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2015 ; 26
(7
): 1395-410
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Heterochromatin formation via recruitment of DNA repair proteins
#MMPMID25631822
Kirkland JG
; Peterson MR
; Still CD 2nd
; Brueggeman L
; Dhillon N
; Kamakaka RT
Mol Biol Cell
2015[Apr]; 26
(7
): 1395-410
PMID25631822
show ga
Heterochromatin formation and nuclear organization are important in gene
regulation and genome fidelity. Proteins involved in gene silencing localize to
sites of damage and some DNA repair proteins localize to heterochromatin, but the
biological importance of these correlations remains unclear. In this study, we
examined the role of double-strand-break repair proteins in gene silencing and
nuclear organization. We find that the ATM kinase Tel1 and the proteins Mre11 and
Esc2 can silence a reporter gene dependent on the Sir, as well as on other repair
proteins. Furthermore, these proteins aid in the localization of silenced domains
to specific compartments in the nucleus. We identify two distinct mechanisms for
repair protein-mediated silencing-via direct and indirect interactions with Sir
proteins, as well as by tethering loci to the nuclear periphery. This study
reveals previously unknown interactions between repair proteins and silencing
proteins and suggests insights into the mechanism underlying genome integrity.
|*Chromatin Assembly and Disassembly
[MESH]
|*DNA Repair
[MESH]
|Cell Cycle Proteins
[MESH]
|Cell Nucleus/metabolism
[MESH]
|Chromosomes, Fungal/*metabolism
[MESH]
|Endodeoxyribonucleases/metabolism
[MESH]
|Exodeoxyribonucleases/metabolism
[MESH]
|Gene Silencing
[MESH]
|Heterochromatin/*metabolism
[MESH]
|Intracellular Signaling Peptides and Proteins/metabolism
[MESH]