Ben Koch 🐛

@benkoch96.bsky.social

Biologist at The Sainsbury Lab in Norwich, UK studying plant-microbe interactions.

this is not my ideal way of seeing my lab published in Science magazine, but, here we are. Roger is well known as a devoted life-long plant scientist, but he is also an incredible human being who shows constant kindness and encouragement to everyone around him. this is simply not fair.

Science Magazine@science.org · 6mo ago

Breaking news: Indiana University plant microbiologist Roger Innes has been locked out of his laboratory by the school in response to a request by one of his federal funders. The move comes after Innes complained about the government’s prosecution of Chinese postdocs. https://scim.ag/4tsDqRr

New Preprint: A specialized ARGONAUTE enables trans-species RNA interference in plant immunity (2026) https://www.tsl.ac.uk/publications/164506

bioRxiv: A specialized ARGONAUTE enables trans-species RNA interference in plant immunity (2026)

Trans-species RNA interference (tsRNAi), in which plants produce small RNAs (sRNAs) to silence target genes in pathogens, has emerged as a promising strategy for disease control. However, whether tsRNAi constitutes an endogenous, regulated immune response remains unclear. Here, we show that ARGONAUTE10 (AGO10) plays a critical role in pathogen-induced tsRNAi. Loss of AGO10 in Arabidopsis abolished pathogen gene silencing during infection, leading to hypersusceptibility to oomycete and fungal pathogens. Importantly, AGO10 rapidly responds to pathogen infection through increased protein accumulation and re-location into discrete cytoplasmic condensates, thus promoting the production of trans-species sRNAs at the pathogen infection sites. This immune responsiveness relies on the N terminal intrinsically disordered region (IDR) of AGO10, which is responsible for sensing and responding to immune activation. Specific features in the IDR partitions AGO10 into two deeply diverged subgroups, AGO10a and AGO10b, with the immune responsiveness and defense function evolutionarily conserved in AGO10a but not AGO10b. Together, these findings establish tsRNAi as a bona fide, evolutionarily conserved immune response and position AGO10 as a signal-responsive hub linking pathogen perception to tsRNAi-based defense.

doi.org