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Updated: Aug 9, 2025

Genome-wide Analysis of Histone Modifications Distribution using the Chromatin Immunoprecipitation Sequencing Method in Magnaporthe oryzae
Published on: June 2, 2021
MoVast2 combined with MoVast1 regulates lipid homeostasis and autophagy in Magnaporthe oryzae
Xue-Ming Zhu1, Lin Li1, Jian-Dong Bao1
1State Key Laboratory for Managing Biotic and Chemical Treats to the Quality and Safety of Agro-products, Institute of Plant Protection and Microbiology, Zhejiang Academy of Agricultural Sciences, Hangzhou, Zhejiang, China.
Abstract:
Macroautophagy/autophagy is an evolutionarily conserved biological process among eukaryotes that degrades unwanted materials such as protein aggregates, damaged mitochondria and even viruses to maintain cell survival. Our previous studies have demonstrated that MoVast1 acts as an autophagy regulator regulating autophagy, membrane tension, and sterol homeostasis in rice blast fungus. However, the detailed regulatory relationships between autophagy and VASt domain proteins remain unsolved. Here, we identified another VASt domain-containing protein, MoVast2, and further uncovered the regulatory mechanism of MoVast2 in M. oryzae. MoVast2 interacted with MoVast1 and MoAtg8, and colocalized at the PAS and deletion of MoVAST2 results in inappropriate autophagy progress. Through TOR activity analysis, sterols and sphingolipid content detection, we found high sterol accumulation in the ΔMovast2 mutant, whereas this mutant showed low sphingolipids and low activity of both TORC1 and TORC2. In addition, MoVast2 colocalized with MoVast1. The localization of MoVast2 in the MoVAST1 deletion mutant was normal; however, deletion of MoVAST2 leads to mislocalization of MoVast1. Notably, the wide-target lipidomic analyses revealed significant changes in sterols and sphingolipids, the major PM components, in the ΔMovast2 mutant, which was involved in lipid metabolism and autophagic pathways. These findings confirmed that the functions of MoVast1 were regulated by MoVast2, revealing that MoVast2 combined with MoVast1 maintained lipid homeostasis and autophagy balance by regulating TOR activity in M. oryzae.
Insights
MoVast2 regulates autophagy and lipid homeostasis in rice blast fungus by interacting with MoVast1. Deleting MoVast2 disrupts autophagy and alters sterol and sphingolipid levels, impacting TOR signaling.
Area of Science:
- Molecular biology
- Cell biology
- Mycology
Background:
- Macroautophagy/autophagy is a conserved eukaryotic process for degrading cellular waste.
- MoVast1 was previously identified as a regulator of autophagy, membrane tension, and sterol homeostasis in rice blast fungus (M. oryzae).
- The precise regulatory roles of VASt domain proteins in autophagy remain unclear.
Purpose of the Study:
- To identify and characterize a novel VASt domain-containing protein, MoVast2, in M. oryzae.
- To elucidate the regulatory mechanism of MoVast2 in autophagy and lipid metabolism.
- To understand the interplay between MoVast1 and MoVast2 in maintaining cellular homeostasis.
Main Methods:
- Protein-protein interaction assays (co-immunoprecipitation).
- Subcellular localization studies (confocal microscopy).
- Autophagy flux assays and TOR activity analysis.
- Sterol and sphingolipid content detection via lipidomic analysis.
- Gene deletion and complementation studies.
Main Results:
- MoVast2 interacts with MoVast1 and MoAtg8, localizing to the phagophore assembly site (PAS).
- Deletion of MoVAST2 impairs autophagy progression and leads to MoVast1 mislocalization.
- The ΔMovast2 mutant exhibits sterol accumulation, sphingolipid depletion, and reduced TORC1/TORC2 activity.
- MoVast2 is crucial for maintaining lipid homeostasis and autophagy balance, regulating TOR activity in conjunction with MoVast1.
Conclusions:
- MoVast2 is a key regulator of autophagy and lipid metabolism in M. oryzae.
- MoVast2 functions in concert with MoVast1 to maintain cellular homeostasis.
- The MoVast2-MoVast1 complex regulates TOR signaling pathways, impacting both autophagy and lipid balance.
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