Defective in mitotic arrest 1 (Dma1) ubiquitin ligase controls G1 cyclin degradation
Autor/a
Hernández-Ortega, Sara
Ricco Pacheco, Natalia
Ramírez, Sara
Casals i Farré, Núria
Jiménez, Javier
Isasa, Marta
Crosas, Bernat
Clotet Erra, Josep
Fecha de publicación
2013-02ISSN
0021-9258
Resumen
Progression through the G1 phase of the cell cycle is controlled by diverse cyclin-dependent kinases (CDKs) that might be associated to numerous cyclin isoforms. Given such complexity, regulation of cyclin degradation should be crucial for coordinating progression through the cell cycle. In Saccharomyces cerevisiae, SCF is the only E3 ligase known to date to be involved in G1 cyclin degradation. Here, we report the design of a genetic screening that uncovered Dma1 as another E3 ligase that targets G1 cyclins in yeast. We show that the cyclin Pcl1 is ubiquitinated in vitro and in vivo by Dma1, and accordingly, is stabilized in dma1 mutants. We demonstrate that Pcl1 must be phosphorylated by its own CDK to efficiently interact with Dma1 and undergo degradation. A nonphosphorylatable version of Pcl1 accumulates throughout the cell cycle, demonstrating the physiological relevance of the proposed mechanism. Finally, we present evidence that the levels of Pcl1 and Cln2 are independently controlled in response to nutrient availability. This new previously unknown mechanism for G1 cyclin degradation that we report here could help elucidate the specific roles of the redundant CDK-cyclin complexes in G1.
Tipo de documento
Artículo
Versión del documento
Versión publicada
Lengua
English
Materias (CDU)
61 - Medicina
Palabras clave
Fisiologia
Cribatge genètic
Fisiología
Genes -- Despistaje
Physiology
Genetic screening
Páginas
11
Publicado por
American Society for Biochemistry and Molecular Biology
Colección
288; 7
Publicado en
Journal of Biological Chemistry
Citación
Hernández-Ortega, Sara; Bru, Samuel; Ricco, Natalia [et al.]. Defective in mitotic arrest 1 (Dma1) ubiquitin ligase controls G1 cyclin degradation. Journal of Biological Chemistry, 2013, 288(7), p. 4704-4714. Disponible en: <https://www.sciencedirect.com/science/article/pii/S0021925820462738?via%3Dihub>. Fecha de acceso: 21 abr. 2021. DOI: 10.1074/jbc.M112.426593
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Under a Creative Commons license
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