Abstract
SummaryThe soil‐borne vascular pathogen Verticillium dahliae infects many dicotyledonous plants to cause devastating wilt diseases. During colonization, V. dahliae spores develop hyphae surrounding the roots. Only a few hyphae that adhere tightly to the root surface form hyphopodia at the infection site, which further differentiate into penetration pegs to facilitate infection. The molecular mechanisms controlling hyphopodium formation in V. dahliae remain unclear. Here, we uncovered a cellophane surface‐induced gene (VdCSIN1) as a regulator of V. dahliae hyphopodium formation and pathogenesis. Deletion of VdCSIN1 compromises hyphopodium formation, hyphal development and pathogenesis. Exogenous application of cyclic adenosine monophosphate (cAMP) degradation inhibitor or disruption of the cAMP phosphodiesterase gene (VdPDEH) partially restores hyphopodium formation in the VdΔcsin1 mutant. Moreover, deletion of VdPDEH partially restores the pathogenesis of the VdΔcsin1 mutant. These findings indicate that VdCSIN1 regulates hyphopodium formation via cAMP‐mediated signalling to promote host colonization by V. dahliae.
Highlights
For effective colonization, fungal pathogens have evolved sophisticated mechanisms to sense the plant surface and initiate infection-related development that promotes infection, penetration and invasive growth (Eynck et al, 2007; Vallad and Subbarao, 2008; Yadeta et al, 2011; Zhang et al, 2013; Zhao P et al, 2014)
Identification of cellophane surface-induced gene, VdCSIN1, which contributes to V. dahliae virulence in cotton plants
To identify V. dahliae components involved in the regulation of initial recognition and surface perception, a number of genes induced by the artificial surface cellophane were individually deleted in the V. dahliae V592 strain and subjected to virulence assessment in its host plants
Summary
Fungal pathogens have evolved sophisticated mechanisms to sense the plant surface and initiate infection-related development that promotes infection, penetration and invasive growth (Eynck et al, 2007; Vallad and Subbarao, 2008; Yadeta et al, 2011; Zhang et al, 2013; Zhao P et al, 2014). Many fungal pathogens develop infection structures, such as appressoria or hyphopodia, to penetrate plant cells. Magnaporthe oryzae employs G-protein-coupled receptors (GPCRs) and cyclic adenosine monophosphate-protein kinase A (cAMP-PKA)-mediated signalling pathways to regulate surface perception and appressorium formation (DeZwaan et al, 1999; Kronstad et al, 2011; Li et al, 2012). Appressorium formation in M. oryzae is regulated by the conserved mitogen-activated protein kinase (MAPK) pathway (Jin et al, 2013; Li et al, 2012; Zhao X et al, 2007). Both the GPCR Pth (Kou et al, 2017) and the putative extracellular chitin-binding protein CBP1 (Kamakura et al, 2002) serve as receptors for the perception of surface signals to induce appressorium formation
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