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Tubulin polyglutamylation regulates flagellar motility by controlling a specific inner‐arm dynein that interacts with the dynein regulatory complex
Author(s) -
Kubo Tomohiro,
Yagi Toshiki,
Kamiya Ritsu
Publication year - 2012
Publication title -
cytoskeleton
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.95
H-Index - 86
eISSN - 1949-3592
pISSN - 1949-3584
DOI - 10.1002/cm.21075
Subject(s) - dynein , biology , axoneme , microbiology and biotechnology , motility , microtubule , dynein atpase , tubulin , mutant , flagellum , chlamydomonas , genetics , gene
The tpg1 mutant of Chlamydomonas lacks the tubulin polyglutamylase TTLL9 and is deficient in flagellar tubulin polyglutamylation. It exhibits slow swimming, whereas the double mutant with oda2 (a slow‐swimming mutant that lacks outer‐arm dynein) is completely nonmotile. Thus, tubulin polyglutamylation must be important for the functioning of inner‐arm dynein(s). In this study, we show that the tpg1 mutation only slightly affects the motility of mutants that lack dynein “e,” one of the seven species of major inner‐arm dyneins, whereas it greatly reduces the motility of mutants lacking other inner‐arm dynein species. This suggests that dynein e is the main target of motility regulation by tubulin polyglutamylation. Furthermore, the motility of various mutants in the background of the tpg1 mutation raises the possibility that tubulin polyglutamylation also affects the dynein regulatory complex, a dynein e–associated key regulator of flagellar motility, which possibly constitutes the interdoublet (nexin) link. Tubulin polyglutamylation thus may play a central role in the regulation of ciliary and flagellar motility. © 2012 Wiley Periodicals, Inc