# Ustilago maydis disrupts carbohydrate signaling networks to induce hypertrophy in host cells

## TL;DR

The fungus Ustilago maydis causes leaf tumors in maize by using a protein called Hap1 to alter plant metabolism and cell growth.

## Contribution

The study identifies Hap1 as a fungal effector that modulates SnRK1 signaling to induce hypertrophy in maize.

## Key findings

- Hap1 promotes endoreduplication and starch accumulation in infected maize tissues.
- Hap1 upregulates starch biosynthesis and cell cycle genes while suppressing plant defense.
- Hap1 interacts with ZmSnRK1α and increases its stability through Hip1 and Hip2.

## Abstract

Ustilago maydis infection in maize causes hypertrophic leaf tumors; however, the underlying mechanisms driving this excessive cell growth are unknown. In this study, we identify Hap1 (hypertrophy-associated protein 1) as an effector and virulence factor that regulates mesophyll cell hypertrophy. Using CRISPR-Cas9 mutagenesis, we demonstrate that Hap1 contributes to endoreduplication and starch accumulation in infected tissues. Transcriptomics revealed Hap1-dependent upregulation of starch biosynthesis and cell cycle genes, as well as suppression of plant defense. This links Hap1 to metabolic and cell cycle reprogramming, and immune suppression. To identify the target of Hap1 that drives metabolic reprogramming, we investigated its interaction with ZmSnRK1α in maize. We found that Hap1 interferes with the phosphorylation of SnRK1 substrates and that two Hap1-interacting effectors, Hip1 and Hip2, enhance its protein stability. We conclude that Hap1 contributes to the reprogramming of maize metabolism and cell cycle, as well as mesophyll cell hypertrophy, by modulating the SnRK1 signaling pathway to regulate starch biosynthesis and host defense responses.

Here the authors identify the fungal effector Hap1 as a key driver of maize leaf tumor growth. Hap1 rewires plant metabolism and the cell cycle via SnRK1 signaling, promoting starch accumulation and cell enlargement.