Abstract：
:Transcription hinders replication fork progression and stability. The ATR checkpoint and specialized DNA helicases assist DNA synthesis across transcription units to protect genome integrity. Combining genomic and genetic approaches together with the analysis of replication intermediates, we searched for factors coordinating replication with transcription. We show that the Sen1/Senataxin DNA/RNA helicase associates with forks, promoting their progression across RNA polymerase II (RNAPII)-transcribed genes. sen1 mutants accumulate aberrant DNA structures and DNA-RNA hybrids while forks clash head-on with RNAPII transcription units. These replication defects correlate with hyperrecombination and checkpoint activation in sen1 mutants. The Sen1 function at the forks is separable from its role in RNA processing. Our data, besides unmasking a key role for Senataxin in coordinating replication with transcription, provide a framework for understanding the pathological mechanisms caused by Senataxin deficiencies and leading to the severe neurodegenerative diseases ataxia with oculomotor apraxia type 2 and amyotrophic lateral sclerosis 4.
journal_name
Celljournal_title
Cellauthors
Alzu A,Bermejo R,Begnis M,Lucca C,Piccini D,Carotenuto W,Saponaro M,Brambati A,Cocito A,Foiani M,Liberi Gdoi
10.1016/j.cell.2012.09.041subject
Has Abstractpub_date
2012-11-09 00:00:00pages
835-846issue
4eissn
0092-8674issn
1097-4172pii
S0092-8674(12)01244-5journal_volume
151pub_type
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