Selection Pressures in Action

Dr Adrian Charbin – the man himself

Here we will discuss hot and current topics in the world of science, where important new discoveries and research flashpoints will be shared and discussed. Oxbridge interviewers often ask about current scientific affairs, so it is very important to be aware of new developments and have informed opinions on them! This blog is written by Dr Adrian Charbin, who studied Natural Sciences at Sidney Sussex, Cambridge. Having specialised in genetics in his final year, Adrian went on to complete a PhD in Biochemistry and Molecular Biology while working for Cancer Research UK and University College London.

What drives can drive evolution to happen rapidly, over a short time period? A strong selection pressure can underpin such a phenomenon, although evidence accurately showing this has not always been easy to come by. A new report by Schal et al in the May 24^th edition of Science provides an excellent demonstration (if slightly gross) of a rapid evolutionary change driven by a strong selection pressure.

In certain groups of the widespread German cockroach (Blattella germanica), nerve cells that normally detect bitter, potentially toxic compounds now also respond to glucose, says entomologist Coby Schal of North Carolina State University in Raleigh. The “bitter” reaction suppresses the “sweet” response from other nerve cells, and the roach stops eating. WATCH the video here.

Normally roaches love sugar. But with these populations, a dab of jelly with glucose in it makes them “jump back,” Schal says. “The response is: ‘Yuck! Terrible!’” This quirk of roach taste explains why glucose-baited poison traps stopped working among certain roaches, Schal says. Such bait traps combining a pesticide with something delicious became popular during the mid-1980s. But in 1993, Jules Silverman, also a coauthor on the new paper, reported roaches avoiding these once-appealing baits.

“This is a fascinating piece of work because it shows how quickly, and how simply, the sense of taste can evolve,” says neurobiologist Richard Benton of the University of Lausanne in Switzerland.

What pest-control manufacturers put in their roach baits now, and whether some still use glucose, isn’t public. Roaches don’t detect taste with tongues, as people do, but instead use hairlike structures that grow in lots of spots on their bodies. “The cockroach can taste things by stepping into them,” Schal says. Taste nerve cells spangle the roach hairs. Co-author Ayako Wada-Katsumata presented various flavors and measured the responses from two types of nerve cells, the GRN1 cells, which detect sugars, and the GRN2 cells, which normally warn of bitter compounds such as caffeine.

In roaches that shied away from glucose, the sweet-detecting nerve cells continued to fire when exposed to various sugars. What differed in these roaches were the bitter-detecting GRN2 cells, which responded to glucose as well as to bitter compounds. In these insects, bitter overwhelms the signal from the sweet detector.

Among the scenarios Schal imagines for the origin of GRN2’s glucose aversion are a chance mating with some other as-yet-unidentified roach species that doesn’t eat glucose. Or he wonders if the bait traps triggered the spread of formerly rare genetic variations in roach taste cells left over from before the species moved in with people. Those outdoor ancestors might have evolved a distaste for glucose because so many plants defend themselves with compounds called glucosides, blends of sweetness and something noxious. An aversion to glucose doesn’t mean distaste for all sugars. The new study found roach enthusiasm for fructose and maltose. During roach courtship, a male roach offers maltose as a gift to win female favour, not dissimilar to how chocolates are used in human courtship…!

Development

Normally all human cells (baring gametes and red blood cells) are diploid, meaning that they contain two copies of each of our chromosomes. When a cell does not contain this usual pairing of chromosomes, that cells is described as being aneuploid, i.e. having an abnormal number of chromosomes present. Aneuploid cells are nearly always unable to survive and die should they form. This is because Aneuploidies disturb the delicate balance of gene products in cells. By definition, aneuploid cells have an abnormal number of chromosomes. Because each chromosome contains hundreds of genes, the addition or loss of even a single chromosome disrupts the existing equilibrium in cells, and in most cases, is not compatible with life.

The most common aneuploidy to occur is trisomy, when three chromosomes are present within a cell instead of the usual two. Any chromosome can become trisomy during development, but the vast majority of these result in non-viable embryos and miscarriages. However trisomy 21, or Down’s Syndrome, is tolerated and the embryo is viable. An interesting question to think about (and heard before in Oxbridge interviews!) is why trisomy 21 is viable whereas nearly all other trisomy’s are not? Children born with Down’s syndrome suffer from a range of mental and physical handicaps, including a greatly lowered IQ and severe learning difficulties.

Above is a karyotype showing the usual pairing of our chromosomes. However, in this particular case there is trisomy of chromosome number 13, called Patau Syndrome. (Bonus question, is the karyotype above from a male or female?)

Recent research by US scientists found a reduction in connections among the brain cells and possible faults in genes that protect the body from ageing, giving an insight into early brain development. A team led by Anita Bhattacharyya, a neuroscientist at the Waisman Center at the University of Wisconsin-Madison, grew brain cells from skin cells of two individuals with Down’s syndrome. This involved reprogramming skin cells to transform them into a type of stem cell that could be turned into any cell in the body. Brain cells were then grown in the lab, providing a way to look at early brain development in Down’s syndrome. One significant finding was a reduction in connections among the neurons, said Dr Bhattacharyya, suggesting that the cells communicate less between each other, fitting in with earlier predictions on how the Down syndrome brain operates.

Brain cells communicate through connections known as synapses. The brain cells in Down’s syndrome individuals had only about 60% of the usual number of synapses and synaptic activity. “This is enough to make a difference,” added Dr Bhattacharyya. “Even if they recovered these synapses later on, you have missed this critical window of time during early development.” The researchers looked at genes that were affected in the stem cells and neurons from two individuals with Down’s syndrome. They found that genes on the extra chromosome, chromosome 21, were increased greatly, particularly genes that responded to damage from free radicals, which may play a role in ageing. This could explain why people with Down’s syndrome appear to age quickly, although this remains to be tested, said the University of Wisconsin-Madison team.