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Tra1 is a component of the Saccharomyces cerevisiae SAGA and NuA4 complexes and a member of the PIKK family, which contain a C-terminal phosphatidylinositol 3-kinase-like (PI3K) domain followed by a 35-residue FATC domain. Single residue changes of L3733A and F3744A, within the FATC domain, resulted in transcriptional changes and phenotypes that were similar but not identical to those caused by mutations in the PI3K domain or deletions of other SAGA or NuA4 components. The distinct nature of the FATC mutations was also apparent from the additive effect of tra1-L3733A with SAGA, NuA4, and tra1 PI3K domain mutations. Tra1-L3733A associates with SAGA and NuA4 components and with the Gal4 activation domain, to the same extent as wild-type Tra1; however, steady-state levels of Tra1-L3733A were reduced. We suggest that decreased stability of Tra1-L3733A accounts for the phenotypes since intragenic suppressors of tra1-L3733A restored Tra1 levels, and reducing wild-type Tra1 led to comparable growth defects. Also supporting a key role for the FATC domain in the structure/function of Tra1, addition of a C-terminal glycine residue resulted in decreased association with Spt7 and Esa1, and loss of cellular viability. These findings demonstrate the regulatory potential of mechanisms targeting the FATC domains of PIKK proteins.
Pubmed ID: 20635087 RIS Download
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View all literature mentionsWelcome to Michael Eisens lab in the Howard Hughes Medical Institute (HHMI) at University of California at Berkeley (UCB) and the Lawrence Berkeley National Lab (LBNL). We are part of the Department of Molecular and Cell Biology of UCB and the Genomics Division of LBNL, and the. We are located in Stanley Hall on the Berkeley campus.Our lab applies computational and experimental genomic approaches to study how genome sequences specify organismal form and function. We are particularly interested in the regulation of gene expression, and focus on how the information that specifies when and where genes are expressed is encoded in genome sequences, the role that regulated gene expression plays in animal development and the response of microbes to their environments, and how variation in and evolution of gene expression contributes to phenotypic variation and the remarkable diversity of life on Earth. This site contains a more detailed description of our research projects, an introduction to members of the lab, reprints of all of our publications, free downloadable and web-based software. Sponsor. Experimental work described here was supported by a Howard Hughes Medical Institute Investigator award to MBE and by National Institutes of Health (NIH) grant GM704403 to MBE and MDB. Computational analyses were supported in by NIH grant HG002779 to MBE. Work at Lawrence Berkeley National Laboratory was conducted under Department of Energy contract DE-AC02-05CH11231. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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