Treating flies with the organophosporous compound tri-ortho-cresyl phosphate (TOCP) results in locomotor deficits and neurodegeneration two weeks after exposure, symptoms similar to organophosphate-induced delayed neuropathy (OPIDN). An acute neurotoxicity is also observed: primary neurons showed signs of axonal degeneration within an hour after treatment. This system has been used to investigate the role of the Drosophila ortholog of PNPLA6, sws, in the development of OPIDN symptoms. Changes in levels of expression of Dmel\sws and Dmel\Pka-C3 (known to interact with sws) were found to impact the delayed symptoms of OPIDN, but not the acute toxicity.
See also the Human Disease Model report 'neurodegenerative disease, PNPLA6-related' (FBhh0000368) and the FlyBase chemical report for Tri-O-cresyl phosphate (FBch0001061).
[updated Mar. 2024 by FlyBase; FBrf0222196]
Certain organophosphorus (OP) compounds produces OP compound-induced delayed neurotoxicity (OPIDN), a distal degeneration of axons in the central nervous system and peripheral nervous system (Richardson et al., 2020; pubmed:32518884).
OPIDN is caused by inhibition of the PNPLA6 (formerly NTE) gene product by the organophosphate (Richardson et al., 2020; pubmed:32518884).