Basics: Synteny

Let’s play the most boring card game in the universe!

Here are the rules. We start with a fully sorted deck of 52 cards, and we deal out four hands. We don’t deal in the ordinary way, either: we give the top 13 cards to the first player, then the next 13 to the second, and so forth. (We could also do the usual deal, but it makes the illustration and logic a little more difficult to see. We’ll keep it simple for now.)

This is what the table will look like.

Hand 1 Ai-233f23e2a2ca8059264849e39e1760d2-heart.gif Ki-233f23e2a2ca8059264849e39e1760d2-heart.gif Qi-233f23e2a2ca8059264849e39e1760d2-heart.gif Ji-233f23e2a2ca8059264849e39e1760d2-heart.gif 10i-233f23e2a2ca8059264849e39e1760d2-heart.gif 9i-233f23e2a2ca8059264849e39e1760d2-heart.gif 8i-233f23e2a2ca8059264849e39e1760d2-heart.gif 7i-233f23e2a2ca8059264849e39e1760d2-heart.gif 6i-233f23e2a2ca8059264849e39e1760d2-heart.gif 5i-233f23e2a2ca8059264849e39e1760d2-heart.gif 4i-233f23e2a2ca8059264849e39e1760d2-heart.gif 3i-233f23e2a2ca8059264849e39e1760d2-heart.gif 2i-233f23e2a2ca8059264849e39e1760d2-heart.gif
Hand 2 Ai-94f8cf214b78029e2cd1e9398229dda0-club.gif Ki-94f8cf214b78029e2cd1e9398229dda0-club.gif Qi-94f8cf214b78029e2cd1e9398229dda0-club.gif Ji-94f8cf214b78029e2cd1e9398229dda0-club.gif 10i-94f8cf214b78029e2cd1e9398229dda0-club.gif 9i-94f8cf214b78029e2cd1e9398229dda0-club.gif 8i-94f8cf214b78029e2cd1e9398229dda0-club.gif 7i-94f8cf214b78029e2cd1e9398229dda0-club.gif 6i-94f8cf214b78029e2cd1e9398229dda0-club.gif 5i-94f8cf214b78029e2cd1e9398229dda0-club.gif 4i-94f8cf214b78029e2cd1e9398229dda0-club.gif 3i-94f8cf214b78029e2cd1e9398229dda0-club.gif 2i-94f8cf214b78029e2cd1e9398229dda0-club.gif
Hand 3 Ai-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif Ki-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif Qi-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif Ji-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif 10i-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif 9i-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif 8i-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif 7i-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif 6i-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif 5i-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif 4i-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif 3i-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif 2i-2b47b78b9878c3d3b29bd4f7d2d03e19-diamond.gif
Hand 4 Ai-37cc42c4042ea4372806e327e67b2e42-spade.gif Ki-37cc42c4042ea4372806e327e67b2e42-spade.gif Qi-37cc42c4042ea4372806e327e67b2e42-spade.gif Ji-37cc42c4042ea4372806e327e67b2e42-spade.gif 10i-37cc42c4042ea4372806e327e67b2e42-spade.gif 9i-37cc42c4042ea4372806e327e67b2e42-spade.gif 8i-37cc42c4042ea4372806e327e67b2e42-spade.gif 7i-37cc42c4042ea4372806e327e67b2e42-spade.gif 6i-37cc42c4042ea4372806e327e67b2e42-spade.gif 5i-37cc42c4042ea4372806e327e67b2e42-spade.gif 4i-37cc42c4042ea4372806e327e67b2e42-spade.gif 3i-37cc42c4042ea4372806e327e67b2e42-spade.gif 2i-37cc42c4042ea4372806e327e67b2e42-spade.gif

Next, we play the game, whatever it is. It really doesn’t matter, since we know exactly what hand everyone has, right? So don’t worry about the rules for that. What’s important is that next the dealer carefully picks up each hand in reverse order and stacks them, restoring the original arrangement of the deck.

[Read more…]

The platypus genome

Blogging on Peer-Reviewed Research

Finals week is upon me, and I should be working on piles of paper work right now, but I need a break … and I have to vent some frustration with the popular press coverage of an important scientific event this week, the publication of a draft of the platypus genome. Over and over again, the newspaper lead is that the platypus is “weird” or “odd” or worse, they imply that the animal is a chimera — “the egg-laying critter is a genetic potpourri — part bird, part reptile and part lactating mammal”. No, no, no, a thousand times no; this is the wrong message. The platypus is not part bird, as birds are an independent and (directly) unrelated lineage; you can say it is part reptile, but that is because it is a member of a great reptilian clade that includes prototherians, marsupials, birds, lizards and snakes, dinosaurs, and us eutherian mammals. We can say with equal justification that we are part reptile, too. What’s interesting about the platypus is that it belongs to a lineage that separated from ours approximately 166 million years ago, deep in the Mesozoic, and it has independently lost different elements of our last common ancestor, and by comparing bits, we can get a clearer picture of what the Jurassic mammals were like, and what we contemporary mammals have gained and lost genetically over the course of evolution.

