Abstract

In eukaryotes, protein phosphatases play a vital role in the control of different cellular activities. Colletotrichum gloeosporioides, an ascomycete, is the cause of anthracnose disease in a number of key crops and plants. CgPPZ1, a protein phosphate gene and a homolog of yeast PPZ1, was discovered in C. gloeosporioides in this investigation. CgPpz1 was found to be critical for vegetative growth and asexual development, conidial germination, and plant infection after targeted gene deletion. CgPpz1 was found to be located in the cytoplasm during cytological tests. Osmotic stresses, cell wall stressors, and oxidative stressors were all hypersensitive in the Cgppz1 mutant. Our findings suggest that CgPpz1 is involved in the fungal development and pathogenicity of C. gloeosporioides, as well as the numerous stress responses that occur [1].

Xanthomonas perforans is a seedborne hemibiotrophic pathogen that infects the tomato phyllosphere. While most investigations on the molecular basis of pathogenesis have focused on apoplastic expansion, variables relevant during asymptomatic colonisation in the early stages of disease development are little known. The tssM gene of the type VI secretion system cluster i3* (T6SS-i3*) plays an important role during initial asymptomatic epiphytic colonisation at various phases during the pathogen's life cycle, according to this study. When dip inoculating 4- to 5-week-old tomato plants, a mutation in a key gene, tssM of T6SS-i3*, conferred stronger pathogen aggressiveness, as seen by higher overall disease severity, higher in planta growth, and shorter latent infection period compared to the wild-type [2]. The role of tssM in aggressiveness was demonstrated during vertical transmission from seed to seedling, with wild-type seedlings demonstrating lower disease severity and in planta populations on seedlings than mutants. When examined in an experimental system that mimicked transplant house high-humidity conditions, the presence of functioning TssM resulted in enhanced epiphytic fitness as well as greater pathogen dissemination potential. We discovered that one mechanism by which TssM promotes epiphytic fitness is through increased osmotolerance. These findings suggest that a functional TssM plays a significant role in the pathogen's ability to gain an ecological advantage. TssM prolongs the hemibiotrophic pathogen's relationship with the host, reducing disease severity while allowing successful diffusion