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Gavin Burns

Researcher at Natural Environment Research Council

Publications -  29
Citations -  3153

Gavin Burns is an academic researcher from Natural Environment Research Council. The author has contributed to research in topics: Gene & Gene expression. The author has an hindex of 21, co-authored 29 publications receiving 2994 citations. Previous affiliations of Gavin Burns include Wellcome Trust Sanger Institute & Australian Antarctic Division.

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Global transcriptional responses of fission yeast to environmental stress

TL;DR: Transcriptional responses of the fission yeast Schizosaccharomyces pombe to various environmental stresses were explored and promoter motifs associated with some of the groups of coregulated genes were identified.
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Periodic gene expression program of the fission yeast cell cycle

TL;DR: The genome-wide transcriptional program of the Schizosaccharomyces pombe cell cycle was studied in this paper, identifying 407 periodically expressed genes of which 136 show high-amplitude changes.
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The transcriptional program of meiosis and sporulation in fission yeast.

TL;DR: Comparison with the meiotic program of the distantly related Saccharomyces cerevisiae reveals an unexpectedly small shared meiotic transcriptome, suggesting that the transcriptional regulation of meiosis evolved independently in both species.
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Whole-genome microarrays of fission yeast: characteristics, accuracy, reproducibility, and processing of array data.

TL;DR: The genome of the fission yeast Schizosaccharomyces pombe has recently been sequenced, setting the stage for the post-genomic era of this increasingly popular model organism and providing data for several microarray properties that are rarely measured.
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Global Effects on Gene Expression in Fission Yeast by Silencing and RNA Interference Machineries

TL;DR: It is indicated that the RNAi and Clr proteins show only a limited functional overlap and that the ClR proteins play more global roles in gene silencing, while the wtf family of repeated sequences seems to be repressed by histone deacetylation independent of RNAi.