Summary
A bioRxiv preprint reports that rice peptide OsRALF7 can trigger infection-structure formation in the rice blast fungus. Experiments in rice plants also suggest the peptide helps guide where those structures form.
A rice peptide involved in immune responses can also act as a cue for the fungus that causes rice blast, according to a bioRxiv preprint. The researchers report that OsRALF7 induced formation of appressoria in Magnaporthe oryzae—specialised structures the fungus needs to penetrate a plant—and that rice plants lacking the peptide had fewer of them.
The findings point to a dual role for a plant signal: it can activate rice defence responses while also helping the pathogen initiate infection. The authors suggest OsRALF7 provides positional information about where infection can begin.
A host signal with two effects
Rapid alkalinization factors, or RALFs, are plant peptide hormones associated with processes including development, stress responses and cell-wall organisation. In the reported experiments, synthetic OsRALF7 activated defence responses in rice suspension cells. The same peptide induced appressorium formation in the blast fungus.
The researchers link the fungal response to activation of the cAMP/PKA and Pmk1 MAPK pathways, which are involved in the fungus’s response to infection-related cues. Appressorium formation in response to OsRALF7 also depended on a hydrophobic surface. The report says the peptide’s activity required a conserved YISY motif and cysteine residues, and that OsRALF7 is located at the plasma membrane and cell wall in rice.
These results describe different responses by the plant and fungus to the same peptide. They suggest the fungus can interpret a rice-derived signal as information relevant to starting infection, even as the signal activates plant defence.
Plant experiments point to a positioning role
When the fungus was inoculated onto rice plants with the OsRALF7 gene knocked out, it formed fewer appressoria. The structures that did form were positioned differently relative to the boundaries between adjacent epidermal cells. Together with the peptide experiments, this supports the authors’ interpretation that OsRALF7 helps guide appressorium placement, rather than simply stimulating formation in any location.
The effect was not shared across the other plant–fungus pairing tested. Arabidopsis RALF23 did not induce appressoria in Colletotrichum higginsianum; instead, it showed antifungal activity. The contrast suggests that the interaction depends on the particular peptide and fungus, rather than representing a universal response to RALF peptides.
The work identifies a possible way a plant pathogen can exploit a host-derived signal during the earliest stages of infection. It is a preprint focused on infection biology; the findings described concern appressorium formation and positioning, not a tested crop-protection treatment or field-level disease outcome.