Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.1 (ACS)
 78,556 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Saccharomyces cerevisiae, chromatin-mediated silencing inactivates transcription of the genes at the HML and HMR cryptic mating-type loci and genes near telomeres. Mutations in the Rap1p and Abf1p binding sites of the HMR-E silencer (HMRa-e**) result in a loss of silencing at HMR. We characterized a collection of 15 mutations that restore the alpha-mating phenotype to MATalpha HMRa-e** strains. These mutations defined three complementation groups, two new groups and one group that corresponded to the previously identified SAS2 gene. We cloned the genes that complemented members of the new groups and identified two previously uncharacterized genes, which we named SAS4 and SAS5. Neither SAS4 nor SAS5 was required for viability. Null alleles of SAS4 and SAS5 restored SIR4-dependent silencing at HMR, establishing that each is a regulator of silencing. Null alleles of SAS4 and SAS5 bypassed the role of the Abf1p binding site of the HMR-E silencer but not the role of the ACS or Rap1p binding site. Previous analysis indicated that SAS2 is homologous to a human gene that is a site of recurring translocations involved in acute myeloid leukemia. Similarly, SAS5 is a member of a gene family that included two human genes that are the sites of recurring translocations involved in acute myeloid leukemia.
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PMID:Identification of SAS4 and SAS5, two genes that regulate silencing in Saccharomyces cerevisiae. 1047 96

Saccharomyces cerevisiae subtelomeric repeats contain silencing elements such as the core X sequence, which is present at all chromosome ends. When transplaced at HML, core X can enhance the action of a distant silencer without acting as a silencer on its own, thus fulfilling the functional definition of a protosilencer. Here we show that an ACS motif and an Abf1p-binding site participate in the silencing capacity of core X and that their effects are additive. In addition, in a variety of settings, core X was found to bring about substantial gene repression only when a low level of silencing was already detectable in its absence. Adjoining an X-STAR sequence, which naturally abuts core X in subtelomeric regions, did not improve the silencing capacity of core X. We propose that protosilencers play a major role in a variety of silencing phenomena, as is the case for core X, which acts as a silencing relay, prolonging silencing propagation away from telomeres.
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PMID:Protosilencers in Saccharomyces cerevisiae subtelomeric regions. 1133 27

The silenced chromatin at the cryptic mating-type loci (HML and HMR) of Saccharomyces cerevisiae requires a cell cycle event between early S phase and G(2)/M phase to achieve repression. Although DNA replication per se is not essential for silencing, mutations in many of the proteins involved in DNA replication affect silencing. Each of the four silencers, which flank the silenced loci, includes an origin recognition complex (ORC) binding site (ACS). ORC directly interacted with Sir1 and recruits Sir1 to the silencers. This study describes additional roles for ORC in the architecture of silenced chromatin. Using chromatin immunoprecipitation (ChIP) analysis, we found that ORC physically interacts throughout the internal regions of HMR as well as with silencers. This interaction depended on the presence of Sir proteins and, in part, on the HMR-I silencer. ORC remained associated with the internal regions of HMR even when these regions were recombinationally separated from the silencers. Moreover, ORC could be recruited to the silencers lacking an ACS through its Sir1 interaction.
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PMID:Expanded roles of the origin recognition complex in the architecture and function of silenced chromatin in Saccharomyces cerevisiae. 1994 82