This study investigates the role of Mid1, a putative stretch-activated calcium channel, in the plant pathogenic fungus Claviceps purpurea. Researchers generated mid1 deletion mutants (Δmid1) and analyzed their phenotypes. The Δmid1 mutants exhibited reduced growth rates in axenic culture compared to wild-type, which could not be complemented by elevated external calcium supplementation. The mutants displayed heightened sensitivity to cell wall stressors and altered calcium homeostasis. Most strikingly, Δmid1 mutants were completely nonpathogenic—infected rye plants showed no disease symptoms. In vitro infection studies revealed that Δmid1 mutants produced excessive apical branches and failed to penetrate host ovarian tissue, suggesting Mid1 is essential for generating the mechanical force required for host cell penetration. This represents the first demonstration that a Mid1 homologue plays a critical role in plant fungal pathogenicity.

Key findings

• Δmid1 mutants showed significantly reduced growth rates in culture that could not be rescued by calcium supplementation, indicating Mid1 role in calcium homeostasis distinct from yeast.
• Δmid1 mutants displayed abnormal cell wall structure with polysaccharide aggregations and altered sensitivity to cell wall stressors and external calcium levels.
• Δmid1 mutants were completely avirulent, causing no disease symptoms in infected rye plants.
• In vitro infection assays demonstrated Δmid1 mutants developed excessive apical branching and were unable to penetrate host tissue, indicating Mid1 is essential for generating penetration force.