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Verticillium dahliae is a soil-borne pathogen that causes vascular wilts in a wide variety of agronomically important crops worldwide. The lack of host specificity and the systemic nature of the infection pose a challenge for the control of this pathogen. Furthermore, V. dahliae produces resistant structures, the microsclerotia, that can remain viable in the soil for long periods of time and are the main source of inoculum for new infections. In this work, using a forward genetic approach and targeted gene deletion we have identified Vmg1, a putative ortholog of the Mediator Complex protein Med15, as a major regulator of morphogenesis and essential for pathogenicity in V. dahliae . Mutants deleted for vmg1 do not sporulate, produce microsclerotia with an aberrant structure, show reduced aerial mycelium formation, and do not induce any Verticillium wilt symptoms. They also exhibit impaired glucose metabolism and altered stress responses. The developmental defects observed in Δ vmg1 strains are consistent with their inability to undergo processes that require cell budding. In planta analyses using confocal and scanning electron microscopy show that the Δ vmg1 strain goes through the prevascular phase of the infection but remains trapped outside the xylem vessels in the vascular tissue. We propose that as previously shown for the well-characterized Saccharomyces cerevisiae Med15 protein, Vmg1 is a major interaction hub of multiple signaling pathways in V. dahliae . Hence, Vmg1 activity integrates the regulation of developmental processes, stress responses, metabolism and other functions required for V. dahliae to cause disease and successfully complete its life cycle.
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Sarmiento-Villamil et al. (2026) studied this question.
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