Abstract
Cover Photograph: Replication stress may constitute a possible source of epigenetic aberrations in cancer. Cancer cells accumulate widespread local and global chromatin changes, and on pages 847–855 of this issue Zuzana Jasencakova and Anja Groth hypothesize as to the source of this instability. Chromatin organization is transiently disrupted during DNA replication, and maintenance of epigenetic information thus relies on faithful restoration of chromatin on the new daughter strands. Replication stress may result in stalled replisomes, thus impairing parental histone recycling and leading to accumulation of lysine 9 monomethylation on new histones stored with Asf1. This could facilitate stochastic epigenetic silencing by laying down repressive histone marks at sites of fork stalling, and promote unwarranted silencing of tumorsuppressor genes.
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