EXPRESSION OF X-LINKED GENES IN ANDROGENETIC, GYNOGENETIC, AND NORMALMOUSE PREIMPLANTATION EMBRYOS

Citation
Ke. Latham et L. Rambhatla, EXPRESSION OF X-LINKED GENES IN ANDROGENETIC, GYNOGENETIC, AND NORMALMOUSE PREIMPLANTATION EMBRYOS, Developmental genetics, 17(3), 1995, pp. 212-222
Citations number
64
Categorie Soggetti
Genetics & Heredity","Developmental Biology
Journal title
ISSN journal
0192253X
Volume
17
Issue
3
Year of publication
1995
Pages
212 - 222
Database
ISI
SICI code
0192-253X(1995)17:3<212:EOXGIA>2.0.ZU;2-3
Abstract
A quantitative RT-PCR approach has been used to examine the expression of a number of X-linked genes during preimplantation development of n ormal mouse embryos and in androgenetic and gynogenetic mouse embryos. The data reveal moderately reduced expression of the Prps1, Hprt and Pdha1 mRNAs in androgenetic eight-cell and morula stage embryos, but n ot in androgenetic blastocysts. Pgk1 mRNA abundance was severely reduc ed in androgenones at the eight-cell and morula stages and remained re duced, but to a lesser degree, in androgenetic blastocysts. These data indicate that paternally inherited X chromosomes are at least partial ly repressed in androgenones, as they are in normal XX embryos, and th at the degree of this repression is chromosome position-dependent or g ene-dependent. Gynogenetic embryos expressed elevated amounts of some mRNAs at the morula and blastocyst stages, indicative of a delay in do sage compensation that may be chromosome position-dependent. The Xist RNA was expressed at a greater abundance in androgenones than in gynog enones at the eight-cell and morula stages, consistent with previous s tudies. Xist expression was observed in both androgenones and gynogeno nes at the blastocyst stage. We conclude that the developmental arrest in early androgenones may be, in part, due to reduced expression of e ssential X-linked genes, particularly those near the X inactivation ce nter, whereas the developmental defects of gynogenones and parthenogen ones, by contrast, may be partially due to overexpression of X-linked genes in extraembryonic tissues, possibly those farthest away from the X inactivation center. (C) 1995 Wiley-Liss, Inc.