Sex specific X chromosome expression caused by genomic imprinting.
The conflict theory of genomic imprinting predicts that imprinted genes are growth enhancing when paternally expressed and growth suppressing when maternally expressed. The expression pattern of autosomal imprinted genes generally fits these predictions. However, the conflict theory cannot easily account for the pattern of X-linked imprinting in humans and mice. This has led us to propose a novel hypothesis that X-linked imprinting has evolved to control sex specific gene expression in early embryos. The hypothesis links paternal X-imprinting (i.e. paternal copy silencing) to random X-inactivation and the retention of Y-linked copies, and links maternal X-imprinting to escape from random X-inactivation and the loss of Y-linked copies. The hypothesis offers a good explanation of the existing data on X-imprinted genes.
Iwasa
Y
Y
Department of Biology, Faculty of Science, Kyushu University, Fukuoka 812-8581, Japan. yiwassch@mbox.nc.kyushu-u.ac.jp
Pomiankowski
A
A
D000818:Animals; D004303:Dosage Compensation, Genetic; D005260:Female; D015870:Gene Expression; D018392:Genomic Imprinting / Q000235:genetics*; D006801:Humans; D008297:Male; D051379:Mice; D008957:Models, Genetic; D012737:Sex Factors; D014960:X Chromosome