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Genetic evidence for an involvement of the TOR complex 1 in the process of transcription elongation in Saccharomyces cerevisiae
Author(s) -
Haller Jasmine Lee,
Allison Mary Kathryn,
Harper Jennifer Aileen,
Outhay Malena Ann,
Warsinske Hayley Catherine,
Duina Andrea Angelo
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.923.1
Subject(s) - chromatin , biology , nucleosome , histone , genetics , transcription coregulator , transcription (linguistics) , microbiology and biotechnology , gene , saccharomyces cerevisiae , eukaryotic transcription , histone code , chromatin remodeling , gene expression , promoter , linguistics , philosophy
In eukaryotic cells, DNA is compacted into chromatin, a structure that includes the nucleosome – a particle consisting of histones and DNA – as its fundamental unit. The presence of nucleosomes across the regulatory and transcribed regions of genes constitutes a physical obstacle for factors that need to access DNA in order to ensure the proper expression of the underlying genetic information. In past studies aimed at better defining the interplay between chromatin and transcription, a histone H3 mutant – H3‐L61W – was isolated that was shown to deleteriously affect the elongation phase of transcription. Here we describe experiments showing that deletions of genes encoding two members of the TOR complex 1 (TORC1) – Tco89 and Tor1 – can suppress a subset of phenotypes conferred by the H3‐L61W mutation. Deletion of TCO89 causes the strongest suppressive effects and additional studies show that deletion of this gene in wild‐type histone H3 cells confers phenotypes indicative of defects in chromatin structure and transcription elongation. Taken together, these and other studies point to a possible role for TORC1 in affecting transcription elongation through effects on chromatin structure. This material is based upon work supported by the National Science Foundation under grant No. 0919241.