The anterior end or head of a devescovinid flagellate from termites continually rotates in a clockwise direction relative to the rest of the cell. Previous laser microbeam experiments showed that rotational motility is caused by a noncontractile axostyle complex which runs from the head through the cell body and generates torque along its length. We report here success in obtaining glycerinated cell models of the rotary axostyle which, upon addition of ATP, undergo reactivation and exhibit rotational movements similar to those observed in vivo. Reactivation of rotational motility and flagellar beating of the models requires ATP or ADP and is competitively inhibited by nonhydrolyzable ATP analogs (AMP-PNP and ATP-gamma-S). N-ethylmaleimide, p-hydroxymercuribenzoate, and mersalyl acid also blocked reactivation of both the rotary axostyle and flagella. Vanadate and erythro-9-[3-(2-hydroxynonyl)]-adenine (EHNA) selectively inhibited flagellar reactivation without effecting rotational motility. These results, together with previous ultrastructural findings, suggest that the rotary axostyle does not operate by a dynein-based mechanism but may be driven by an actomyosin system with a circular arrangement of interacting elements.
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1 November 1982
Article|
November 01 1982
ATP reactivation of the rotary axostyle in termite flagellates: effects of dynein ATPase inhibitors.
M A Yamin
S L Tamm
Online ISSN: 1540-8140
Print ISSN: 0021-9525
J Cell Biol (1982) 95 (2): 589–597.
Citation
M A Yamin, S L Tamm; ATP reactivation of the rotary axostyle in termite flagellates: effects of dynein ATPase inhibitors.. J Cell Biol 1 November 1982; 95 (2): 589–597. doi: https://doi.org/10.1083/jcb.95.2.589
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