Journal
DEVELOPMENTAL CELL
Volume 14, Issue 5, Pages 762-774Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2008.03.002
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Funding
- NCRR NIH HHS [S10RR16708, S10 RR016708-01] Funding Source: Medline
- NIGMS NIH HHS [R01 GM056223-11, GM56223, R37 GM056223, R01 GM056223] Funding Source: Medline
- NINDS NIH HHS [P30NS45713, P30 NS045713, P30 NS045713-049001] Funding Source: Medline
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Nonmotile primary cilia are sensory organelles composed of a microtubular axoneme and a surrounding membrane sheath that houses signaling molecules. Optimal cellular function requires the precise regulation of axoneme assembly, membrane biogenesis, and signaling protein targeting and localization vi as yet poorly understood mechanisms. Here, we show that sensory signaling is required to maintain the architecture of the specialized AWB olfactory neuron cilia in C. elegans. Decreased sensory signaling results in alteration of axoneme length and expansion of a membraneous structure, thereby altering the topological distribution of a subset of ciliary transmembrane signaling molecules. Signaling-regulated alteration of ciliary structures can be bypassed by modulation of intracellular cGMP or calcium levels and requires kinesin-II-driven intraflagellar transport (IFT), as well as BBS- and RAB8-related proteins. Our results suggest that compensatory mechanisms in response to altered levels of sensory activity modulate AWB cilia architecture, revealing remarkable plasticity in the regulation of cilia structure.
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