Abstract:
:Fragile X syndrome, a common form of inherited intellectual disability, is caused by loss of the fragile X mental retardation protein FMRP. FMRP is present predominantly in the cytoplasm, where it regulates translation of proteins that are important for synaptic function. We identify FMRP as a chromatin-binding protein that functions in the DNA damage response (DDR). Specifically, we show that FMRP binds chromatin through its tandem Tudor (Agenet) domain in vitro and associates with chromatin in vivo. We also demonstrate that FMRP participates in the DDR in a chromatin-binding-dependent manner. The DDR machinery is known to play important roles in developmental processes such as gametogenesis. We show that FMRP occupies meiotic chromosomes and regulates the dynamics of the DDR machinery during mouse spermatogenesis. These findings suggest that nuclear FMRP regulates genomic stability at the chromatin interface and may impact gametogenesis and some developmental aspects of fragile X syndrome.
journal_name
Celljournal_title
Cellauthors
Alpatov R,Lesch BJ,Nakamoto-Kinoshita M,Blanco A,Chen S,Stützer A,Armache KJ,Simon MD,Xu C,Ali M,Murn J,Prisic S,Kutateladze TG,Vakoc CR,Min J,Kingston RE,Fischle W,Warren ST,Page DC,Shi Ydoi
10.1016/j.cell.2014.03.040subject
Has Abstractpub_date
2014-05-08 00:00:00pages
869-81issue
4eissn
0092-8674issn
1097-4172pii
S0092-8674(14)00415-2journal_volume
157pub_type
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