Molecular Mechanisms of Chemotaxis to Sodium Chloride in Caenorhabditis elegans

CHAPTER 5 Overexpression of Subunit c, the main component of the storage material in Juvenile Neuronal Ceroid Lipofuscinosis (JNCL), causes disruption of mitochondria in C.

CLN5, a novel gene encoding a putative transmembrane protein mutated in Finnish variant late infantile neuronal ceroid lipofuscinosis. Schuchman EH,

We have compiled a list of thirteen disease genes encoding proteins without lysosomal localization in the most affected cell types or organs and their worm homologues (Table

In order to get more insight in gene functions CLN3 deletion mutants were isolated from an ethyl methanesulphonate (EMS)-induced deletion mutant library 18.. The primary screening of

Supplementary figure S2 Electron microscopical analysis of adult cln-3 triple mutant and wild type worms No changes in the ultrastructural morphology of lysosomes, mitochondria,

For easy detection of Subunit c overexpression in living worms, we also generated a GFP-Subunit c fusion construct, containing the 41 amino acid mitochondrial targeting signal of

Comparison of the life span of the different models to wild type worms suggested the cln-3.1 mutant has a shorter life span than wild type worms, while cln-3.2 and cln-3.3

which Subunit c of the mitochondrial ATP synthase, the main component of the stored material in patients, was inducibly overexpressed and these transgenes were crossed into