A novel and conserved protein AHO‐3 is required for thermotactic plasticity associated with feeding states in Caenorhabditis elegans

Although a large proportion of molecules expressed in the nervous system are conserved from invertebrate to vertebrate, functional properties of such molecules are less characterized. Here, we show that highly conserved hydrolase AHO‐3 acts as a novel regulator of starvation‐induced thermotactic pla...

Full description

Saved in:
Bibliographic Details
Published in:Genes to cells : devoted to molecular & cellular mechanisms 2012-05, Vol.17 (5), p.365-386
Main Authors: Nishio, Nana, Mohri‐Shiomi, Akiko, Nishida, Yukuo, Hiramatsu, Naoya, Kodama‐Namba, Eiji, Kimura, Kotaro D., Kuhara, Atsushi, Mori, Ikue
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Animals, Genetically Modified
Behavior, Animal - physiology
Caenorhabditis elegans
Caenorhabditis elegans - genetics
Caenorhabditis elegans - physiology
Caenorhabditis elegans Proteins - genetics
Caenorhabditis elegans Proteins - metabolism
Cell migration
Cysteine
Feeding
Food
Food Deprivation
Guanine nucleotide-binding protein
Humans
hydrolase
Hydrolases - genetics
Hydrolases - metabolism
Locomotion - physiology
Migration
Molecular Sequence Data
Nematoda
Nervous system
Original
Sequence Alignment
Temperature
Temperature effects
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Although a large proportion of molecules expressed in the nervous system are conserved from invertebrate to vertebrate, functional properties of such molecules are less characterized. Here, we show that highly conserved hydrolase AHO‐3 acts as a novel regulator of starvation‐induced thermotactic plasticity in Caenorhabditis elegans. As wild‐type animals, aho‐3 mutants migrated to the cultivation temperature on a linear thermal gradient after cultivation at a particular temperature with food. Whereas wild‐type animals cultivated under food‐deprived condition showed dispersed distribution on the gradient, aho‐3 mutants exhibited tendency to migrate toward higher temperature. Such an abnormal behavior was completely rescued by the expression of human homologue of AHO‐3, indicating that the molecular function of AHO‐3 is highly conserved between nematode and human. The behavioral regulation by AHO‐3 requires the N‐terminal cysteine cluster, which ensures the proper subcellular localization of AHO‐3 to sensory endings. Double‐mutant analysis suggested that AHO‐3 acts in the same pathway with ODR‐3, a heterotrimeric G protein alpha subunit. Our results unveiled a novel neural protein in C. elegans, confirming its conserved role in behavioral regulation.
ISSN:1356-9597
1365-2443
DOI:10.1111/j.1365-2443.2012.01594.x