The Saccharomyces cerevisiae 14-3-3 Proteins Are Required for the G1/S Transition, Actin Cytoskeleton Organization and Cell Wall Integrity
| Autor: | Francisca Lottersberger, Giovanna Lucchini, Simonetta Piatti, Andrea Panza, Maria Pia Longhese |
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| Přispěvatelé: | Lottersberger, F, Panza, A, Lucchini, G, Piatti, S, Longhese, M |
| Rok vydání: | 2006 |
| Předmět: |
Osmosis
Saccharomyces cerevisiae Proteins actin cytoskeleton Genes Fungal Saccharomyces cerevisiae Gene Dosage S. cerevisiae BIO/18 - GENETICA Investigations Actin cytoskeleton organization S Phase Calcium-binding protein Genetics DNA Fungal Genes Suppressor Cytoskeleton Protein Kinase C 14-3-3 Membrane Glycoproteins Base Sequence biology Calcium-Binding Proteins G1 Phase Intracellular Signaling Peptides and Proteins Temperature DNA replication Membrane Proteins G1/S transition biology.organism_classification Actin cytoskeleton Actins Cell biology 14-3-3 Proteins Membrane protein Mutation cell wall cell cycle |
| Zdroj: | Genetics. 173:661-675 |
| ISSN: | 1943-2631 |
| Popis: | 14-3-3 proteins are highly conserved polypeptides that participate in many biological processes by binding phosphorylated target proteins. The Saccharomyces cerevisiae BMH1 and BMH2 genes, whose concomitant deletion is lethal, encode two functionally redundant 14-3-3 isoforms. To gain insights into the essential function(s) shared by these proteins, we searched for high-dosage suppressors of the growth defects of temperature-sensitive bmh mutants. Both the protein kinase C1 (Pkc1) and its upstream regulators Wsc2 and Mid2 were found to act as high dosage suppressors of bmh mutants' temperature sensitivity, indicating a functional interaction between 14-3-3 and Pkc1. Consistent with a role of 14-3-3 proteins in Pkc1-dependent cellular processes, shift to the restrictive temperature of bmh mutants severely impaired initiation of DNA replication, polarization of the actin cytoskeleton, and budding, as well as cell wall integrity. Because Pkc1 acts in concert with the Swi4-Swi6 (SBF) transcriptional activator to control all these processes, the defective G1/S transition of bmh mutants might be linked to impaired SBF activity. Indeed, the levels of the G1 cyclin CLN2 transcripts, which are positively regulated by SBF, were dramatically reduced in bmh mutants. Remarkably, budding and DNA replication defects of bmh mutants were suppressed by CLN2 expression from an SBF-independent promoter, suggesting that 14-3-3 proteins might contribute to regulating the late G1 transcriptional program. |
| Databáze: | OpenAIRE |
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