TY - JOUR
T1 - Sex specific X chromosome expression caused by genomic imprinting
AU - Iwasa, Y.
AU - Pomiankowski, A.
N1 - Funding Information:
We are grateful for support received from The Royal Society "AP# and from a Grant!in!Aid from the Ministry of Education\ Science\ Sports and Culture "YI#[ Our collaboration was made possible by Fellowships we both held at the Wissenschaftskolleg zu Berlin[ Thanks also to Matteo Adinol_\ Paul Burgoyne\ Greg Hurst and Laurence Hurst[
PY - 1999/4/21
Y1 - 1999/4/21
N2 - 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.
AB - 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.
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U2 - 10.1006/jtbi.1998.0888
DO - 10.1006/jtbi.1998.0888
M3 - Article
C2 - 10196091
AN - SCOPUS:0033590911
SN - 0022-5193
VL - 197
SP - 487
EP - 495
JO - Journal of Theoretical Biology
JF - Journal of Theoretical Biology
IS - 4
ER -