Chromosome imprinting and the mammalian X chromosome

Chandra, H. Sharat; Brown, Stephen P. A.

doi:10.1038/253165a0

Cited by 99 publications

(35 citation statements)

References 31 publications

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“…In male mealybug embryos an entire haploid set of paternal chromosomes becomes facultatively heterochromatinised and genetically inert at the early cleavage (blastoderm) stage of development; in females both parental sets remain euchromatic and active (Hughes-Schrader, 1948;Brown and Nur, 1964;Chandra and Brown, 1975). In Sciaridae, a similar phenomenon has been observed during late blastoderm, just before cellularization, where the paternal X chromosomes are selectively eliminated in male embryos (reviewed by Metz, 1938).…”

Section: Introductionmentioning

confidence: 79%

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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Section: Introductionmentioning

confidence: 79%

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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“…The regulation of chromatin activity is believed to be integrated with sexual processes including meiosis, hence restoration of gene expression after a sexual New Zealand Journal of Botany, 1979, Vol. 17 cycle (Cooper 1971, Lyon 1974, Chandra & Brown 1975. Delayed expression of additional DNA has also been found in other organisms under different circumstances, for example, in Drosophila melanogaster where the ribosomal RNA cistrons are susceptible to both deletion and magnification.…”

Section: Gametic Transformationmentioning

confidence: 96%

Overcoming incompatibility and promoting genetic recombination in flowering plants

Pandey

1979

New Zealand Journal of Botany

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A critical review of observations regarding physiology of pollen-style incompatibility in plants led to the conclusion that the widely occurring evolutionary relationships between genetic systems of self-incompatibility, floral morphology, site of inhibition, and pollen cytology are best understood in the light of two-phase S gene physiology -S specificity detennination (transcription), and S protein synthesis or precursor conversion (translation).

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“…Imprinting has also been identified in maize (14), zebra fish (15), and a variety of other insects including Drosophila melanogaster in which the phenomenon has been referred to as parental effects (13,(16)(17)(18)(19). The viability of both gynogenic and androgenic flies and zebra fish (20)(21)(22) indicates, however, that imprinted genes are not as developmentally essential in these species as in mammals (23)(24)(25)(26).…”

Section: Imprint Gene Identificationmentioning

confidence: 99%

Imprinted genes as potential genetic and epigenetic toxicologic targets.

Murphy

Jirtle

2000

Environ Health Perspect

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Genomic imprinting is an epigenetic phenomenon in eutherian mammals that results in the differential expression of the paternally and maternally inherited alleles of a gene. Imprinted genes are necessary for normal mammalian development. This requirement has been proposed to have evolved because of an interparental genetic battle for the utilization of maternal resources during gestation and postnatally. The nonrandom requisite for monoallelic expression of a subset of genes has also resulted in the formation of susceptibility loci for neurobehavioral disorders, developmental disorders, and cancer. Since imprinting involves both cytosine methylation within CpG islands and changes in chromatin structure, imprinted genes are potential targets for dysregulation by epigenetic toxicants that modify DNA methylation and histone acetylation.

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Chromosome imprinting and the mammalian X chromosome

Cited by 99 publications

References 31 publications

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

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

Overcoming incompatibility and promoting genetic recombination in flowering plants

Imprinted genes as potential genetic and epigenetic toxicologic targets.

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