English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/129949
Share/Impact:
Statistics
logo share SHARE   Add this article to your Mendeley library MendeleyBASE
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:
Title

Controlling mitotic commitment from the G2 spindle pole

AuthorsTallada, Víctor A. ; Hagan, Iain M.
Issue Date2009
CitationXXXVII Congreso de la SEG (2009)
AbstractThe activation of MPF to promote mitotic commitment is regulated by the co-ordination of the signals from a number of signalling cascades. MPF is held in check in interphase cells by phosphorylation in the ATP binding site of the catalytic, Cdk1, subunit. This phosphate is then removed by a phosphatase called Cdc25 to activate the Cdk1 kinase and promote entrance into mitosis. The essential spindle pole body (SPB) component Cut12 appears to play a key role in the activation of MPF in fission yeast. The cut12.1 loss of function mutation leads to insertion defects of the new SPB and blocks spindle formation while the gain of function mutation cut12.s11 enable cells to live without the otherwise essential phosphatase Cdc25. Increasing Cdc25 levels suppresses the conditional lethality and the spindle formation defect of cut12.1, indicating that these cells are unable to form a spindle because of a defect in MPF activation. Thus, this SPB component seems to play a critical role in regulating entrance to mitosis. We think that this function is fulfilled by alteration of the activity of the polo kinase Plo1. Polo has been implicated in a positive feedback loop that boosts Cdc25 and inhibits Wee1 during mitotic entry in a variety of systems. We found that boosting Plo1 activity independently of any change in Cut12 also suppresses cdc25.22 defects. Furthermore the gain of function cut12.s11 mutation boosts global and SPB associated Plo1 activity and the loss of function mutant cut12.1 reduces both. Importantly, at 30°C Plo1 is recruited to the SPB in G2 100 mins before commitment to mitosis. The cdc25 bypassing cut12.s11 mutation promotes this recruitment 25 minutes earlier. Fluorescence Recovery After Photobleaching (FRAP) experiments demonstrate that this premature recruitment is not due to turnover increase. Live imaging experiments with analogue sensitive cdc2.as mutant establish that recruitment of Plo1 to the G2 SPB relies upon the activity of MPF itself. Thus from a point in G2 there is a futile cycle that involves MPF activity on the SPB.
DescriptionResumen del trabajo presentado al XXXVII Congreso de la Sociedad Española de Genética, celebrado en Torremolinos (Málaga) del 29 de septiembre al 2 de octubre de 2009.
URIhttp://hdl.handle.net/10261/129949
Appears in Collections:(CABD) Comunicaciones congresos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.