| Description |
cln-3.2 encodes a predicted transmembrane protein that comprises one of three C. elegans homologs of human CLN3 (OMIM:607042, mutations are associated with Batten disease (also known as juvenile neuronal ceroid lipofuscinosis), a recessively inherited childhood neurodegenerative disorder characterized by progressive loss of vision, seizures, and psychomotor abnormalities); by homology, CLN-3.2 is predicted to localize to Golgi and lysosomal membranes, where its proposed functions include that of a chaperone and/or a regulator of intracellular trafficking; in C. elegans, loss of cln-3.2 activity via mutation or RNA-mediated interference (RNAi) does not result in any obvious abnormalities (nor does loss of all three CLN3 homologs, cln-3.1, cln-3.2, and cln-3.3), suggesting that these genes do not play an essential role in development and/or behavior. |
![Adult](JavaScript:void
window.open("/cgi-bin/rnaidb/popUpImage.cgi?imgName=N2wormfinal.png",
"RNAiDB Help","toolbar=no, location=no, directories=no,
status=no, menubar=no, scrollbars=yes, resizable=no,
copyhistory=no, width=1000, height=550"))
