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Published on: July 30, 2017
The secretory protein COA1 enables Metarhizium robertsii to evade insect immune recognition during cuticle
Qiangqiang Zhang1,2, Xuanlian Wei3, Weiguo Fang4
1Shandong Provincial Key Laboratory of Synthetic Biology, Qingdao Institute of Bioenergy and Bioprocess Technology, Chinese Academy of Sciences, Qingdao, 266101, Shandong, China.
Abstract:
The interplay between the insect immune system and entomopathogenic fungi during cuticle penetration is not yet fully understood. Here, we show that a secretory protein COA1 (coat of appressorium 1) from Metarhizium robertsii, an entomopathogenic fungus causing diseases in a wide range of insects, is required to avoid host immune recognition during cuticle penetration. COA1 is highly expressed on the cuticle and translocated to the cell surface, where it directly binds with and masks carbohydrates of the fungal cell wall to avoid provoking the host's intense immune response. Deletion of Coa1 results in a robust immune response, leading to a reduction in bacterial load in both the gut and hemocoel and ultimately attenuating fungal virulence. Our work reveals a novel cell surface protein indispensable for fungal pathogenicity via masking cell wall carbohydrates to avert a hypersensitive response from the host.
Insights
Metarhizium robertsii fungus uses COA1 protein to evade insect immunity during cuticle invasion. This coat of appressorium 1 protein masks fungal cell walls, preventing host immune detection and ensuring pathogenicity.
Area of Science:
- Mycology
- Insect Pathology
- Immunology
Background:
- The interaction between insects and entomopathogenic fungi during cuticle penetration is complex and not fully understood.
- Entomopathogenic fungi, like Metarhizium robertsii, cause significant insect diseases, necessitating research into their infection mechanisms.
Purpose of the Study:
- To investigate the role of the secretory protein COA1 from Metarhizium robertsii in evading insect immune recognition during cuticle penetration.
- To elucidate the mechanism by which COA1 facilitates fungal pathogenicity.
Main Methods:
- Analysis of COA1 protein expression and localization in Metarhizium robertsii.
- Genetic deletion of the Coa1 gene to assess its impact on fungal virulence.
- Investigation of host immune responses upon fungal interaction with and without COA1.
Main Results:
- COA1 is expressed on the fungal cuticle and translocates to the cell surface.
- COA1 directly binds and masks fungal cell wall carbohydrates, preventing immune recognition.
- Deletion of Coa1 triggers a strong insect immune response, reducing fungal load and virulence.
Conclusions:
- COA1 is a novel cell surface protein essential for Metarhizium robertsii pathogenicity.
- COA1 functions by masking fungal cell wall carbohydrates to avert host hypersensitive responses.
- Understanding COA1's role provides insights into fungal-insect immune system interactions.
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