English   español  
Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/128869
Título

Antagonistic roles of PP2A-Pab1 and Etd1 in the control of cytokinesis in fission yeast

AutorLahoz, Aurelia; Alcaide, María; Daga, Rafael R. ; Jiménez-Martínez, Juan
Fecha de publicación2010
EditorGenetics Society of America
CitaciónGenetics 186(4): 1261-1270 (2010)
ResumenIn Schizosaccharomyces pombe, Etd1 is a positive regulator of the septation initiation network (SIN), a conserved GTPase-regulated kinase cascade that triggers cytokinesis. Here we show that a mutation in the pab1 gene, which encodes the B-regulatory subunit of the protein phosphatase 2A (PP2A), suppresses mutations in the etd1 gene. Etd1 is required for the function of the GTPase Spg1, a key regulator of SIN signaling. Interestingly, the loss of Pab1 function restored the activity of Spg1 in Etd1-deficient cells. This result suggests that PP2A-Pab1-mediated dephosphorylation inhibits Spg1, thus antagonizing Etd1 function. The loss of pab1 function also rescues the lethality of mutants of other genes in the SIN cascade such as mob1, sid1, and cdc11. Two-hybrid assays indicate that Pab1 physically interacts with Mob1, Sid1, Sid2, and Cdc11, suggesting that the phosphatase 2A B-subunit is a component of the SIN complex. Together, our results indicate that PP2A-Pab1 plays a novel role in cytokinesis, regulating SIN activity at different levels. Pab1 is also required to activate polarized cell growth. Thus, PP2A-Pab1 may be involved in coordinating polar growth and cytokinesis.
URIhttp://hdl.handle.net/10261/128869
DOI10.1534/genetics.110.121368
Identificadoresdoi: 10.1534/genetics.110.121368
issn: 0016-6731
e-issn: 1943-2631
Aparece en las colecciones: (CABD) Artículos
Ficheros en este ítem:
Fichero Descripción Tamaño Formato  
accesoRestringido.pdf15,38 kBAdobe PDFVista previa
Visualizar/Abrir
Mostrar el registro completo
 

Artículos relacionados:


NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.