Defects in yeast RNA polymerase II transcription elicit hypersensitivity to G1 arrest induced by Kluyveromyces lactis zymocin View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2002-09

AUTHORS

H. Kitamoto, D. Jablonowski, J. Nagase, R. Schaffrath

ABSTRACT

The G1 cell cycle arrest imposed by Kluyveromyces lactis zymocin on Saccharomyces cerevisiae requires a functional RNA polymerase II (pol II) TOT/Elongator complex. In a study of zymocin's mode of action, genetic scenarios known to impair transcription or affect the pol II machinery itself were found to elicit hypersensitivity to zymocin. Thus, mutations in components of SAGA, SWI/SNF, Mediator and Ccr4-Not, complexes involved in transcriptionally relevant functions such as nucleosome modification, chromatin remodelling and formation of the preinitiation complex, make yeast cells hypersensitive to the lethal effects of zymocin. The defects at the level of transcriptional elongation displayed by rtf1Delta, ctk1, fcp1 and rpb2 mutants also result in zymocin hypersensitivity. Intriguingly, inactivation of histone deacetylase (HDAC) activity, which is expected to reduce the demand for the histone acetyltransferase (HAT) function of TOT/Elongator, also reduces sensitivity to zymocin. Thus, zymocin interferes with pol II-dependent transcription, and this effect requires the HAT function of TOT, presumably while the Elongator complex is associated with pol II. More... »

PAGES

49-55

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00438-002-0720-3

DOI

http://dx.doi.org/10.1007/s00438-002-0720-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1023739147

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12242498


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