Parental influences on X chromosome expression

Abstract

Using mice that were mosaics for both Xce and phosphoglycerate kinase (Pgk-l) alleles, we have established that the parental source of the Xce gene may affect the probability with which the X chromosome carrying it will remain active. This effect was seen in one allelic combination of Xce but not in another. The relationship between these effects and other phenomena of maternal 'imprinting' is discussed.

Further evidence for the importance of parental source of the Xce allele in X chromosome inactivation

“…The direction of the reciprocal cross differences in AKR/J heterozygotes described in Table 1 agrees with that of Forrester & Ansell (1985), although actual percentages differ: they found 52% PGK-1 A (data combined from two groups) when Xce c was of paternal origin compared to 60% in crosses A and C above (P < 0-001) and 60% PGK-1 A (data combined from three groups) when Xce c was of maternal origin compared to 65 % in cross B (P < 0-001) and D (P<001). These data suggest the existence of a fourth allele for Xce carried by the AKR/J mouse strain, subject to parental influences on its expression, but distinct from the ' b ' allele.…”

“…CBA(Pgk-l a ) mice were produced in this laboratory by backcrossing C3Yl(Pgk-l a ) mice onto a CQA./C2L{Pgk-l") background for 20 generations. Pgk-1 and Xce are tightly linked on the X chromosome and no recombination was observed between these loci in our backcrossing programme (Forrester & Ansell, 1985). This observation was confirmed by Krietsch et al (1986), who similarly observed no recombinants after 15 generations of backcrossing.…”

“…when X p carries the Xce c allele, these tissues do not exclusively express X M . Similarly, no parental effects on PGK-1 expression were seen in reciprocal crosses carrying extreme alleles at the Xce locus (Forrester & Ansell, 1985) although Bucher & Krietsch (1988) have detected parental effects in those situations. Background genetic effects may influence the direction and degree of parental effects, although in different strain combinations the data presented above supports the conclusion of Forrester & Ansell (1985) that maternal inheritance of Xce alleles mitigates against X M being inactivated.…”

“…Forrester & Ansell (1985) described reciprocal cross difference in X-inactivation frequencies in heterozygotes derived from C57BL and C3H/HeHa-Pgk-l a parental strains carrying the ' b' and ' c' alleles of Xce respectively. The direction of the reciprocal cross differences in AKR/J heterozygotes described in Table 1 agrees with that of Forrester & Ansell (1985), although actual percentages differ: they found 52% PGK-1 A (data combined from two groups) when Xce c was of paternal origin compared to 60% in crosses A and C above (P < 0-001) and 60% PGK-1 A (data combined from three groups) when Xce c was of maternal origin compared to 65 % in cross B (P < 0-001) and D (P<001).…”

“…Parental effects on X-inactivation were reported for adult tissue in Xce"/Xce c heterozygotes by Forrester & Ansell (1985). Sixty per cent PGK-1 A expression was found when the Xce" was paternally derived, while Xinactivation was equally balanced when the Xce" was maternally derived.…”