Selective Mitophagy Enables Invasive Growth of Anthracnose Pathogen

Anthracnose is one of the most damaging fungal diseases affecting woody oil crops and many other plants, causing severe yield losses worldwide. Successful infection requires fungal pathogens to survive environmental stress, penetrate host tissues, and sustain invasive growth. Mitochondria play a critical role in energy production and stress adaptation, but damaged mitochondria can impair cellular fitness if not properly removed. Mitophagy allows cells to selectively degrade dysfunctional mitochondria, maintaining metabolic balance and survival under stress. Although mitophagy has been linked to fungal development, its precise molecular role in plant-pathogenic fungi remains poorly understood. Based on these challenges, it is necessary to conduct in-depth research into how mitophagy contributes to fungal pathogenicity.

In a study published (DOI: 10.1093/hr/uhaf121) on May 2, 2025, in Horticulture Research, scientists from Zhejiang Agriculture and Forestry University, Huazhong Agricultural University, and collaborating institutes report the discovery of a key mitophagy regulator in Colletotrichum camelliae, the fungus responsible for anthracnose in tea oil trees. The research reveals that a SUN family protein, CaSun1, directly recruits the autophagy protein CaAtg8 to mitochondria, enabling mitophagy during infection. This mechanism proves essential for fungal virulence and invasive growth in host plants.

Using immunoprecipitation–mass spectrometry, the researchers first identified CaSun1 as a potential interacting partner of CaAtg8, a conserved autophagy protein. Genetic deletion experiments showed that loss of CaSun1 severely impaired fungal growth, spore formation, stress tolerance, and pathogenicity. In infected leaves, CaSun1-deficient strains produced much smaller lesions and displayed blocked invasive hyphal development.

Fluorescence imaging demonstrated that CaSun1 localizes to mitochondria and colocalizes with CaAtg8 under nutrient starvation. Importantly, CaSun1 was not required for general autophagy but was indispensable for mitophagy. Without CaSun1, damaged mitochondria failed to be delivered to vacuoles for degradation, leading to mitochondrial accumulation and physiological dysfunction.

Further molecular analysis revealed that CaSun1 binds CaAtg8 through two specific AIM/LIR motifs. Mutating these motifs disrupted the interaction, abolished mitophagy, and reproduced the loss-of-virulence phenotype. Together, the results establish CaSun1 as a mitophagy-specific receptor that links mitochondrial surveillance to fungal pathogenicity, defining a previously unrecognized layer of infection control.

"This study reveals how mitochondrial quality control directly shapes fungal virulence," the authors note. "By uncovering a mitophagy-specific regulator rather than a general autophagy factor, we show that pathogenic fungi depend on highly targeted cellular recycling pathways during infection." They emphasize that disrupting this process does not kill the fungus outright but weakens its ability to invade and spread. "This makes mitophagy regulators particularly attractive targets for disease control strategies that aim to reduce pathogen aggressiveness while minimizing broader ecological impact."

The discovery of CaSun1-mediated mitophagy opens new avenues for controlling anthracnose and related fungal diseases. Targeting mitophagy-specific regulators could offer a precision strategy to suppress fungal virulence without relying on conventional fungicides. Such approaches may reduce resistance development and environmental burden. Beyond agriculture, the findings also advance understanding of mitophagy in eukaryotic pathogens, highlighting conserved links between mitochondrial maintenance and infectious behavior. As mitophagy emerges as a core determinant of pathogen fitness, manipulating this pathway may become a powerful tool for safeguarding crop health and improving sustainable disease management.