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Genome-wide control of H4 K16 acetylation by the SAS-I complex in Saccharomyces cerevisiae
The MYST HAT Sas2 is part of the SAS-I complex, which includes the subunits Sas4 and Sas5 and acetylates histone H4 lysine 16 (H4 K16Ac). This Sas2-mediated H4 K16Ac blocks the propagation of heterochromatin at the telomeres of Saccharomyces cerevisiae and is further involved in silencing at the HM loci and the rDNA locus. In this study, we investigated Sas2 mediated H4 K16Ac on a genome-wide scale, by using chromatin immunoprecipitations combined with high resolution tiling arrays. Because Sas2 interacts with the chromatin assembly factors CAF-I and Asf1, we furthermore investigated the dependence of the Sas2-mediated H4 K16Ac on these factors and found a partial influence of CAF-I and Asf1 on H4 K16Ac. Globally, H4 K16Ac was reduced in the absence of Sas2. Interestingly, H4 K16Ac loss in sas2∆ cells outside of the telomeric regions showed a distinctive pattern in that there was a pronounced decrease of H4 K16Ac within the majority of open reading frames (ORFs), but little change in intergenic regions. Significantly, high Sas2-dependent H4 K16Ac correlated with low histone H3 exchange and low H3 K56 acetylation, indicating that this modification was placed on chromatin independently of histone exchange. Consistent with this notion we found evidence that Sas2 mediated H4 K16 acetylation coupled to the S-Phase of the cell cycle. In agreement with the effect of Sas2 within ORFs, sas2∆ caused resistance to 6-azauracil, and RNA polymerase II (PolII) occupancy in the 3’ region of genes was increased in sas2∆ cells, suggesting a positive effect on transcription elongation in the absence of H4 K16Ac. Additionally, we observed a slight accumulation of transcripts at the 3’ end of the majority of genes in sas2∆ cells. This effect for several reasons was distinct from short transcripts that are caused by cryptic transcription initiation. Nonetheless, this finding completed our picture of the positive impact of sas2∆ on PolII-dependent transcription. In summary, our data suggest that Sas2 dependent H4 K16Ac is distributed ...
Genome-wide control of H4 K16 acetylation by the SAS-I complex in Saccharomyces cerevisiae
The MYST HAT Sas2 is part of the SAS-I complex, which includes the subunits Sas4 and Sas5 and acetylates histone H4 lysine 16 (H4 K16Ac). This Sas2-mediated H4 K16Ac blocks the propagation of heterochromatin at the telomeres of Saccharomyces cerevisiae and is further involved in silencing at the HM loci and the rDNA locus. In this study, we investigated Sas2 mediated H4 K16Ac on a genome-wide scale, by using chromatin immunoprecipitations combined with high resolution tiling arrays. Because Sas2 interacts with the chromatin assembly factors CAF-I and Asf1, we furthermore investigated the dependence of the Sas2-mediated H4 K16Ac on these factors and found a partial influence of CAF-I and Asf1 on H4 K16Ac. Globally, H4 K16Ac was reduced in the absence of Sas2. Interestingly, H4 K16Ac loss in sas2∆ cells outside of the telomeric regions showed a distinctive pattern in that there was a pronounced decrease of H4 K16Ac within the majority of open reading frames (ORFs), but little change in intergenic regions. Significantly, high Sas2-dependent H4 K16Ac correlated with low histone H3 exchange and low H3 K56 acetylation, indicating that this modification was placed on chromatin independently of histone exchange. Consistent with this notion we found evidence that Sas2 mediated H4 K16 acetylation coupled to the S-Phase of the cell cycle. In agreement with the effect of Sas2 within ORFs, sas2∆ caused resistance to 6-azauracil, and RNA polymerase II (PolII) occupancy in the 3’ region of genes was increased in sas2∆ cells, suggesting a positive effect on transcription elongation in the absence of H4 K16Ac. Additionally, we observed a slight accumulation of transcripts at the 3’ end of the majority of genes in sas2∆ cells. This effect for several reasons was distinct from short transcripts that are caused by cryptic transcription initiation. Nonetheless, this finding completed our picture of the positive impact of sas2∆ on PolII-dependent transcription. In summary, our data suggest that Sas2 dependent H4 K16Ac is distributed ...
Genome-wide control of H4 K16 acetylation by the SAS-I complex in Saccharomyces cerevisiae
Heise, Franziska (author) / Ehrenhofer-Murray, Ann
2011-06-28
Theses
Electronic Resource
English
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