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ChIP-chip data of Npl3-Myc and Rrm3-Flag in wild-type and npl3M-bM-^HM-^F cells

ABSTRACT: Transcription is a major obstacle for replication fork progression and a cause of genome instability. Such instability increases in mutants with a suboptimal assembly of the nascent messenger ribonucleo-protein particle (mRNP), as THO/TREX and some heterogeneous nuclear ribonucleoproteins (hnRNPs) mutants. Here we show that yeast npl3M-bM-^HM-^F cells show genome-wide replication obstacles as determined by accumulation of the Rrm3 helicase. Such obstacles preferentially occur at long and highly expressed genes, to which Npl3 is preferentially bound in wild-type cells. ChIP-chip studies were perfomed with antibodies against Myc-tagged Npl3 protein in wild-type cells of the yeast S. Cerevisiae, as well as Flag-tagged Rrm3 protein in both wild-type and npl3M-bM-^HM-^F cells.

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: AndrM-CM-)s Aguilera

PROVIDER: E-GEOD-50185 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ChIP-chip data of Thp1-Flag and Sac3-Flag in wild-type cells, and Rrm3-Flag in sac3M-bM-^HM-^F and thp1M-bM-^HM-^F cells

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ChIP-chip data of Npl3-Myc and Rrm3-Flag in wild-type and npl3∆ cells

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Rad53-mediated regulation of Rrm3 and Pif1 DNA helicases contributes to prevention of aberrant fork transitions under replication stress.

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The shuttling SR-like proteins Gbp2 and Hrb1 mediate the nuclear export of spliced mRNAs

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