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Abnormal X‐Chromosome Dosage Compensation as a Possible Cause of Early Developmental Failure in Mice
Author(s) -
Takagi Nobuo
Publication year - 1991
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/j.1440-169x.1991.00429.x
Subject(s) - imprinting (psychology) , biology , x inactivation , genomic imprinting , dosage compensation , genetics , x chromosome , embryogenesis , endoderm , ectoderm , embryonic stem cell , embryo , microbiology and biotechnology , gene , dna methylation , gene expression
An extra maternally derived X chromosome (X M ) but not a paternally derived one (X P ) is detrimental in early mouse embryogenesis resulting in failure to form the ectoplacental cone and extra‐embryonic ectoderm. Cytogenetic studies suggested that two X M chromosomes remain active in the trophectoderm and possibly also the primitive endoderm, in which X P is preferentially inactivated in normal female embyos. Two copies of an active X chromosome due to maternal imprinting seem to prevent further differentiation of the trophectoderm.