Mutation of the feh-1 gene, the Caenorhabditis elegans orthologue of mammalian Fe65, decreases the expression of two acetylcholinesterase genes.

摘要: The molecular adaptor Fe65 is one of the cytosolic ligands Alzheimer's β-amyloid precursor protein (APP), and this complex believed to play important roles in mammalian cells. Upon cleavage APP by specific processing activities, between intracellular domain (AICD) translocates nucleus. Experimental evidence suggests that Fe65-AICD regulates gene transcription. In Caenorhabditis elegans orthologue gene, feh-1, pharyngeal activity. fact, rate contraction increased following transient or stable suppression feh-1 expression. Here we show pharynx mutant worms associated decreased acetylcholinesterase activity accompanied reduced expression ace-1 ace-2 transcripts, coding for two major activities nematode. These results indicate a target regulatory mechanisms based on Fe65-APP could be relevant pathogenesis disease.