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首页> 外文期刊>Nucleic acids research >INO1–100: an allele of the Saccharomyces cerevisiae INO1 gene that is transcribed without the action of the positive factors encoded by the INO2, INO4, SWI1, SWI2 and SWI3 genes
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INO1–100: an allele of the Saccharomyces cerevisiae INO1 gene that is transcribed without the action of the positive factors encoded by the INO2, INO4, SWI1, SWI2 and SWI3 genes

机译:INO1–100:酿酒酵母INO1基因的等位基因,其转录不受INO2,INO4,SWI1,SWI2和SWI3基因编码的阳性因子的作用

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摘要

ABSTRACT A dominant allele of the INO1locus, INO1–100, does not require the positive regulators encoded by INO2 and INO4 for expression. Sequence analysis showed that INO1–-100 had a 239 bp deletion in the INO1 promoter. INO1–-100 suppressed the Inositol auxotrophy of Ino2, Ino4, swi1, swi2 and swi3 mutants. Transcription of INO1–100 was constitutive and independent of these regulators. A 20 bp deletion from ?247 to ?228 caused a similar phenotype. A 38 bp deletion from ?245 to ?208 suppressed the inositol auxotrophy of an ino2 mutant, but not an ino4 mutant, indicating that ino2p and lno4p may function alone as well as in a complex. A 40 bp deletion from ?287 to ?248 that removed a URS1 site caused constitutive transcription that required INO2 and INO4. A deletion from ?167 to ?128 suppressed the inositol auxotrophy of swi,ino2 and ino4 mutants, indicating the presence of a previously unidentified URS1. Mutation of the specific negative regulator of phospholipld synthesis encoded by OPI1 suppressed the inositol auxotrophy of swi2 mutants. This study indicates that negative regulation of INO1 is chromatin mediated and provides in vivo information on the interaction of both general and specific regulatory factors that function to accomplish negative and positive regulation of the INO1 promoter in response to inositol.
机译:摘要INO1基因座的一个主要等位基因INO1–100,不需要由INO2和INO4编码的正调控子来表达。序列分析表明,INO1-100在INO1启动子中缺失了239 bp。 INO1--100抑制了Ino2,Ino4,swi1,swi2和swi3突变体的肌醇营养缺陷。 INO1-100的转录是组成性的,并且独立于这些调节剂。从?247到?228的20bp缺失引起相似的表型。从?245至?208缺失38 bp抑制了ino2突变体的肌醇营养缺陷,但没有抑制ino4突变体,表明ino2p和lno4p可能单独起作用,也可能在复合物中起作用。从?287到?248的40 bp缺失删除了URS1位点,导致组成型转录需要INO2和INO4。从?167到?128的缺失抑制了swi,ino2和ino4突变体的肌醇营养缺陷,表明存在以前未鉴定的URS1。 OPI1编码的磷脂合成的特定负调控因子的突变抑制了swi2突变体的肌醇营养缺陷。这项研究表明,INO1的负调控是由染色质介导的,并提供了体内有关一般和特定调控因子相互作用的信息,这些因子可完成对肌醇的INO1启动子的负调控和正调控。

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