A mutation of a single core gene, tssM, of Type VI secretion system of Xanthomonas perforans influences virulence, epiphytic survival and transmission during pathogenesis on tomato

Xanthomonas perforans is a seed-borne hemi-biotrophic pathogen that successfully establishes infection in the phyllosphere of tomato. While the majority of the studies investigating mechanistic basis of pathogenesis have focused on successful apoplastic growth, factors important during asymptomatic colonization in the early stages of disease development are not well understood. In this study, we show that tssM gene of the type VI secretion system cluster i3* (T6SS-i3*) plays a significant role during initial asymptomatic epiphytic colonization at different stages during the life cycle of the pathogen. Mutation in a core gene, tssM of T6SS-i3*, imparted higher aggressiveness to the pathogen, as indicated by higher overall disease severity, higher in planta growth as well as shorter latent infection period compared to the wild-type upon dip-inoculation of 4-5-week-old tomato plants. Contribution of tssM towards aggressiveness was evident during vertical transmission from seed-to-seedling with wild-type showing reduced disease severity as well as lower in planta populations on seedlings compared to the mutant. Presence of functional TssM offered higher epiphytic fitness as well as higher dissemination potential to the pathogen when tested in an experimental setup mimicking transplant house high-humidity conditions. We showed higher osmotolerance being one mechanism by which TssM offers higher epiphytic fitness. Taken together, these data reveal that functional TssM plays a larger role in offering ecological advantage to the pathogen. TssM prolongs the association of hemi-biotrophic pathogen with the host, minimizing overall disease severity, yet facilitating successful dissemination.

The Plant Salicylic Acid Signalling Pathway Regulates the Infection of a Biotrophic Pathogen in Grasses Associated with an Epichloë Endophyte

The study of the contribution of the plant defence hormones, salicylic acid (SA) and jasmonic acid (JA), in the resistance against pathogens of plants associated with Epichloë fungal endophytes has been scanty. We hypothesised that Epichloë spp., capable of inducing host plant SA-dependent defences, would increase the levels of plant resistance against biotrophic pathogens. Plants of Achnatherum inebrians, with and without the fungal endophyte Epichloë gansuensis, were inoculated with the biotrophic fungal pathogen Blumeria graminis. We measured the status of plant defences (associated with SA and JA signalling pathways) and the levels of resistance to the pathogen. Plants associated with the endophyte showed less disease symptoms caused by the biotrophic pathogen than plants without the endophyte. In agreement with our hypothesis, the Epichloë endophyte increased the plant production of SA and enhanced the expression levels of plant genes of synthesis and response to the SA hormone. The elevated expression of SA-related genes coding for putative plant enzymes with anti-fungal activities promoted by the endophyte may explain the enhanced resistance to the pathogen. The present study highlights that interaction between the plant immune system and Epichloë fungal endophytes can contribute significantly to the resistance of endophyte-symbiotic plants against pathogens.

Transformation of Endophytic Bipolaris spp. Into Biotrophic Pathogen Under Auxin Cross-Talk With Brassinosteroids and Abscisic Acid

Auxin is the reciprocal signaling molecule, which interferes with other phyto-hormonal and physiological processes during plant–microbes interaction. In this regard, Bipolaris spp., a growth-promoting endophytic fungus was used to inoculate pre-stressed Zea mays seedlings with yucasin (IAA inhibitor). The IAA-deficient host was heavily colonized by the endophyte that subsequently promoted the host growth and elevated the IAA levels with a peak value at 72 h. However, the seedling growth was inhibited later (i.e., at 120 h) due to the high levels of IAA that interfered with the activity of phytoalexins and brassinosteroids. Such interference also modulated the endophytic fungus from symbiotic to biotrophic pathogen that left the host plants defenseless.

The hijacking of a receptor kinase–driven pathway by a wheat fungal pathogen leads to disease

Necrotrophic pathogens live and feed on dying tissue, but their interactions with plants are not well understood compared to biotrophic pathogens. The wheatSnn1gene confers susceptibility to strains of the necrotrophic pathogenParastagonospora nodorumthat produce the SnTox1 protein. We report the positional cloning ofSnn1, a member of the wall-associated kinase class of receptors, which are known to drive pathways for biotrophic pathogen resistance. Recognition of SnTox1 bySnn1activates programmed cell death, which allows this necrotroph to gain nutrients and sporulate. These results demonstrate that necrotrophic pathogens such asP. nodorumhijack host molecular pathways that are typically involved in resistance to biotrophic pathogens, revealing the complex nature of susceptibility and resistance in necrotrophic and biotrophic pathogen interactions with plants.