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Verticillium dahliae Asp1 regulates the transition from vegetative growth to asexual reproduction by modulating microtubule dynamic organization

Juan Tian; Mengli Pu; Bin Chen; Guangda Wang; Chunli Li; Xiaxia Zhang; Yanjun Yu; Zhi Wang; Zhaosheng Kong
Environmental Microbiology · Vol. 25, Issue 3 · pp. 738-750 · 2023

Abstract

Verticillium dahliae is a devastating pathogenic fungus that causes severe vascular wilts in more than 400 dicotyledonous plants. The conidiation of V. dahliae in plant vascular tissues is the key strategy for its adaptation to the nutrient‐poor environment and is required for its pathogenicity. However, it remains unclear about the regulatory mechanism of conidium production of V. dahliae in vascular tissues. Here, we found that VdAsp1 , encoding an inositol polyphosphate kinase, is indispensable for the pathogenicity of V. dahliae . Loss of VdAsp1 function does not affect the invasion of the host, but it impairs the colonization and proliferation in vascular tissues. The Δ VdAsp1 mutant shows defective initiation of conidiophore formation and reduced expression of genes associated with the central developmental pathway. By live‐cell imaging, we observed that some of Δ VdAsp1 mutant hyphae are swollen, and microtubule arrangements at the apical region of these hyphae are disorganized. These results indicate that VdAsp1 regulates the transition from vegetative growth to asexual reproduction by modulating microtubule dynamic organization, which is essential for V. dahliae to colonize and proliferate in vascular tissues. These findings provided a potential new direction in the control of vascular wilt pathogen by targeting conidium production in vascular tissues.

Bibliographic Information

JournalEnvironmental Microbiology
PublisherWiley
Publication Date2023-03-01
Publication Year2023
Volume25
Issue3
Pages738-750
Document TypeJournal Article
Print ISSN1462-2912
eISSN1462-2920
DOI10.1111/1462-2920.16320
SubjectMicrobial Ecology

Access Information

NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/14622920
Publisher PageOpen Publisher Page
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