Ability of paralyzed flagella mutants of Chlamydomonas to move

Abstract

Chlamydomonas mutants missing the central pair or radial spokes are paralyzed despite the fact that they have the full wild-type complement of functional dynein ATPases. We show here that these mutants can move under conditions of low ATP concentration, a combination of ATP and ADP, and a combination of ATP and ribose-modified ATP analogs. These conditions suggest an inhibitory role of ATP and that this inhibition can be relieved by ADP or analogs. The function of the central-pair/radial spoke complex may be to release this ATP inhibition in a controlled manner.

TheChlamydomonas PF6Locus Encodes a Large Alanine/Proline-Rich Polypeptide That Is Required for Assembly of a Central Pair Projection and Regulates Flagellar Motility

“…For instance, wild-type Chlamydomonas cells can switch from an asymmetric (ciliary) beat pattern to a symmetric (flagellar) beat pattern in response to elevated calcium levels, and the central pair appears to be required for this conversion at physiological ATP levels (Hosokawa and Miki-Noumura, 1987). Central pair mutants can be induced to produce asymmetric waveforms under altered nucleotide or buffer conditions (Omoto et al, 1996;Yagi and Kamiya, 2000). Yet, a great majority of motile axonemes possess a central apparatus, and most central pair defective mutants are paralyzed under physiological conditions (Witman et al, 1978;Afzelius, 1985), consistent with an essential role in regulating motility.…”

Thinking about flagellar oscillation

“…Most of these mutants appear to have switching defects that cause the flagella to become arrested at or near temporal switch points. They typically show no deficit when tested for sliding disintegration, and paralysis can be overcome, partially or completely, by altered chemical conditions [Goldstein, 1982;Omoto et al, 1996;Frey et al, 1997], mechanical forces [Hayashibe et al, 1997], or extragenic suppressor mutants that do not restore structural proteins missing in the mutants. In many cases, pf mutants show defects in protein components of the central apparatus, in contrast to dynein mutants, which often show reduced frequency or bend amplitude rather than arrest.…”

The radial spokes and central apparatus: Mechano‐chemical transducers that regulate flagellar motility

“…Presumably, the paralysis caused by radial spoke and central pair defects reveals a control system that inhibits flagellar movement when these components are missing; the suppressor mutations restore motility by bypassing the inhibited state. Omoto et al [1996] have proposed that the inhibited state may be due to ATP interaction with the regulatory P-loops of the dynein heavy chains. By using ATP analogs or low concentrations of ATP (Ͻ50 M ATP), axonemes isolated from radial spoke or central apparatus defective mutants could be reactivated to produce modest waveforms at very low beat frequency (Ͻ5 Hz) [Omoto et al, 1996].…”

“…Omoto et al [1996] have proposed that the inhibited state may be due to ATP interaction with the regulatory P-loops of the dynein heavy chains. By using ATP analogs or low concentrations of ATP (Ͻ50 M ATP), axonemes isolated from radial spoke or central apparatus defective mutants could be reactivated to produce modest waveforms at very low beat frequency (Ͻ5 Hz) [Omoto et al, 1996]. These results suggest that ATP plays an inhibitory role, and that the function of the CP/RS system may be to release the ATP inhibition in a controlled manner.…”