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.
Sorghum ( Sorghum bicolor L.) is a globally important crop used for food, fodder, and biofuel production; however, its productivity is severely constrained by insect pests such as sugarcane aphid (SCA). Previous studies have shown that loss of LIGULELESS1 ( LG1 ) function activates jasmonate signaling and enhances maize resistance to corn leaf aphids. Here, we investigated the role of LG1 in sorghum defense against SCA. Aphid no-choice bioassays revealed that loss of LG1 significantly reduced aphid settling and reproduction. EPG analysis further revealed that lg1 mutant significantly increased aphid probing/pathway phase while reducing sieve element phase duration, suggesting impaired phloem feeding and altered aphid feeding behavior on lg1 plants. Gene expression analysis using RT-qPCR showed that SCA feeding suppressed key jasmonic acid (JA) signaling genes in lg1 plants, while hormone profiling revealed enhanced salicylic acid (SA) accumulation and altered JA and abscisic acid responses in lg1 plants following infestation. Notably, this shift is consistent with the well-established antagonistic crosstalk between JA and SA pathways, where activation of SA signaling often suppresses JA-mediated responses. Growth-associated hormones were also differentially affected by SCA feeding. Together, these results demonstrate that LG1 modulates hormone-dependent defense responses in sorghum and represents a promising target for improving resistance to aphid pests.
The bacterial plant pathogen Pseudomonas syringae uses a type III secretion system (T3SS) to translocate, or inject, type III effector (T3E) proteins into plant cells. The T3SS is required for pathogenicity. For T3Es to be translocated, P. syringae must create an opening in the plant plasma membrane, using a group of proteins known as a translocon, through which the T3E proteins can be delivered. The translocon is composed of membrane proteins called translocators that span the plant plasma membrane. HrpK1 exhibits many of the characteristics of a translocator, including being a type III-secreted protein, possessing a transmembrane domain, and being crucial for pathogenicity. Most importantly, hrpK1 mutants are secretion competent but defective in T3E translocation. Here, we confirm that HrpK1 can act as a translocator for multiple T3Es and find that it interacts with liposomes, consistent with the properties of other established translocators. HrpK1 is more important to T3E translocation than other P. syringae proteins known as harpins, which have been implicated in translocation. Both HrpK1 and HrpZ1, one of the harpins, interact with phosphatidic acid, and when infiltrated into the apoplast, this compound can block T3E translocation in a HrpK1 and HrpZ1-specific manner. In contrast, injection of phospholipase D, an enzyme that increases phosphatidic acid in the membrane, allowed for increased T3E translocation. These experiments support that HrpK1 is a primary translocator for the P. syringae T3SS and that it may function by binding phospholipids in the plant plasma membrane.
Hemibiotrophic fungi of the genus Colletotrichum provide valuable systems for studying plant immunity and pathogen lifestyle transitions; however, compatible and incompatible interactions have rarely been compared within the same host species. Here, we show that Arabidopsis thaliana exhibits contrasting responses to two phylogenetically distinct hemibiotrophic fungi, Colletotrichum coccodes KACC40803 and Colletotrichum scovillei KC05. Multilocus phylogenetic analyses using ITS, ACT, GAPDH, and TUB2 sequences confirmed their taxonomic identities. The two fungi also differed morphologically, particularly in colony characteristics and appressorial structures. Inoculation of Arabidopsis leaves with C. coccodes caused progressive chlorosis, necrotic lesions, extensive fungal colonization, acervulus formation, and increasing fungal biomass, indicating a compatible susceptible interaction. Host defense-related genes associated with salicylic acid– and jasmonic acid–mediated pathways were suppressed during infection. By contrast, C. scovillei induced restricted lesion development, rapid accumulation of callose and reactive oxygen species, localized plasma membrane disruption, and strong induction of defense-related genes in Arabidopsis leaves, consistent with an incompatible hypersensitive response (HR)–like cell death. Fungal biomass remained low throughout infection, demonstrating effective restriction of colonization. Together, these findings establish a dual Arabidopsis–Colletotrichum pathosystem that enables comparative analysis of susceptibility and HR-like resistance within a single host, providing a tractable model for dissecting host specificity, immune signaling, and regulated cell death during hemibiotrophic infection. [Figure: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
