Poster
Matthew Macleod (he/him/his)
Sainsbury Laboratory Cambridge University
Cambridge, Cambridge, UNITED KINGDOM
Sabine Brumm (she/her/hers)
Phytopathology - TUM School of Life Sciences
Freising-Weihenstephan, Bayern, Germany
Isaac Coven
Research Technician
Sainsbury Laboratory Cambridge University
Cambridge, England, United Kingdom
Fabio Dos Santos Barbosa
The Sainsbury Laboratory
Norwich, England, United Kingdom
Matthew Moscou
USDA
St Paul, Minnesota, United States
Sebastian Schornack
Sainsbury Laboratory (SLCU), University of Cambridge
Cambridge, England, United Kingdom
Plant-microbe interactions are shaped by host molecular processes, including cytoskeletal reorganization. Susceptibility (S) genes, often linked to broader metabolic functions, play key roles in pathogen infection and are promising targets for improving crop resistance. SCAR/WAVE proteins are part of the SCAR/WAVE complex which regulates ARP2/3-mediated actin filament nucleation. In Medicago truncatula, the SCAR protein API is a susceptibility factor to the oomycete pathogen Phytophthora palmivora by controlling cell wall properties near the root tip. However, a conserved role for SCARs as S genes in monocots has not yet been demonstrated. To explore this, we generated barley lines where individual SCAR/WAVE proteins are inactivated and assessed their impact on plant development and microbial interactions. We find that HvSCAR-B and HvSCAR-C contribute to root susceptibility to P. palmivora, with stronger resistance in double mutants. Plants in which HvSCAR B and HvSCAR-C were mutated also did not show any pleiotropic defects in growth or fertility and colonization by Arbuscular Mycorrhiza (AM) was either unaffected or enhanced, suggesting a differential role for SCARs in different microbial interactions. These findings establish SCAR/WAVE proteins as susceptibility factors in monocots but reveal distinct functional roles among SCAR paralogs. Future research should explore their biochemical impact on root-microbe interactions, particularly in localised cell wall remodelling.