We can see that the journalistic convention of emphasizing the platypus as an odd duck of a composite creature is missing the whole point if we just look at the title of the paper: “Genome analysis of the platypus reveals unique signatures of evolution.” This is work that is describing the evidence for evolution in a comparative analysis of the genomes of multiple organisms, with emphasis on the newly revealed data from the platypus.

[Read more…]


That’s the sound you should hear when Joe Felsenstein takes on an idiotic claim by Sal Cordova. Would you believe that Cordova claims that Kimura and Ohta’s classic 1971 paper “shatters the modern synthesis”? That’s what he claims, on the basis of his poor understanding of the mathematics of population genetics, which is ridiculous on the face of it. So it’s very satisfying to see one of the big guns of population genetics take him down with one brief explanation: contrary to Cordova, the principle he’s describing confirms the effectiveness of natural selection.

Just to help everyone follow along, here’s the simple explanation. As Kimura and Ohta explained, most mutations, even advantageous ones, do not go to fixation in a population, and are lost. Slimy Sal just reports only that much, and declares the end of evolution, to huzzahs from his equally ignorant cronies. What he ignores, and what Felsenstein explains, is that 1) the frequency of fixation of advantageous alleles will be much, much greater than for neutral or deleterious alleles, and 2) that there are many mutations being generated — so natural selection is an effective filter.

It’s a kind of mathematical quote mine, where Cordova only tells a tiny part of the story and leaves out the important bit that destroys his thesis.

Basics: How can chromosome numbers change?

There in the foaming welter of email constantly flooding my in-box was an actual, real, good, sincere question from someone who didn’t understand how chromosome numbers could change over time — and he also asked with enough detail that I could actually see where his thinking was going awry. This is great! How could I not take time to answer?

So here’s the question:

How did life evolve from one (I suspect) chromosome to… 64 in horses, or whatever organism you want to pick. How is it possible for a sexually reproducing population of organisms to change chromosome numbers over time?

Firstly: there would have to be some benefit to the replication probability of the organisms which carry the chromosomes. I don’t see how this would work. How is having more chromosomes of any extra benefit to an organism’s replicative success? Yes, perhaps if those chromosomes were full of useful information… but the chances of that happening are non existent and fly in the face of ‘small adaptations over time’.

Secondly, the extra chromosomes need to come from somewhere. I’m not sure about this, but I believe chromosome number are not determined by genes, are they? There isn’t a set of genes which determines the number of chromosomes an organism has. So the number is fixed, determined by the sexually reproducing parents. Which leads me to believe that if the number does change, and by chance the organism is still alive and capable of sexual reproduction, that the number will start swinging back and forward, by 1 or 2, every generation, and never stabilising. The chances of this happening are also very very slim.

[Read more…]

A neurological mechanism for Fragile-X disease

Blogging on Peer-Reviewed Research

I’m busy preparing my lecture for genetics this morning, in which I’m going to be talking about some chromosomal disorders … and I noticed that this summary of Fragile-X syndrome that was on the old site hadn’t made it over here yet. A lot of the science stuff here actually gets used in my lectures, so they represent a kind of scattered online notes, so I figured I’d better put this one where I can find it.

I haven’t even finished grading the last of the developmental biology papers, and already my brain is swiveling towards the genetics literature, as I get in the right frame of mind to teach our core genetics course in the spring. And, lo, here is a new paper in PNAS that addresses details of a topic I bring up every time.

There are a surprising number of heritable diseases that share a couple of common traits: they are neurodegenerative, causing progressive loss of neural control, and they also exhibit a phenomenon called genetic anticipation—they tend to get worse, with earlier onset and more severe affects with each generation. Some of these diseases may be rather obscure, for instance
Haw-River Syndrome (AKA Dentatorubral-pallidoluysian atrophy),
Friedreich Ataxia,
Machado-Joseph Disease, or
X-linked Spinal and Bulbar Atrophy Disease (AKA Kennedy Disease), but others you’ve probably heard of, like
Myotonic dystrophy and
Huntington Disease. These are dreadful diseases that are variable in their pattern of appearance, and have terrible symptoms, like loss of motor control, chorea, seizures, dementia, and eventually, death.

