CSL protein regulates transcription of genes required to prevent catastrophic mitosis in fission yeast
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F16%3A10330079" target="_blank" >RIV/00216208:11310/16:10330079 - isvavai.cz</a>
Result on the web
<a href="http://dx.doi.org/10.1080/15384101.2016.1235100" target="_blank" >http://dx.doi.org/10.1080/15384101.2016.1235100</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1080/15384101.2016.1235100" target="_blank" >10.1080/15384101.2016.1235100</a>
Alternative languages
Result language
angličtina
Original language name
CSL protein regulates transcription of genes required to prevent catastrophic mitosis in fission yeast
Original language description
For every eukaryotic cell to grow and divide, intricately coordinated action of numerous proteins is required to ensure proper cell-cycle progression. The fission yeast Schizosaccharomyces pombe has been instrumental in elucidating the fundamental principles of cell-cycle control. Mutations in S. pombe 'cut' (cell untimely torn) genes cause failed coordination between cell and nuclear division, resulting in catastrophic mitosis. Deletion of cbf11, a fission yeast CSL transcription factor gene, triggers a 'cut' phenotype, but the precise role of Cbf11 in promoting mitotic fidelity is not known. We report that Cbf11 directly activates the transcription of the acetyl-coenzyme A carboxylase gene cut6, and the biotin uptake/biosynthesis genes vht1 and bio2, with the former 2 implicated in mitotic fidelity. Cbf11 binds to a canonical, metazoan-like CSL response element (GTGGGAA) in the cut6 promoter. Expression of Cbf11 target genes shows apparent oscillations during the cell cycle using temperature-sensitive cdc25-22 and cdc10-M17 block-release experiments, but not with other synchronization methods. The penetrance of catastrophic mitosis in cbf11 and cut6 mutants is nutrient-dependent. We also show that drastic decrease in biotin availability arrests cell proliferation but does not cause mitotic defects. Taken together, our results raise the possibility that CSL proteins play conserved roles in regulating cell-cycle progression, and they could guide experiments into mitotic CSL functions in mammals.
Czech name
—
Czech description
—
Classification
Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
EB - Genetics and molecular biology
OECD FORD branch
—
Result continuities
Project
<a href="/en/project/GPP305%2F12%2FP040" target="_blank" >GPP305/12/P040: Fission yeast CSL proteins in the maintenance of genome integrity</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2016
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Cell Cycle
ISSN
1538-4101
e-ISSN
—
Volume of the periodical
15
Issue of the periodical within the volume
22
Country of publishing house
US - UNITED STATES
Number of pages
12
Pages from-to
3082-3093
UT code for WoS article
000388374500023
EID of the result in the Scopus database
2-s2.0-84992036641