Abstract |
Most eukaryotes have motile cilia/flagella as cell organelles for swimming, locomotion, or
generating extracellular fluid flow. Recent studies have revealed that dysfunctions in ciliary/flagellar
motility engender human disease. Most motile cilia/flagella possess the inner structure called the
axoneme with “9 + 2” pattern, in which the nine doublet microtubules surround two central singlet
microtubules. This structural pattern is evolutionally conserved. The axoneme comprises many structural
components aligned on the microtubules, including axonemal dyneins, radial spokes, and projections on
the central pair microtubules. Ciliary/flagellar movements are generated by dynein-driven microtubule
sliding, and are controlled by second messengers such as Ca2+ and cAMP. However, molecular
mechanisms of ciliary/flagellar movements in response to Ca2+ and cAMP, and the individual roles of the
axonemal components in the mechanisms remain unclear. Furthermore, mechanisms by which the energy
is supplied for ciliary/flagellar movement are not well defined. Paramecium has long been used as a
model organism for studying ciliary motility, because of its valuable experimental systems. For example, cell excitement can be analyzed elecrophysiologically, and cilia on demembranated cell models and
cortical sheets can be reactivated in vitro. Furthermore, protocols for RNAi depletion of specific genes,
as well as the genome and the ciliary proteome databases, became available recently. This review
describes recent studies on molecular mechanisms of ciliary movements in Paramecium, highlighting
intraciliary energy-supply systems and regulatory systems by Ca2+ and cAMP.
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