Matrin3 promotes homologous recombinational repair by regulation of RAD51

Lin Shi; Jiying Sun; Aiko Kinomura; Atsuhiko Fukuto; Yasunori Horikoshi; Satoshi Tashiro

doi:10.1093/jb/mvz041

Matrin3 promotes homologous recombinational repair by regulation of RAD51

J Biochem. 2019 Oct 1;166(4):343-351. doi: 10.1093/jb/mvz041.

Authors

Lin Shi¹, Jiying Sun¹, Aiko Kinomura¹, Atsuhiko Fukuto^{1

2}, Yasunori Horikoshi¹, Satoshi Tashiro¹

Affiliations

¹ Department of Cellular Biology, Research Institute for Radiation Biology and Medicine.
² Department of Ophthalmology and Visual Science, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

PMID: 31119278
DOI: 10.1093/jb/mvz041

Abstract

Matrin3 is a highly conserved inner nuclear matrix protein involved in multiple stages of RNA metabolism. Although Matrin3 may also play a role in DNA repair, its precise roles have remained unclear. In this study, we showed that the depletion of Matrin3 led to decreased homologous recombination (HR) efficiency and increased radiation sensitivity of cells. Matrin3-depleted cells showed impaired DNA damage-dependent focus formation of RAD51, a key protein in HR. These findings suggest that Matrin3 promotes HR by regulating RAD51.

Keywords: DNA double-strand breaks; DNA repair; Matrin3; RAD51; homologous recombination.