Actin filaments are essential for plant cellular functions, and their dynamics are altered in response to fungal infection, contributing to defense responses. However, the mechanisms by which pathogens suppress actin-mediated immunity remain largely unknown. Here, we report that infection by the adapted fungus Colletotrichum higginsianum induces actin fragmentation in Arabidopsis thaliana leaf cells. Imaging analyses revealed that actin fragmentation with increased apparent actin thickness occurred following C. higginsianum inoculation. Actin fragmentation was observed two days after inoculation, preceding hyphal invasion on day three. Rhodamine-phalloidin staining confirmed that endogenous actin filaments were disrupted in infected cells. Pretreatment with latrunculin B, which induces actin fragmentation, significantly increased the rate of C. higginsianum hyphal invasion, suggesting that fragmented actin filaments may facilitate fungal entry. Notably, actin fragmentation occurred even in pattern recognition receptor mutants, indicating that it is not triggered by pathogen-associated molecular patterns (PAMP) perception. No obvious changes in microtubule organization were observed. Inoculation with the non-adapted C. tropicale did not induce actin fragmentation in A. thaliana. In contrast, C. higginsianum induced actin fragmentation in cucumber and Brassica crops, whereas C. orbiculare did not, despite being pathogenic to cucumber. These findings suggest that C. higginsianum employs a distinctive infection strategy involving actin fragmentation that is independent of canonical immune recognition.
Shimada et al. (Fri,) studied this question.