Plasticity in Caenorhabditis elegans

All animals have the ability to perceive and respond to external cues. Cuesmay signify the presence of good things, such as food, a potential mate or shelter, or bad things, such as predators, competitors, or a hazardous environment. Typically, an organism will be exposed to a mixture of positive and negative cues, requiring the animal to weigh the inputs and subsequently determine its behavioural response based on that information. However, the response may vary: a certain stimulus may elicit different behavioural responses, depending on the context of the stimulus, previous experiences of the organism, its age or developmental stage. This variability is called plasticity, and is well known in many animal species. The ensuing flexibility is thought to enhance the chances of survival and to be essential for memory formation and for many aspects of development. It has even been proposed to be one of the driving forces of natural selection and evolution (Price et al., 2003; Agrawal 2001). However, despite the broad impact of behavioural plasticity, the cellular and molecular mechanisms are thus far poorly understood

Signaling proteins that regulate NaCl [corrected] chemotaxis responses modulate longevity in C. elegans

The lifespan of the nematode Caenorhabditis elegans is regulated by sensory signals detected by the amphid neurons. In these neurons, C. elegans expresses at least 14 Galpha s

Dauer pheromone and G-protein signaling modulate the coordination of intraflagellar transport kinesin motor proteins in C. elegans

Cilia length and function are dynamically regulated by modulation of intraflagellar transport (IFT). The cilia of C. elegans amphid channel neurons provide an excellent model to study this process, since they use two different kinesins for anterograde transport: kinesin-II and OSM-3 kinesin together in the cilia middle segments, but only OSM-3 in the distal segments. To address whether sensory signaling modulates the coordination of the kinesins, we studied IFT protein motility in gpa-3 mutant animals, since dominant active mutation of this sensory Gα protein GPA-3QL) affects cilia length. In addition, we examined animals exposed to dauer pheromone, since dauer formation, which involves gpa-3, induces changes in cilia morphology. Live imaging of fluorescently tagged IFT proteins showed that in gpa-3 mutants and in larvae exposed to dauer pheromone, kinesin-II speed is decreased and OSM-3 speed is increased, whereas structural IFT proteins move at an intermediate speed. These results indicate that mutation of gpa-3 and exposure to dauer pheromone partially uncouple the two kinesins. We propose a model in which GPA-3-regulated docking of kinesin-II and/or OSM-3 determines entry of IFT particles into the cilia subdomains, allowing structural and functional plasticity of cilia in response to environmental cues

PACRG, a protein linked to ciliary motility, mediates cellular signaling

Cilia are microtubule-based organelles that project from nearly all mammalian cell types. Motile cilia generate fluid flow, whereas nonmotile (primary) cilia are required for sensory physiology and modulate various signal transduction pathways. Here we investigate the nonmotile ciliary signaling roles of parkin coregulated gene (PACRG), a protein linked to ciliary motility. PACRG is associated with the protofilament ribbon, a structure believed to dictate the regular arrangement of motility-associated ciliary components. Roles for protofilament ribbon-associated proteins in nonmotile cilia and cellular signaling have not been investigated. We show that PACRG localizes to a small subset of nonmotile cilia in Caenorhabditis elegans, suggesting an evolutionary adaptation for mediating specific sensory/signaling functions. We find that it influences a learning behavior known as gustatory plasticity, in which it is functionally coupled to heterotrimeric G-protein signaling. We also demonstrate that PACRG promotes longevity in C. Elegans by actiong upstream of the lifespan-promoting FOXO transcription factor DAF-16 and likely upstream of insulin/IGF signaling. Our findings establish previously unrecognized sensory/signaling functions for PACRG and point to a role for this protein in promoting longevity. Furthermore, our work suggests additional ciliary motility-signaling connections, since EFHC1 (EF-hand containing 1), a potential PACRG interaction partner similarly associated with the protofilament ribbon and ciliary motility, also positively regulates lifespan