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Methylation-specific PCR: A novel PCR assay for methylation status of CpG islands tumor p16 is “off” in the tumor Following bisulfite treatment of the DNA, DNA sequencing of a normal (H249) and tumor (H157) cell line for the promoter region of the p16 tumor suppressor gene. bisulfite converts C to U but doesn’t affect 5 Me-C. Medical Sciences: Herman et al. Proc. Natl. Acad. Sci. USA 93 (1996) 9823 reactivation of a epigenetically silenced Mlh1 gene by aza-C aza-cytidine Swain JL, Stewart TA, Leder P. Parental legacy determines methylation and expression of an autosomal transgene: a molecular mechanism for parental imprinting. Cell. 1987 Aug 28;50(5):719-27. We have created a transgenic mouse strain in which an autosomal transgene bearing elements of the RSV LTR and a translocated c-myc gene obeys very unusual rules. If the transgene is inherited from the male parent, it is expressed in the heart and no other tissue. If it is inherited from the female parent, it is not expressed at all. This pattern of expression correlates precisely with a parentally imprinted methylation state evident in all tissues. Methylation of the transgene is acquired by its passage through the female parent and eliminated during gametogenesis in the male. These observations provide direct molecular evidence that autosomal gene expression can depend upon the sex of the parent from which the gene is inherited. They also provide a plausible mechanism for understanding parental imprinting that may be relevant to the failure of parthenogenesis in mammals, the apparent non-Mendelian behavior of some autosomal genes, and the role of methylation in gene regulation. http://genet.annualreviews.org/cgi/content-nw/full/31/1/493/F3 FIGURE 1. Typical phenotypes of Angelman (left) and Prader-Willi (right) syndrome patients. The difference between them belies the fact they they are caused by the same chromosomal deletion. (From Nicholls, 1994; Photographs courtesy of R. D. Nicholls). Prader-Willi uniparental (maternal) inheritance In the example shown, the parents were concerned about the recurrence of a child affected with AS despite a very low recurrence risk in AS shown to be due to a deletion of maternal origin or paternal uniparental disomy. In this case, the AS patient shows absence of maternal alleles at GABRB3 and D15S113. D15S11 was uninformative. In the current pregnancy, normal maternal and paternal contributions were observed at all three loci. Fly dosage compensation: The single male X gets transcribed about 2X. The MSL complex is a Histone H4 K16 HAT. anti-HA HA-tagged MSL2 Dosage compensation in worms: both Xs are down-regulated by a condensin-like complex XO XB XO Y or XB Y XO XB Y XO XB XO XB homologous mouse sequences in the human genome Inactive X is hypoacetylated at H4-K19 http://www.hgu.mrc.ac.uk/Research/Chrombio/ChromOrg/peterj.htm Figure 2 | Xist transcription in embryonic stem cells. Patterns of Xist RNA expression in female ES cells undergoing differentiation using RNA fluorescence in situ hybridization. The left panel shows that undifferentiated ES cells have two punctate Xist RNA signals, representing the presence of unstable Xist transcripts at the site of transcription on both (active) X chromosomes. The middle panel shows that, upon differentiation, Xist RNA from one of the two alleles becomes stabilized and coats the X chromosome that is to be inactivated in cis . The X chromosome that remains active continues to express Xist in its unstable form. The right panel shows that, in fully differentiated cells, Xist RNA coats the inactive X chromosome and the Xist gene on the active X has been silenced.