[Read more…]

The genome is not a computer program

The author of All-Too-Common Dissent has found a bizarre creationist on the web; this fellow, Randy Stimpson, isn’t at all unusual, but he does represent well some common characteristics of creationists in general: arrogance, ignorance, and projection. He writes software, so he thinks we have to interpret the genome as a big program; he knows nothing about biology; and he thinks his expertise in an unrelated field means he knows better than biologists. And he freely admits it!

I am not a geneticist or a molecular biologist. In fact, I only know slightly more about DNA than the average college educated person. However, as a software developer I have a vague idea of how many bytes of code is needed to make complex software programs. And to think that something as complicated as a human being is encoded in only 3 billion base pairs of DNA is astounding.

Wow. I know nothing about engine repair, but if I strolled down to the local garage and tried to tell the mechanics that a car was just like a zebrafish, and you need to throw a few brine shrimp in the gas tank now and then, I don’t think I would be well-received. Creationists, however, feel no compunction about expressing comparable inanities.

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Bisexual flies and the neurochemistry of behavior

Blogging on Peer-Reviewed Research

On the one hand, this is a strange tale of mutant, bisexual, necrophiliac flies, and you’ve got to love it for the titillating nature of the experiments. But on the other, much more interesting hand, it’s a story about drilling down deeply into the causes of a complex behavior, and tracing it to a single gene product — and it also reveals much about the way the chemicals sloshing about in the brain can modulate responses to stimuli. Work by Grosjean and others on a simple Drosophila mutant, genderblind, which causes flies to be indiscriminate about gender in their courtship, opens up a window into how sexual responses are shaped and specified.

Think about human sexual responses. Some of us, when we see an attractive woman, are at least mildly aroused; others are have their sexual interest picqued when they see an attractive man; still others might feel sexual urges when they see a shoe, or a plush animal, or a pot of baked beans. No matter what the stimulus, these are all biological responses, with something in the environment matching some trigger in our brains and initiating a cascade of neural, neurochemical, and hormonal activity that leads to sexual behaviors. The question we want to address is what every step in the biology is doing; unfortunately, human behaviors are both too complex and not amenable to ethical experimentation, so we turn instead to simpler organisms that allow us to find simpler causes and carry out thorough experiments to probe the behavior.

[Read more…]

Dubious parentage

It would seem like sweet poetic justice if James Watson were found to be 1/8th African, but I’m afraid I don’t quite believe it. This is news coming from a company called deCODE genetics, an Icelandic outfit that analyzes an individual’s racial background on the basis of various genetic markers. While I can buy the claim that they can assess the distribution of various alleles in populations, I really dislike the game of trying to work in reverse and assign the fraction of a race to an individual.

I don’t think Larry is much impressed with them, either. Here’s another article that brings up the flaws.

The problem is compounded by the increasing improbability of the company’s claims. Watson is also 9% Asian. He’s got a 31% lesser chance than average of getting asthma, and a 2% greater chance of prostate cancer. These kinds of numbers are meaningless when applied to individuals. We don’t even know all the genetic factors that contribute to the various diseases listed, so it’s ludicrous to pretend they can quantify the total risk for a single person that way. While I’ve got no problem thinking there are shared alleles percolating through African and European populations, there are much more reliable ways of determining that a person has an African great grandparent.

(via Accidental Blogger)

Student Post: Immortalized Mules

I spent a summer working on an Arabian horse ranch when i was 17. I loved that place and am crazy about Arabians but… let’s face it. We’ve severely inbred horses for show. Exhibit A:

It’s not uncommon for an Arabian pedigree to boast seven lines of relation to one horse. Bask, for instance, was a famous Arabian stallion and today a large percentage of Arabs are his decendents including my horse, Rebel, of whom I’m foolishly fond:


Well, I learned some interesting news at today’s Senior Seminar. Why inbreed when you can clone! It’s all the rage among mule racing enthusiasts. Don Jacklin, president of the American Mule Racing Association, almost single-handedly funded cloning research at the University of Idaho of his champion mule line. Cloning champion horses has been made into a very lucrative business in France. Cryozootech turns a large profit cloning gelded or aged horses so that their clones can be used for breeding. If I had 300 grand I could clone Rebel.

It will be really interesting to see what happens to these animals as they age. The mules are reported to be healthy and competitive racers but concerns over telomere length have yet to be addressed.

…And yes. I did just want to use the phrase “mule racing enthusiasts.”