[lbo-talk] Y: Ain't as Good as X

Les Schaffer schaffer at optonline.net
Sat Nov 26 11:10:20 PST 2005


Yoshie Furuhashi wrote:


> Rumors of the demises of Y may have been exaggerated, but Y still
> ain't as good as X. :->

from: http://www.devbio.com/article.php?ch=5&id=47 :

Since only half the human population has a Y chromosome, the Y

chromosome does not have genes that are important to the vital body

functions. Basically, it contains genes for testes formation and

sperm maturation. Everyone has at least one X chromosome, however,

and it contains numerous genes that are essential for normal

development and body function.

also, an interesting article in Nature last week on X-chromosome inactivation:

Nature 438, 297-298 (17 November 2005) | doi:10.1038/438297a

Developmental biology: The X-inactivation yo-yo Wolf Reik and Anne C. Ferguson-Smith

Abstract In female mammals, one of two X chromosomes has to be shut down during early development. To what extent does this 'imprinted X-chromosome inactivation' involve the history of the chromosome?

In most mammals, males have the male sex-determining Y chromosome and a single X chromosome, whereas females have two X chromosomes. In females, the resulting imbalance in the 'dosage' of genes on the X chromosomes needs to be compensated so that gene expression from the X chromosome is equivalent in males and females. Mammals have evolved a unique form of dosage compensation, called X-chromosome inactivation, in which one of the two X chromosomes in female cells is silenced epigenetically[1] — that is, by factors such as chemical modification of the DNA, or of the histone proteins that package DNA into chromosomes, often involving non-coding RNAs. Many aspects of mammalian X inactivation remain mysterious. But through elegant studies in the mouse, Okamoto and colleagues (page 369 of this issue)[2] have unravelled some of the earliest events in the process.

During early development of female mouse embryos, and in extra-embryonic tissues such as the placenta, it is always the X chromosome derived from the father that is inactivated3. Gene expression from only one parental member of a chromosome pair is known as imprinting, and is caused by an epigenetic memory first arising in the egg or the sperm. Later on, in the embryonic tissues, X inactivation is random with respect to the parental origin of the X chromosomes[4].

There is considerable interest in understanding the mechanisms that specifically silence the paternal X chromosome in early development, and the extent to which the history of that chromosome is involved.

[snip]

The latest work illustrates the amazing plasticity and dynamic nature of epigenetic programming and reprogramming in germ cells and early embryos.

les schaffer



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