RETARDED POSTIMPLANTATION DEVELOPMENT OF XO MOUSE EMBRYOS - IMPACT OFTHE PARENTAL ORIGIN OF THE MONOSOMIC X-CHROMOSOME

About 12-17% of the embryos obtained by mating mice carrying the In(X) 1H or Paf mutations are of the 39,X (X0) genotype. Depending on the mu tant mice used for mating, the monosomic X chromosome can be inherited from the paternal (X-P) Or the maternal (X-M) parent. The X(P)0 embry os display developmental retardation at gastrulation and early organog enesis. X(P)0 embryos also display poor development of the ectoplacent al cone, which is significantly smaller in size and contains fewer tro phoblasts than XX siblings. In contrast, X(M)0 embryos develop normall y and are indistinguishable from XX littermates. In both types of X0 e mbryos, an X-linked lacZ transgene is expressed in nearly all cells in both the embryonic and the extraembryonic tissues, suggesting that X inactivation does not occur when only one X is present. Of particular significance is the maintenance of an active X-P chromosome in the ext raembryonic tissues where normally the paternal X chromosome is prefer entially inactivated in XX embryos. The differential impact of the inh eritance of X chromosomes from different parents on the development of the X0 embryos raises the possibility that the X-P is less capable th an the X-M in providing the appropriate dosage of X-linked activity th at is necessary to support normal development of the embryo and the ec toplacental cone. Alternatively, the development of the X(P)0 embryo m ay be compromised by the lack of activity of one or several X-linked g enes which are expressed only from the maternal X chromosome. Without the activity of these genes, embryonic development may be curtailed ev en though all other loci on the X-P chromosome are actively transcribe d. (C) 1998 Academic Press.