Caenorhabditis elegans integrates the signals of butanone and food to enhance chemotaxis to butanone

Ichiro Torayama, Takeshi Ishihara, Isao Katsura

研究成果: Contribution to journalArticle査読

57 被引用数 (Scopus)

抄録

Behavioral plasticity induced by the integration of two sensory signals, such as associative learning, is an important issue in neuroscience, but its evolutionary origin and diversity have not been explored sufficiently. We report here a new type of such behavioral plasticity, which we call butanone enhancement, in Caenorhabditis elegans adult hermaphrodites: C. elegans specifically enhances chemotaxis to butanone by preexposure to butanone and food. Mutant analysis revealed that this plasticity requires the AWC ON olfactory neuron, whose fate is known to be determined by the NSY-1/ASK1 MAPKKK (mitogen-activated protein kinase kinase kinase) cascade as well as the DAF-11 and ODR-1 guanylyl cyclases. These proteins also control many aspects of olfactory sensation/plasticity in AWC neurons and seem to provide appropriate cellular conditions for butanone enhancement in the AWCON neuron. Butanone enhancement also required the functions of Bardet-Biedl syndrome genes in the AWCON neuron but not other genes that control ciliary transport. Furthermore, preexposure to butanone and the odor of food was enough for the enhancement of butanone chemotaxis. These results suggest that the AWCON olfactory neuron may conduct a behavioral plasticity resembling associative learning and that the functions of Bardet-Biedl syndrome genes in sensory cilia may play an important role in this plasticity.

本文言語英語
ページ(範囲)741-750
ページ数10
ジャーナルJournal of Neuroscience
27
4
DOI
出版ステータス出版済み - 1 24 2007
外部発表はい

All Science Journal Classification (ASJC) codes

  • 神経科学(全般)

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