Genetic impairment of autophagy intensifies expanded polyglutamine toxicity in Caenorhabditis elegans.
Neuronal homeostasis requires a balance between anabolic and catabolic processes. Eukaryotic cells use two distinct systems for the degradation of unused proteins: the ubiquitin-proteasome system and the autophagic system. The autophagic system is also necessary for the degradation of bulk amounts of proteins and organelles. We have searched for new autophagy-related genes in the Caenorhabditis elegans genome and investigated their role in a polyglutamine (polyQ) disease model. Here, we have shown that inactivation of these genes intensified the toxicity of expanded polyQ in C. elegans neurons and muscles, and at the same time inactivation of CeTor reduced the polyQ toxicity.
Khan
Liakot A
LA
Laboratory of Structural Neuropathology, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.
Yamanaka
Tomoyuki
T
Nukina
Nobuyuki
N
D000818:Animals; D001343:Autophagy / Q000235:genetics*; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000254:growth & development*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics*; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease / Q000235:genetics; D020271:Heredodegenerative Disorders, Nervous System / Q000235:genetics*; D010455:Peptides / Q000235:genetics*
D029742:Caenorhabditis elegans Proteins; D010455:Peptides; C097188:polyglutamine