12 February 2024
Clement Pellegrin, Anika Damm, Alexis L. Sperling, Beth Molloy, Dio S. Shin, Jonathan Long, Paul Brett, Andrea Díaz-Tendero Bravo, Sarah Jane Lynch, Beatrice Senatori, Paulo Vieira, Joffrey Mejias, Anil Kumar, Rick E. Masonbrink, Tom R. Maier, Thomas J. Baum, Sebastian Eves-van den Akker - Biorxiv, 2024
All pathogens must tailor their gene expression to their environment. Therefore, targeting host:parasite biology that regulates these changes in gene expression could open up routes to pathogen control. Here, we show that in the plant-parasitic nematode Heterodera schachtii, host signals (termed effectostimulins) within plant roots activate the master regulator sugr1. SUGR1, then, directly binds effector promoters, and orchestrates their production. Effector production, in turn, facilitates host entry, releasing more effectostimulins. These data show that gene expression during the very earliest stages of parasitism is defined by a feed forward loop for host entry. Importantly, we demonstrate that blocking SUGR1 blocks parasitism, underlining the SUGR1 signalling cascade as a valuable target for crop protection. Given that nematodes also parasitise humans and other animals, the potential impact is broad: disrupting effector production could, in principle, be applied to any pathogen that secrets effectors.
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