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Doctoral thesis
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Mechanisms and Persistence of Chromatin-Mediated Antisense Transcription Interference

ContributorsKaur, Jatinder
Defense date2020-10-16
Abstract

Eukaryotic genomes are transcribed almost entirely in an interleaved manner giving rise to manynon-coding RNA (ncRNA) transcripts overlapping coding gene promoters. In the compact genome ofthe yeast S.cerevisiae, these non-coding transcripts end up being in antisense orientation to theupstream mRNA. Nuclear surveillance mechanisms restrict non-coding transcription through early-termination and degradation by Nrd1/Nab3/Sen1(NNS) pathway. The act of non-coding RNAtranscription by itself causes gene repression by a poorly understood mechanism of transcriptioninterference (TI). The thesis discusses a chromatin-mediated mechanism of transcriptioninterference. It begins with Antisense-mediated co-transcriptional deposition of H3K36 methylationat sense promoter and Rpd3 histone deacetylase recognizes and deacetylates the promoter. This leads to closing of the promoter NDR due to reduced occupancy of RSC chromatin remodeler, that restrictsTBP binding and results in TI. Furthermore, persistence of antisense-mediated repression is also addressed.

eng
Keywords
  • Non-coding transcription
  • Transcription interference
  • Promoter
  • Nucleosome-Depleted Region
  • Histone deacetylase
  • Histone methyltransferase
  • Nucleosome positioning
Research group
Citation (ISO format)
KAUR, Jatinder. Mechanisms and Persistence of Chromatin-Mediated Antisense Transcription Interference. 2020. doi: 10.13097/archive-ouverte/unige:148174
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