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Jürg Bähler

Researcher at University College London

Publications -  237
Citations -  24955

Jürg Bähler is an academic researcher from University College London. The author has contributed to research in topics: Schizosaccharomyces pombe & Gene. The author has an hindex of 67, co-authored 227 publications receiving 21327 citations. Previous affiliations of Jürg Bähler include University of Debrecen & European Bioinformatics Institute.

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H3K9me-independent gene silencing in fission yeast heterochromatin by Clr5 and histone deacetylases.

TL;DR: It is found that Clr5 controls gene expression at multiple chromosomal locations in addition to affecting the mating-type region, and like the multi-functional Atf1 transcription factor, controls sexual differentiation and genome integrity at several levels.
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Contributions of transcription and mRNA decay to gene expression dynamics of fission yeast in response to oxidative stress.

TL;DR: A dominant role of transcriptional regulation in response to stress is revealed, but this study points to the first minutes after stress induction as a critical time when the coordinated control of mRNA turnover can support the control of transcription for rapid gene regulation.
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Cyclin-dependent kinase inhibits reinitiation of a normal S-phase program during G2 in fission yeast.

TL;DR: It is concluded that CDK inhibits reinitiation of S phase during G2, and if G2/M CDK is depleted, replication results from induction of a largely normal S-phase program with only small differences in origin usage and efficiency.
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Sites of strong Rec12/Spo11 binding in the fission yeast genome are associated with meiotic recombination and with centromeres

TL;DR: Rec12 binding showed preference for large intergenic regions and was found to bind preferentially near to genes expressed strongly in meiosis, which raises the intriguing possibility that Rec12 plays additional roles in meiotic chromosome dynamics.
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The roles of stress-activated Sty1 and Gcn2 kinases and of the protooncoprotein homologue Int6/eIF3e in responses to endogenous oxidative stress during histidine starvation.

TL;DR: It is shown that mutants lacking sty1(+) or gcn2(+) display reduced viabilities during histidine depletion stress in a manner suppressible by the antioxidant N-acetyl cysteine, suggesting that these protein kinases function to alleviate endogenous oxidative damage generated during nutrient starvation.