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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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Widespread exon skipping triggers degradation by nuclear RNA surveillance in fission yeast.

TL;DR: RNA-seq data from 116 transcriptomes in fission yeast is analyzed, highlighting widespread but low frequency alternative or aberrant splicing events that are targeted by nuclear RNA surveillance.
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Mfc1 is a novel forespore membrane copper transporter in meiotic and sporulating cells.

TL;DR: Analysis of DNA microarrays in the model yeast Schizosaccharomyces pombe revealed a novel meiosis-specific gene, termed mfc1+, that encodes a putative major facilitator superfamily-type transporter that serves to transport copper for accurate and timely meiotic differentiation under copper-limiting conditions.
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A CRISPR/Cas9-based method and primer design tool for seamless genome editing in fission yeast

TL;DR: Applying this optimized CRISPR/Cas9-based approach, this work has successfully deleted over 80 different non-coding RNA genes, which are generally lowly expressed, and have inserted 7 point mutations in 4 different genomic regions.
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Int6/eIF3e promotes general translation and Atf1 abundance to modulate Sty1 MAPK-dependent stress response in fission yeast.

TL;DR: It is found that Int6 is required for maintaining the basal level of Atf1 and for rapid transcriptional activation of the CESR on 3AT-insult, and Pulse labeling experiments indicate that int6Δ significantly slows down de novo protein synthesis.
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The Role of Topoisomerase II in Meiotic Chromosome Condensation and Segregation in Schizosaccharomyces pombe

TL;DR: It is suggested that the inability to decatenate the replicated DNA is the primary defect in top2, which leads to a loss of chromatin condensation shortly before meiosis I, failure of sister chromatid separation, and a nonregulatory arrest.