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Of Male and Female

Jed Bland

 
GENDYS JOURNAL

Issue 8
November 1999

 
It has for years been the dogma that development as a female is some sort of passive default option due to the lack of a Y chromosome.

The search for the gene or genes responsible for male development ended in a region of only 250 base pairs, compared to an average length of many thousands, which was christened the SRY gene. It probably has a long evolutionary history, being almost identical to gene involved in reproduction in yeast.

It seems that the protein produced by the SRY gene binds to the DNA molecule in specific places, and causes it to bend sharply. It is believed that this change in the three dimensional geometric structure alters the action of a range of other genes. For instance, there are many factors affecting rate of growth, both genetic and environmental, but it is believed that it accounts for the average larger size of men compared to women.

Sometimes the SRY gene is missing from the Y chromosome, or doesn't activate. The fetus grows, is born, and lives as a little girl, and later as a woman, but her chromosomes are XY. Such people are, usually, clearly women to themselves and everyone else. The first premonition that something is wrong may be when menstruation doesn't begin. Occasionally, during meiosis a piece of a Y chromosome transfers to the X, and is carried on into the sperm. Thus the female embryo that results is XX, but develops as a male.

So far so good - nothing to challenge the idea that women are men with something missing. However recently a number of researchers have begun to challenge this assumption. and evidence has come to light of genes that might actively promote the formation and function of the ovaries.

One such candidate was AHC (also known as DAX1). In Nature Science Update, 10th. December, 19.98, Henry Gee reported work by J. Larry Jameson of Northewestern University Medical School, Chicago, Illinois which provides evidence to show that, in fact, the role of AHC is not to promote ovarian function, but instead to act as an 'anti-testis' factor, which is something rather different.

Combined with earlier observations on AHC in humans, it would seem that AHCh acts to regulate the activities of genes carried on the Y chromosome that are known to be testis-determining factors, in other words, the SRY gene.

However there is another report in Nature Science Update of the work of Andrew P. McMahon and colleagues from the Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts, who have identified a positive female "switch" gene, whose expression in the female fetus is esential for female development. If this gene is absent, the otherwise female fetus develops testes and other parts of the male reproductive tract.

McMahon and colleagues have found that far from being an inevitable consequence of a lack of the testis-determining gene, development as a female absolutely requires the action of another gene-Wnt-4-which actively suppresses male development and provides positive signals for the developing female reproductive organs. In its absence, chromosomally female mice do not develop internal female reproductive organs, but make testes and Wolffian ducts which are indistinguishable from those of their male counterparts. Male mice lacking Wnt-4 on the other hand simply develop normally, proving that Wnt-4 is a genuine female developmental switch. Although it is present in both male and female animals, and is expressed in both early in fetal development, it appears to be turned off in males.

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