The emerging regulatory potential of SCFMet30-mediated polyubiquitination and proteolysis of the Met4 transcriptional activator Public Deposited

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Creator
  • Skowyra, Dorota
    • Other Affiliation: Edward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, MO, 63104, USA
  • Chandrasekaran, Srikripa
    • Affiliation: School of Medicine, Department of Biochemistry and Biophysics
    • Other Affiliation: Edward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, MO, 63104, USA
Abstract
  • Abstract The yeast SCFMet30 ubiquitin ligase plays a critical role in cell division by regulating the Met4 transcriptional activator of genes that control the uptake and assimilation of sulfur into methionine and S-adenosyl-methionine. The initial view on how SCFMet30 performs its function has been driven by the assumption that SCFMet30 acts exclusively as Met4 inhibitor when high levels of methionine drive an accumulation of cysteine. We revisit this model in light of the growing evidence that SCFMet30 can also activate Met4. The notion that Met4 can be inhibited or activated depending on the sulfur metabolite context is not new, but for the first time both aspects have been linked to SCFMet30, creating an interesting regulatory paradigm in which polyubiquitination and proteolysis of a single transcriptional activator can play different roles depending on context. We discuss the emerging molecular basis and the implications of this new regulatory phenomenon.
Date of publication
Identifier
  • 18655704
  • doi:10.1186/1747-1028-3-11
Resource type
  • Article
Rights statement
  • In Copyright
Rights holder
  • Srikripa Chandrasekaran et al.; licensee BioMed Central Ltd.
License
Journal title
  • Cell Division
Journal volume
  • 3
Journal issue
  • 1
Page start
  • 11
Language
  • English
Is the article or chapter peer-reviewed?
  • Yes
ISSN
  • 1747-1028
Bibliographic citation
  • Cell Division. 2008 Jul 25;3(1):11
Access
  • Open Access
Publisher
  • BioMed Central Ltd