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How Sex Keeps The Species Healthy

February 19, 2015 | by Stephen Luntz

photo credit: Creations/Shutterstock. We may have worked out why the seemingly inefficient process of combining sperm and egg is so widespread

A theory for why sexual reproduction is usually a better method for transferring genes than asexual reproduction has gained support. In the process, scientists have gained another tool to help them search for genetic disease mutations.

Most animals, and many plants, reproduce sexually. While it might be fun for us, rueful comments at its expense are even truer for species that waste most of their energy trying to have sex, or kill themselves in the act. Yet sexual reproduction must have advantages, or else creatures that reproduce asexually would long ago have overrun us.

One theory holds that the shuffling of chromosomes from genetically different parents helps us do a better job at fighting off parasites. A related idea is that a more diverse genome is beneficial for responding to changing environmental conditions.

Now, one long-standing explanation has received empirical support. The deleterious mutation hypothesis proposes that when an individual of an asexual species has a mutation, that gene will be passed on to all its offspring. Since most mutations that alter proteins are harmful, this would not be good for the survival of the line. However, in sexual reproduction, some offspring will have more mutations and others less. The ones with fewer mutations will generally thrive while those with more tend to die out, keeping the population as a whole healthy.

However, even mathematical models constructed by the leading advocate of the hypothesis require an average of more than one new deleterious mutation per individual if sex is to provide a benefit. The evidence for whether living species actually match this rate remains disputed.

In Nature Genetics, Dr. Philip Awadalla of the University of Montreal has provided powerful new evidence for the deleterious mutation hypothesis. Contrary to high school genetics classes, parental genomes do not recombine evenly. Some segments combine frequently, while others only once in many generations.

If the hypothesis is correct, then the parts of our genome that seldom combine should have more mutations. This is indeed what Awadalla found. Mutations build up from parent to child on these stretches of chromosome until recombination finally occurs. “But since these mutations rest on less dynamic segments of our genome, the process can potentially take many hundreds of generations,” Awadalla says.

By identifying the parts of the genome that rarely combine, Awadalla is providing scientists seeking genetic disease mutations a suggestion on the best places to start looking. Rather than having to hunt through the entire human genome, researchers can focus on slow-combining “coldspots” which make up a third of the genome and are most likely to harbor mutations. Awadalla also found that mutations in the coldspots tend to be more serious than those elsewhere in the genome.

The study was done with genomes from four human populations, and found that the difference between coldspots and rapidly combining regions was smaller for people of African than European descent. According to the authors, this demonstrates that new selection pressures can change the speed at which mutations are removed over short evolutionary periods.

Source: IFLS

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This entry was posted on February 26, 2015 by in Biology, General and tagged , , , , , , , , , .

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