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First published online November 4, 2009

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Myo52 spells catastrophe for MTs

Polarised growth – which determines cell shape – has been closely studied in the fission yeast Schizosaccharomyces pombe, in which cell growth occurs exclusively at cell tips and requires the actin cytoskeleton. To switch from monopolar to bipolar growth in preparation for cell division, S. pombe cells also require the activity of the microtubule (MT) cytoskeleton – but how do the two cytoskeletal networks interact? On page 3862, Rebeca Martín-García and Daniel Mulvihill identify a role for the actin-associated myosin motor Myo52 in actin-MT interactions. The authors first show that, in yeast lacking fully functional Myo52, MTs that contact the cell end keep growing and curl around the end of the cell; by contrast, MTs in wild-type S. pombe undergo catastrophe (a switch from growth to shrinking). Moreover, in myo52 mutant yeast, the removal of the MT-plus-end-binding protein Tip1 from MT tips at cell ends (an event that is associated with MT catastrophe) is inhibited. The authors next show that Tip1 undergoes ubiquitylation and proteolysis, and that this is regulated by Myo52 and the ubiquitin receptor Dph1, both of which interact with Tip1. They conclude that Myo52 promotes MT catastrophe at cell ends by facilitating Tip1 removal and degradation. These results provide fresh insight into interactions between the MT and actin cytoskeletons.

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Related articles in JCS:

Myosin V spatially regulates microtubule dynamics and promotes the ubiquitin-dependent degradation of the fission yeast CLIP-170 homologue, Tip1

Rebeca Martín-García and Daniel P. Mulvihill
JCS 2009 122: 3862-3872. [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 Social Bookmarking                         What's this?