|
|
|
|
|
|
|
||
Department of Molecular, Cellular, and Developmental Biology, University of Colorado at Boulder, Boulder, Colorado 80309-0347
To gain a further understanding of axonemal
dynein regulation, mutant strains of Chlamydomonas
reinhardtii that had defects in both phototactic behavior and flagellar motility were identified and characterized. ptm1, ptm2, and ptm3 mutant strains exhibited motility phenotypes that resembled those of known inner dynein arm region mutant strains, but did not have
biochemical or genetic phenotypes characteristic of
other inner dynein arm mutations. Three other mutant
strains had defects in the f class of inner dynein arms.
Dynein extracts from the pf9-4 strain were missing the
entire f complex. Strains with mutations in pf9/ida1,
ida2, or ida3 failed to assemble the f dynein complex
and did not exhibit phototactic behavior. Fractionated
dynein from mia1-1 and mia2-1 axonemes exhibited a
novel f class inner dynein arm biochemical phenotype;
the 138-kD f intermediate chain was present in altered phosphorylation forms. In vitro axonemal dynein activity was reduced by the mia1-1 and mia2-1 mutations.
The addition of kinase inhibitor restored axonemal dynein activity concomitant with the dephosphorylation of the 138-kD f intermediate chain. Dynein extracts
from uni1-1 axonemes, which specifically assemble only
one of the two flagella, contained relatively high levels
of the altered phosphorylation forms of the 138-kD intermediate chain. We suggest that the f dynein complex
may be phosphoregulated asymmetrically between the
two flagella to achieve phototactic turning.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
