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Updated: Aug 12, 2025
Author Spotlight: Investigating Fungal Pathogenicity Mechanisms in Maize
Published on: September 15, 2023
The COPII subunit MoSec24B is involved in development, pathogenicity and autophagy in the rice blast fungus
Hui Qian1, Lixiao Sun1, Minghua Wu1
1State Key Laboratory for Managing Biotic and Chemical Treats to the Quality and Safety of Agro-products, Institute of Biotechnology, Zhejiang University, Hangzhou, China.
Abstract:
The endoplasmic reticulum (ER) acts as the starting point of the secretory pathway, where approximately one-third of the proteins are correctly folded and modified, loaded into vesicles, and transported to the Golgi for further processing and modification. In this process, COPII vesicles are responsible for transporting cargo proteins from the ER to the Golgi. Here, we identified the inner shell subunit of COPII vesicles (MoSec24B) and explored the importance of MoSec24B in the rice blast fungus. The targeted disruption of MoSec24B led to decreased growth, reduced conidiation, restricted glycogen and lipids utilization, sensitivity to the cell wall and hypertonic stress, the failure of septin-mediated repolarization of appressorium, impaired appressorium turgor pressure, and decreased ability to infect, which resulted in reduced pathogenicity to the host plant. Furthermore, MoSec24B functions in the three mitogen-activated protein kinase (MAPK) signaling pathways by acting with MoMst50. Deletion of MoSec24B caused reduced lipidation of MoAtg8, accelerated degradation of exogenously introduced GFP-MoAtg8, and increased lipidation of MoAtg8 upon treatment with a late inhibitor of autophagy (BafA1), suggesting that MoSec24B regulates the fusion of late autophagosomes with vacuoles. Together, these results suggest that MoSec24B exerts a significant role in fungal development, the pathogenesis of filamentous fungi and autophagy.
Insights
The inner shell subunit of COPII vesicles, MoSec24B, is crucial for fungal development and pathogenicity in rice blast fungus. Its disruption impairs growth, infection, and autophagy, highlighting its role in cellular processes.
Area of Science:
- Cell Biology
- Mycology
- Molecular Biology
Background:
- The endoplasmic reticulum (ER) is central to protein folding and transport via vesicles.
- COPII vesicles mediate cargo transport from the ER to the Golgi apparatus.
- Understanding vesicle components is key to deciphering fungal pathogenesis.
Purpose of the Study:
- To identify and characterize the function of the COPII vesicle inner shell subunit, MoSec24B, in the rice blast fungus (Magnaporthe oryzae).
- To investigate the role of MoSec24B in fungal growth, development, stress response, and pathogenicity.
- To elucidate the involvement of MoSec24B in mitogen-activated protein kinase (MAPK) signaling and autophagy.
Main Methods:
- Targeted gene disruption of MoSec24B in Magnaporthe oryzae.
- Phenotypic analysis of MoSec24B deletion mutants, including growth, conidiation, and stress sensitivity.
- Assessment of appressorium formation, turgor, and infection efficiency.
- Analysis of MAPK pathway interactions and autophagy-related protein dynamics (lipidation and degradation).
Main Results:
- Disruption of MoSec24B significantly reduced fungal growth, conidiation, and nutrient utilization.
- MoSec24B is essential for appressorium function, leading to impaired turgor and reduced pathogenicity.
- MoSec24B interacts with MoMst50 in MAPK pathways and regulates autophagy, specifically the fusion of late autophagosomes with vacuoles.
- MoSec24B deletion resulted in altered MoAtg8 lipidation and degradation patterns.
Conclusions:
- MoSec24B is a critical component of COPII vesicles involved in the secretory pathway.
- MoSec24B plays a vital role in the development, stress tolerance, and pathogenesis of filamentous fungi like rice blast fungus.
- MoSec24B regulates essential cellular processes including MAPK signaling and autophagy, impacting fungal survival and infection.
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