P53 and the defenses against genome instability caused by transposons and repetitive elements

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Abstract

The recent publication by Wylie et al. is reviewed, demonstrating that the p53 protein regulates the movement of transposons. While this work presents genetic evidence for a piRNA-mediated p53 interaction with transposons in Drosophila and zebrafish, it is herein placed in the context of a decade or so of additional work that demonstrated a role for p53 in regulating transposons and other repetitive elements. The line of thought in those studies began with the observation that transposons damage DNA and p53 regulates DNA damage. The presence of transposon movement can increase the rate of evolution in the germ line and alter genes involved in signal transduction pathways. Transposition can also play an important role in cancers where the p53 gene function is often mutated. This is particularly interesting as recent work has shown that de-repression of repetitive elements in cancer has important consequences for the immune system and tumor microenvironment.

There is a history of associating p53 with transposon activity repression and of transposons spreading p53 binding sites throughout the genome. Presumably this emanates from p53 regulating DNA damage, and the DNA damage associated with transposition. Wylie et al. present evidence for direct interaction between p53 and transposon regulating piRNA.

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