The study, published in the Jan. 23, 2004, issue of Science, shows that an excess of genes on the X chromosome "jump" to a non-sex chromosome, or autosome, during germline cell division. This finding contradicts the historic human genome project paper published in Science Feb. 16, 2001, that claimed the X chromosome had an average rate of traffic similar to all autosomes. The discovery also torpedoes the conventional theory that the X chromosome is the 'hot bed' for sex-related genes.
"That's just not true," said Manyuan Long, the associate professor of ecology and evolution who led the study.
Since the X chromosome becomes inactive meaning it shuts down during male meiosis, the U. Chicago researchers suggest the male-expressed genes must flee the X before this phenomenon takes place.
Long and his colleagues propose that sexual antagonism may also cause this high traffic volume on the X. Since females have two X chromosomes and males have only one, the X is more likely to end up in a female. And if there is a beneficial gene mutation on the X, there is a higher chance that it would help the female, despite its affect on the man. The researchers suggest that the male-expressed genes leave the X for an autosome, where each gene would have the same share of the chromosome and therefore a better environment to carry out its function more effectively.
"An X-linked gene spends two-thirds of its time in females compared with one-half for an autosomal gene, thus the X chromosome becomes 'demasculinized,'" the researchers wrote in the paper.
The research team contends that either theory justifies male-expressed genes leaving the X chromosome, whether the X kicks them out or they merely jump ship before the X shuts down
Contact: Catherine Gianaro
University of Chicago Medical Center