Document Type

Article

Language

eng

Format of Original

13 p.

Publication Date

1-2008

Publisher

Rockefeller University Press

Source Publication

Journal of Cell Biology

Source ISSN

0021-9525

Original Item ID

doi: 10.1083/jcb.200705069; PubMed Central, PMCID: PMC2213584

Abstract

T-shape radial spokes regulate flagellar beating. However, the precise function and molecular mechanism of these spokes remain unclear. Interestingly, Chlamydomonas reinhardtii flagella lacking a dimeric heat shock protein (HSP) 40 at the spokehead–spokestalk juncture appear normal in length and composition but twitch actively while cells jiggle without procession, resembling a central pair (CP) mutant. HSP40 cells begin swimming upon electroporation with recombinant HSP40. Surprisingly, the rescue doesn't require the signature DnaJ domain. Furthermore, the His-Pro-Asp tripeptide that is essential for stimulating HSP70 adenosine triphosphatase diverges in candidate orthologues, including human DnaJB13. Video microscopy reveals hesitance in bend initiation and propagation as well as irregular stalling and stroke switching despite fairly normal waveform. The in vivo evidence suggests that the evolutionarily conserved HSP40 specifically transforms multiple spoke proteins into stable conformation capable of mechanically coupling the CP with dynein motors. This enables 9 + 2 cilia and flagella to bend and switch to generate alternate power strokes and recovery strokes.

Comments

Published version. Journal of Cell Biology, Vol. 180, No. 2 (January 2008): 403-415. DOI. © Rockefeller University Press 2008. Used with permission.

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