Yeast Genetics and Molecular Biology 1998
College Park, Maryland
August 1998


Name: Ramos, Paula C.
Mailing Address: Institut für Mikrobiologie, Heinrich-Heine-Universität, Universitätsstr.1, Düsseldorf, 40225, Germany
Email Address: ramos@uni-duesseldorf.de
Phone and Fax numbers: 49-211-81-13724, 49-211-81-14908

070

Maturation of the proteasome.


Paula C. Ramos (1) , Jörg Höckendorff (1), Birgit Keck (1), Erica Johnson (2), Alexander Varshavsky (3), Jürgen Dohmen (1)
(1) Institut für Mikrobiologie, Heinrich-Heine-Universität, Universitätsstr.1, Düsseldorf, 40225, Germany; (2) Laboratory of Cell Biology, The Rockefeller University, New York, NY 10021; (3) Division of Biology, California Institute of Technology, Pasadena, CA 91125

In eukaryotes, ubiquitin-mediated proteolysis (UMP) is the main pathway for selective degradation of short-lived proteins. These include many regulators with diverse functions in cell biology, e.g. cyclins, Cdk inhibitors and transcriptional activators or repressors as Gcn4p or Matalpha2p. Substrates that are marked for degradation by the attachment of multi-ubiquitin chains are degraded by the 26S proteasome. It is composed of a catalytic core, the 20S proteasome, and two 19S regulators that are specifically required for the degradation of ubiquitylated proteins. We have isolated several mutants, ump1-ump5 , with defects in this pathway. These mutants directly affect the function of the proteasome. The UMP1 gene was found to be required for proper maturation of the proteasome (Ramos et al., Cell 92, 489-499). Ump1p is a short-lived chaperone present in half-proteasome precursors characterized by the presence of unprocessed beta-subunits. Upon formation of the 20S particle from these precursors, Ump1p becomes encased and assists in activation of the protease (processing of beta-subunits). Ump1p is degraded after activation of the proteolytic sites making it the first substrate of the newly formed proteasome. The ump2 and ump4 mutations were localized to genes encoding 20S proteasome subunits. Our analyses revealed that both mutants are deficient in beta-subunit processing, and suggested a defined order of processing events.


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