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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
VmPma1 contributes to virulence via regulation of the acidification process during host infection in Valsa mali
Feiran Zhang1, Yangguang Meng1, Yinghao Wang1
1State Key Laboratory of Crop Stress Biology for Arid Areas, College of Plant Protection, Northwest A&F University, Yangling 712100, Shaanxi, China.
Abstract:
Valsa mali is a destructive phytopathogenic fungus that mainly infects apple and pear trees. Infection with V. mali results in host tissue acidification via the generation of citric acid, which promote invasion. Here, two plasma membrane H+-ATPases, VmPma1 and VmPma2, were identified in V. mali. The VmPma1 deletion mutant (∆VmPma1) displayed higher intracellular acid accumulation and a lower growth rate compared to the wild type. In contrast, the VmPma2 deletion mutant (∆VmPma2) showed no obvious phenotypic differences. Meanwhile, loss of VmPma1, but not VmPma2, in V. mali led to a significant decrease in growth under acidic or alkaline conditions compared with WT. More importantly, ∆VmPma1 showed a greater reduction in ATPase hydrolase activity and acidification of the external environment, more sensitivity to abiotic stress, and weaker pathogenicity than ∆VmPma2. This evidence indicates that VmPma1 is the main gene of the two plasma membrane H+-ATPases. Transcriptomic analysis indicated that many metabolic processes regulated by VmPma1 are strictly pH-regulated. Besides, we identified two genes (named VmAgn1p and Vmap1) that contribute to the pathogenicity of V. mali by differentially regulating external acidification capacity. Overall, our findings show that VmPma1 plays a pivotal role in pathogenicity by affecting the acidification of V. mali.
Insights
Valsa mali uses plasma membrane H+-ATPases to acidify host tissues. VmPma1 is crucial for Valsa mali growth, stress tolerance, and pathogenicity, unlike VmPma2.
Area of Science:
- Plant Pathology
- Mycology
- Biochemistry
Background:
- Valsa mali causes significant damage to apple and pear trees.
- Fungal invasion is facilitated by host tissue acidification through citric acid production.
Purpose of the Study:
- To investigate the roles of two plasma membrane H+-ATPases, VmPma1 and VmPma2, in Valsa mali.
- To determine the contribution of these ATPases to fungal growth, stress response, and pathogenicity.
Main Methods:
- Gene deletion mutants (∆VmPma1, ∆VmPma2) were created and analyzed.
- Phenotypic characterization included growth rates, acid accumulation, and response to pH.
- Transcriptomic analysis was performed to understand gene regulation.
- Pathogenicity assays were conducted on host plants.
Main Results:
- Deletion of VmPma1 led to increased intracellular acid accumulation and reduced growth rate.
- VmPma1, but not VmPma2, deletion significantly impacted growth under acidic/alkaline conditions.
- ∆VmPma1 exhibited reduced ATPase activity, external acidification, stress tolerance, and pathogenicity compared to WT and ∆VmPma2.
- Transcriptomic data revealed VmPma1 regulates pH-dependent metabolic processes.
- VmAgn1p and Vmap1 were identified as additional pathogenicity factors affecting acidification.
Conclusions:
- VmPma1 is the primary plasma membrane H+-ATPase in Valsa mali, essential for its growth and pathogenicity.
- VmPma1's role in regulating external acidification is critical for Valsa mali virulence.
- Understanding VmPma1 function offers potential targets for controlling Valsa mali infections.
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