OriDB Curated Paper

Please contact OriDB if you think this paper has been mis-annotated.

Replication stress checkpoint signaling controls tRNA gene transcription.

Vesna C Nguyen, Brett W Clelland, Darren J Hockman, Sonya L Kujat-Choy, Holly E Mewhort, Michael C Schultz

Nat. Struct. Mol. Biol. (2010), 17(8):976-81PubMed | Nat. Struct. Mol. Biol.

In budding yeast, the transcriptional machinery at tRNA genes naturally interferes with replication in a way that can promote chromosome breakage. Here we show that a signaling module composed of core components of the replication stress checkpoint pathway represses this fork-pausing machinery in normally cycling and genotoxin-treated cells. Specifically, the sensor kinase Mec1, the signaling adaptor Mrc1 and the transducer kinase Rad53 relay signals that globally repress tRNA gene transcription during unchallenged proliferation and under conditions of replication stress. Repressive signaling in genotoxin-treated cells requires Rad53-dependent activation of a conserved repressor of tRNA gene transcription, Maf1. Cells lacking Maf1 are sensitive to replication stress under conditions of elevated tRNA gene transcription. We propose that checkpoint control of the fork-pausing activity of tRNA genes complements the repertoire of replisome-targeted mechanisms by which checkpoint proteins promote faithful DNA replication.

OriDB annotation of this paper:

ARS assay

None curated.

2D gel

None curated.

ChIP of replication origin proteins

None curated.

Replication timing

None curated.

Replication in hydroxyurea

None curated.

Predicted origins

None curated.

Confirmed sequence element

None curated.

Predicted sequence element

None curated.

The data on this page come directly from PubMed and OriDB databases, please report any errors to OriDB.
This page is new! Please let us know of any problems you experience.