%0 Journal Article
%T The replicative lifespan©\extending deletion of SGF73 results in altered ribosomal gene expression in yeast
%A Amanda G. Mason
%A Bhumil Patel
%A Brian K. Kennedy
%A Lorraine Pillus
%A Mark A. McCormick
%A Renee M. Garza
%J Archive of "Aging Cell".
%D 2017
%R 10.1111/acel.12611
%X Sgf73, a core component of SAGA, is the yeast orthologue of ataxin©\7, which undergoes CAG¨Cpolyglutamine repeat expansion leading to the human neurodegenerative disease spinocerebellar ataxia type 7 (SCA7). Deletion of SGF73 dramatically extends replicative lifespan (RLS) in yeast. To further define the basis for Sgf73©\mediated RLS extension, we performed ChIP©\Seq, identified 388 unique genomic regions occupied by Sgf73, and noted enrichment in promoters of ribosomal protein (RP)©\encoding genes. Of 388 Sgf73 binding sites, 33 correspond to 5¡ä regions of genes implicated in RLS extension, including 20 genes encoding RPs. Furthermore, half of Sgf73©\occupied, RLS©\linked RP genes displayed significantly reduced expression in sgf73¦¤ mutants, and double null strains lacking SGF73 and a Sgf73©\regulated, RLS©\linked RP gene exhibited no further increase in replicative lifespan. We also found that sgf73¦¤ mutants display altered acetylation of Ifh1, an important regulator of RP gene transcription. These findings implicate altered ribosomal protein expression in sgf73¦¤ yeast RLS and highlight altered acetylation as a pathway of relevance for SCA7 neurodegeneration
%K genome©\wide occupancy
%K longevity gene
%K Neurodegeneration
%K replicative lifespan
%K Sgf73
%K yeast
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5506417/