The Expression of X-Linked Phosphoglycerate Kinase in the Early Mouse Embryo

Krietsch, Wolfgang K. G.; Fundele, Reinald; Kuntz, Günter W. K.; Fehlau, Monika; Bürki, Kurt; Illmensee, Karl

doi:10.1111/j.1432-0436.1982.tb01276.x

Cited by 43 publications

(24 citation statements)

References 23 publications

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“…Previous studies had suggested that genes may be expressed at a lower level from the X p in preimplantation embryos. (11)(12)(13) The current papers (1)(2)(3) that we discuss here further challenge the view that both X chromosomes are expressed in early stages of development by providing clear evidence of X p inactivation in preimplantation embryos.…”

Section: Introductionmentioning

confidence: 78%

Silence of the fathers: Early X inactivation

Cheng

Distèche

2004

BioEssays

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Section: Introductionmentioning

confidence: 78%

Silence of the fathers: Early X inactivation

Cheng

Distèche

2004

BioEssays

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“…For example, imprinted facultative heterochromatinisation of the paternal X chromosome occurs in all tissues of marsupials (Cooper, 1971). In the mouse, paternal X-chromosome inactivation occurs during early pre-implantation embryogenesis (Krietsch et al, 1982) and is maintained in the trophectoderm (Takagi and Sasaki, 1975) but is reversed in the inner cell mass before random X-inactivation in the embryo proper (Mak et al, 2004;Okamoto et al, 2004). More recent work on epigenetic silencing of imprinted genes reveals similarities to imprinted X-chromosome inactivation.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic regulation of facultative heterochromatinisation inPlanococcus citrivia the Me(3)K9H3-HP1-Me(3)K20H4 pathway

Bongiorni

Pasqualini

Taranta

et al. 2007

Journal of Cell Science

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Using RNA interference (RNAi) we have conducted a functional analysis of the HP1-like chromobox gene pchet2 during embryogenesis of the mealybug Planococcus citri. Knocking down pchet2 expression results in decondensation of the male-specific chromocenter that normally arises from the developmentally-regulated facultative heterochromatinisation of the paternal chromosome complement. Together with the disappearance of the chromocenter the staining levels of two associated histone modifications, tri-methylated lysine 9 of histone H3 [Me(3)K9H3] and tri-methylated lysine 20 of histone H4 [Me(3)K20H4], are reduced to undetectable levels. Embryos treated with double-stranded RNA (dsRNA) targeting pchet2 also exhibit chromosome abnormalities, such as aberrant chromosome condensation, and also the presence of metaphases that contain `lagging' chromosomes. We conclude that PCHET2 regulates chromosome behavior during metaphase and is a crucial component of a Me(3)K9H3-HP1-Me(3)K20H4 pathway involved in the facultative heterochromatinisation of the (imprinted) paternal chromosome set.

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“…However, a different picture was obtained from studies on the X-linked Pgk-J gene, which lies close to the X chromosome controlling element (Xce) (10,11), in the region of the center of X chromosome inactivation (12). No zygotic expression of the paternal PGK-1 allozyme was seen until day 6 or 7, 2 days after detection of the allozyme encoded by the maternal X chromosome (13)(14)(15). This led to the idea that PGK-1 expression from the paternal X chromosome is delayed until the developmental stage at which X chromosome inactivation occurs (14), as may be true for the X-linked Xist gene, which also maps in the vicinity of the X inactivation center (16,17).…”

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confidence: 99%

“…Models favored prior to this work were based on an apparent delay in expression of paternally derived PGK-1 until about the time of random X chromosome inactivation in the inner cell mass (13,15). The models suggested a limited spread of a chromatin modification from the X inactivation center to the nearby Pgk-1 locus but not to the more distant genes for a-galactosidase and HPRT.…”

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confidence: 99%