Human embryos are particularly susceptible to chromosome instability (CIN) and errors in chromosome segregation, but the molecular mechanisms that regulate and sense CIN in mammalian embryos are unclear. Here, on p. 1806, Maria Viveiros and colleagues investigate the role of the chromatin remodelling protein ATRX in early mouse embryos. They first show that ATRX, which is transmitted to the early zygote through the maternal germ line, localises to pericentric heterochromatin (PCH) within the maternal pronucleus, where it is required for the transcriptional repression of major satellite transcripts. The loss of ATRX hence leads to the abnormal expression of maternal satellite transcripts. The authors also demonstrate that the maternal inheritance of ATRX helps to set up an epigenetic asymmetry between the maternal and paternal chromosomes, which might be implicated in facilitating chromosome segregation. In line with this, ATRX loss, they report, causes abnormal centromeric mitotic recombination and an increase in double-strand DNA breaks. Overall, these data highlight an important role for ATRX in the early mouse embryo and provide new insights into how CIN is controlled in early mammalian development.
ATRX: keeping quiet in the embryo
ATRX: keeping quiet in the embryo. Development 15 May 2015; 142 (10): e1003. doi:
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