SAGA Complex Components and Acetate Repression in Aspergillus nidulans

G3: Genes, Genomes, Genetics

Joan M. Kelly¹  Robin A. Lockington¹  Paraskevi Georgakopoulos¹ 

[1] School of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA, 5006, AustraliaSchool of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA, 5006, AustraliaSchool of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA, 5006, Australia

关键词: acetate repression;    SAGA complex;    carbon catabolite repression;    creA;    creB;    creC;   

DOI  :  10.1534/g3.112.003913

学科分类：生物科学（综合）

来源: Genetics Society of America

【 摘 要 】

Alongside the well-established carbon catabolite repression by glucose and other sugars, acetate causes repression in Aspergillus nidulans. Mutations in creA, encoding the transcriptional repressor involved in glucose repression, also affect acetate repression, but mutations in creB or creC, encoding components of a deubiquitination system, do not. To understand the effects of acetate, we used a mutational screen that was similar to screens that uncovered mutations in creA, creB, and creC, except that glucose was replaced by acetate to identify mutations that were affected for repression by acetate but not by glucose. We uncovered mutations in acdX, homologous to the yeast SAGA component gene SPT8, which in growth tests showed derepression for acetate repression but not for glucose repression. We also made mutations in sptC, homologous to the yeast SAGA component gene SPT3, which showed a similar phenotype. We found that acetate repression is complex, and analysis of facA mutations (lacking acetyl CoA synthetase) indicates that acetate metabolism is required for repression of some systems (proline metabolism) but not for others (acetamide metabolism). Although plate tests indicated that acdX- and sptC-null mutations led to derepressed alcohol dehydrogenase activity, reverse-transcription quantitative real-time polymerase chain reaction showed no derepression of alcA or aldA but rather elevated induced levels. Our results indicate that acetate repression is due to repression via CreA together with metabolic changes rather than due to an independent regulatory control mechanism.

【 授权许可】

Unknown