The Cysteine Protease CfAtg4 Interacts with CfAtg8 to Govern the Growth, Autophagy and Pathogenicity of Colletotrichum fructicola

TL;DR

This study shows how the proteins CfAtg4 and CfAtg8 work together to control the growth, autophagy, and ability to cause disease in a fungus that infects Camellia oleifera.

Contribution

The study identifies a novel interaction between CfAtg4 and CfAtg8 that regulates autophagy and pathogenicity in Colletotrichum fructicola.

Findings

CfAtg4 interacts with CfAtg8 to form autophagosomes in the fungus.

A truncated version of CfAtg8 partially restores autophagy and growth defects in the absence of CfAtg4.

The interaction between CfAtg8 and CfAtg4 is critical for appressoria formation and pathogenicity.

Abstract

Camellia oleifera is a native woody oil plant in southern China and is infected with anthracnose wherever it is grown. We previously identified Colletotrichum fructicola as the major causal agent of anthracnose on C. oleifera and found that CfAtg8 regulates the pathogenicity and development of C. fructicola. Here, we revealed that CfAtg4 interacts with CfAtg8, contributing to the formation of autophagosomes. The CfAtg81–160 allele, which only contains 1–160 amino acids of the CfAtg8, partially recovered the autophagosome numbers and autophagy defects of the ΔCfatg4 mutant. Consequently, these recoveries resulted in the restoration of the defects of the ΔCfatg4 mutant in growth and responses to different external stresses, albeit to an extent. Importantly, we illustrated the critical roles of CfAtg81–160 in appressoria formation, and pathogenicity. Collectively, our findings provide new insights into the importance of the interaction between CfAtg8 and CfAtg4 in the growth, autophagy and pathogenicity of the phytopathogenic fungi.

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