作者: Jacquetta M. Trasler , Daphne G. Trasler , Timothy H. Bestor , En Li , Felicia Ghibu
DOI: 10.1002/(SICI)1097-0177(199607)206:3<239::AID-AJA2>3.0.CO;2-J
关键词:
摘要: The mouse genome experiences a large decrease in net 5-methylcytosine between fertilization and implantation; de novo methylation brings to adult somatic cell levels implantation gastrulation. Very little is known of the regulation demethylation or methylation. Levels one form DNA methyltransferase are very high early embryos, but enzyme localized cytoplasm during most preimplantation development. We show here that found exclusively nuclei conceptus after implantation, proximal decidual cells free detectable methyltransferase. High were seen all tissues, including developing nervous system, 9.5- 12.5-day embryos. maternal stores become limiting prior embryonic day 9.5, as shown by barely immunostaining 9.5-day embryos homozygous for loss-of-function mutation (Dnmtn) gene. These mutant failed develop past 25-somite stage showed evidence developmental delay some asynchrony. Normal extraembryonic tissues contained similar methyltransferase, even though severely reduced loss imprinting have previously been observed tissues. findings suggest patterns not simple function concentration unidentified factors must be involved development mouse. © 1996 Wiley-Liss, Inc.