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First published online December 17, 2008

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CME effectors – making the connection

The phosphoinositide PtdIns(4,5)P₂ and the small GTPase Rab5 both have key roles during the early stages of clathrin-mediated endocytosis (CME) – PtdIns(4,5)P₂ is important in clathrin-coated-vesicle (CCV) formation, whereas Rab5 promotes the budding and maturation of CCVs. Now, Antoine Guichet and colleagues (p. 25) explore how the roles of Rab5 and PtdIns(4,5)P₂ interconnect. The authors analyse early endocytic events during yolk-protein uptake in Drosophila oocytes, showing that oocytes that lack Rab5 cannot endocytose yolk proteins. Moreover, in wild-type oocytes, depletion of PtdIns(4,5)P₂ [through loss of function of the PtdIns(4,5)P₂-synthesising enzyme Skittles] impedes recruitment of Rab5 to a site below the plasma membrane, and diminishes the formation of early endocytic vesicles (EEVs). The authors next demonstrate that Rab5 mediates the removal of PtdIns(4,5)P₂ from EEVs; notably, oocytes that overexpress Skittles [and therefore overproduce PtdIns(4,5)P₂] fail to endocytose yolk proteins, and echo the phenotype of Rab5-deficient oocytes. The authors propose that the Rab5-dependent removal of PtdIns(4,5)P₂ from EEVs is necessary for CME to proceed. Their results shed light on the complex interplay between effectors of CME.

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Related articles in JCS:

Interplay between Rab5 and PtdIns(4,5)P₂ controls early endocytosis in the Drosophila germline

Julien Compagnon, Louis Gervais, Mabel San Roman, Sophy Chamot-Bœuf, and Antoine Guichet
JCS 2009 122: 25-35. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?