Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/1208
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dc.contributor.authorArimbasseri, Gopalakrishnan Aneeshkumar-
dc.contributor.authorSandhu, Kuljeet Singh-
dc.contributor.authorBhargava, Purnima-
dc.contributor.authorBhalla, Pratibha-
dc.contributor.authorShukla, Ashutosh-
dc.contributor.authorVernekar, Dipti Vinayak-
dc.date.accessioned2021-03-25T09:08:36Z-
dc.date.available2021-03-25T09:08:36Z-
dc.date.issued2019-09-
dc.identifier.urihttp://hdl.handle.net/123456789/1208-
dc.description.abstractThe RNA polymerase (pol) III transcribes mostly short, house-keeping genes, which produce stable, non-coding RNAs. The tRNAs genes, highly transcribed by pol III in vivo are known replication fork barriers. One of the transcription factors, the PAF1C (RNA polymerase II associated factor 1 complex) is reported to associate with pol I and pol II and influence their transcription. We found low level PAF1C occupancy on the yeast pol III-transcribed genes, which is not correlated with nucleosome positions, pol III occupancy and transcription. PAF1C interacts with the pol III transcription complex and causes pol III loss from the genes under replication stress. Genotoxin exposure causes pol III but not Paf1 loss from the genes. In comparison, Paf1 deletion leads to increased occupancy of pol III, γ-H2A and DNA pol2 in gene-specific manner. Paf1 restricts the accumulation of pol III by influencing the pol III pause on the genes, which reduces the pol III barrier to the replication fork progression.en_US
dc.language.isoenen_US
dc.publisherSpringer Nature Limiteden_US
dc.titleYeast PAF1 complex counters the pol III accumulation and replication stress on the tRNA genesen_US
dc.typeArticleen_US
dc.journalSci Repen_US
dc.volumeno9en_US
dc.issueno1en_US
dc.pages12892en_US
Appears in Collections:Molecular Genetic, Publications

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