Title:

argeting cyclic nucleotide phosphodiesterase as a potential nematicide by using chemical and biochemical agents

Nearly 4,100 species of plant parasitic nematodes seriously constrain global food security, and about ~100B crops are damaged due to them. Nematode behavior and lifecycle depend on cyclic nucleotide signaling. PDEs are major determinants of cellular levels of cyclic nucleotides because the main process of lowering active intracellular cyclic nucleotide second messengers (cAMP and cGMP) in the cells is through PDEs. However, there is currently limited knowledge of the role of individual PDEs in mediating C. elegans signaling pathways. Mammals possess 11 PDE families (PDE1-PDE11), and nematodes have six PDE genes representing six families. Our studies show that exposing wildtype C. elegans N2 strain to a human PDE1-specific inhibitor reduced chemotactic response to the odorant. To mimic the phenotype observed by exposing human PDE1- specific inhibitor, exposed C. elegans strain in which PDE1 was ablated (“knocked out”) can also disrupt chemosensation. In addition, exposing a PDE-1/PDE-4 double mutant C. elegans strain to the pde-3 RNAi construct showed a greater reduction in reproduction and developmental delays, and nematodes appeared to be lethargic. Altogether, these findings will help us to understand the role of individual PDEs in C. elegans and lay the foundation for discovering novel chemical or genetic controls for phyto parasitic nematodes that minimize adverse effects on the host or the environment. The outcome of this work may lead to increased crop productivity globally, thereby enhancing access to a safe and secure food supply.

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