and hyenas (Jenks, 1995). In both these systems, offspring inherit their mother’s rank and a mother is willing to engage in physical combat or establish social coalitions designed to elevate their offspring in rank. Because rank determined ability to procure resources, survive and reproduce, and females had high parental investment, there was sufficient evolutionary pressure for females to evolve the capacity to establish dominance even over males on their offsprings’ behalf.
I’ve written a long introduction to the work I’m about to describe, but here’s the short summary: the parts of organisms are interlinked by what has historically been called laws of correlation, which are basically sets of rules that define the relationship between different characters. An individual attribute is not independent of all others: vary one feature, and as Darwin said, “other modifications, often of the most unexpected nature, will ensue”.
Now here’s a beautiful example: the regulation of the growth of mammalian molars. Teeth have long been a useful tool in systematics—especially in mammals, they are diverse, they have important functional roles, and they preserve well. They also show distinct morphological patterns, with incisors, canines, premolars, and molars arranged along the jaw, and species-specific variations within each of those tooth types. Here, for example, is the lower jaw of a fox. Look at the different kinds of teeth, and in particular, look at the differences within just the molars.
Note that in this animal, there are three molars (the usual number for most mammals, although there are exceptions), and that the frontmost molar, M1, is the largest, M2 is the second largest, and M3, the backmost molar, is the smallest. This won’t always be the case! Some mammals have a larger M3, and others may have three molars of roughly equal size. What rules regulate the relative size of the various molars, and are there any consistent rules that operate across different species?
To answer those questions, we need to look at how the molars develop, which is exactly what Kavanagh et al. have done.
Cuvier, and his British counterpart, Richard Owen, had an argument against evolution that you don’t hear very often anymore. Cuvier called it the laws of correlation, and it was the idea that organisms were fixed and integrated wholes in which every character had a predetermined value set by all the other characters present.
In a word, the form of the tooth involves that of the condyle; that of the shoulder-blade; that of the claws: just as the equation of a curve involves all its properties. And just as by taking each property separately, and making it the base of a separate equation, we should obtain both the ordinary equation and all other properties whatsoever which it possesses; so, in the same way, the claw, the scapula, the condyle, the femur, and all the other bones taken separately, will give the tooth, or one another; and by commencing with any one, he who had a rational conception of the laws of the organic economy, could reconstruct the whole animal.
Cuvier famously (and incorrectly) argued that he could derive the whole of the form of an animal from a single part, and that this unity of form meant that species were necessarily fixed. An organism was like a complex, multi-part equation that used only a single variable: you plugged a parameter like ‘ocelot’ into the Great Formula, and all the parts and pieces emerged without fail; plug in a different parameter, say ‘elephant’, and all the attributes of an elephant would be expressed. By looking at one element, such as the foot, you could determine whether you were looking at an elephant or an ocelot, and thereby derive the rest of the animal.
All of us mammals have pretty much the same set of genes, yet obviously there have to be some significant differences to differentiate a man from a mouse. What we currently think is a major source of morphological diversity is in the cis regulatory regions; that is, stretches of DNA outside the actual coding region of the gene that are responsible for switching the gene on and off. We might all have hair, but where we differ is when and where mice and men grow it on their bodies, and that is under the control of these regulatory elements.
A new paper by Fondon and Garner suggests that there is another source of variation between individuals: tandem repeats. Tandem repeats are short lengths of DNA that are repeated multiple times within a gene, anywhere from a handful of copies to more than a hundred. They are also called VNTRs, or variable number tandem repeats, because different individuals within a population may have different numbers of repeats. These VNTRs are relatively easy to detect with molecular tools, and we know that populations (humans included) may carry a large reservoir of different numbers of repeats, but what exactly the differences do has never been clear. One person might carry 3 tandem repeats in a particular gene, while her neighbor might bear 15, with no obvious differences between them that can be traced to that particular gene. So the question is what, if anything, does having a different number of tandem repeats do to an organism?
Casey Luskin has to be a bit of an embarrassment to the IDists…at least, he would be, if the IDists had anyone competent with whom to compare him. I tore down a previous example of Luskin’s incompetence at genetics, and now he’s gone and done it again. He complains about an article by Richard Dawkins that explains how gene duplication and divergence are processes that lead to the evolution of new information in the genome. Luskin, who I suspect has never taken a single biology class in his life, thinks he can rebut the story. He fails miserably in everything except revealing his own ignorance.
It’s quite a long-winded piece of blithering nonsense, so I’m going to focus on just three objections.
Cosma has to go and show off with a magisterial demonstration of why he is the smartest man on the internet: he’s written an exceptionally thorough description of heritability and IQ. It’s not a light read (statistics and genetics!), but it’s probably the most informative thing I’ve read in a month or more.
I’m sure I’m going to have to read it a few more times before I’ve absorbed it all.
One concept that is sometimes used in developmental biology is the idea of the “master control gene” or “master switch” — a single gene whose expression is both necessary and sufficient to trigger activation of many other genes in a coordinated fashion, leading to the development of a specific tissue or organ. It’s a handy concept on which to hang a discussion of transcription factors, but it may actually be of rather limited utility in the real world of molecular genetics: there don’t seem to be a lot of examples of master control genes out there! Pax-6 is the obvious one, a gene that initiates development of the eye, and other genes may be mentioned in certain stem cell pathways, but even in the eyes of vertebrates, for example, eye development is more complicated than a single switch, and similarly, many other developmental processes seem to use multiple or redundant regulatory controls — the cases where we have a single gene bottleneck are either rare or poorly represented in the literature.
They’re still at least pedagogically useful, though — it’s a simple case of imposition of a specific developmental pathway on a patch of tissue.
Hmmm. Estimates of the cost of the war in Iraq range from $4.4 to 7.1 billion per month. If I assume about $5 billion, it looks like we’re throwing away about $7 million per hour in that effort; so it looks like a little bit more than a half-hours worth of bloody war costs us $4 million. So let’s just stop for about 40 minutes, OK?
What was the point of that calculation? The government is threatening to shut down the Arecibo Observatory unless they can cough up $4 million dollars for its operating budget for the next three years. Wow.
The National Science Foundation, which has long funded the dish, has told the Cornell University-operated facility that it will have to close if it cannot find outside sources for half of its already reduced $8 million budget in the next three years — an ultimatum that has sent ripples of despair through the scientific community.
Shall we trade three years of science for less than an hour’s worth of war? That sounds like a no-brainer to me. The observatory doesn’t even kill anybody in normal operation. Or is that considered a strike against it?
