# The Phytophthora parasitica effector AVH195 interacts with ATG8, attenuates host autophagy, and promotes biotrophic infection

## TL;DR

A plant pathogen uses a protein called AVH195 to interfere with the plant's autophagy process, preventing cell death and promoting infection.

## Contribution

AVH195 is a novel effector that interacts with ATG8 to suppress autophagy and promote biotrophic infection in plants.

## Key findings

- AVH195 prevents cell death in tobacco caused by pathogen effectors and BAX protein.
- AVH195 interacts with ATG8 and delays autophagy in Chlamydomonas reinhardtii and Arabidopsis thaliana.
- AVH195 promotes susceptibility to Phytophthora parasitica and Hyaloperonospora arabidopsidis in Arabidopsis.

## Abstract

Plant pathogens secrete effector proteins into host cells to suppress immune responses and manipulate fundamental cellular processes. One of these processes is autophagy, an essential recycling mechanism in eukaryotic cells that coordinates the turnover of cellular components and contributes to the decision on cell death or survival.

We report the characterization of AVH195, an effector from the broad-spectrum oomycete plant pathogen, Phytophthora parasitica. We show that P. parasitica expresses AVH195 during the biotrophic phase of plant infection, i.e., the initial phase in which host cells are maintained alive. In tobacco, the effector prevents the initiation of cell death, which is caused by two pathogen-derived effectors and the proapoptotic BAX protein. AVH195 associates with the plant vacuolar membrane system and interacts with Autophagy-related protein 8 (ATG8) isoforms/paralogs. When expressed in cells from the green alga, Chlamydomonas reinhardtii, the effector delays vacuolar fusion and cargo turnover upon stimulation of autophagy, but does not affect algal viability. In Arabidopsis thaliana, AVH195 delays the turnover of ATG8 from endomembranes and promotes plant susceptibility to P. parasitica and the obligate biotrophic oomycete pathogen Hyaloperonospora arabidopsidis.

Taken together, our observations suggest that AVH195 targets ATG8 to attenuate autophagy and prevent associated host cell death, thereby favoring biotrophy during the early stages of the infection process.

The online version contains supplementary material available at 10.1186/s12915-024-01899-w.