Figure - available from: Frontiers in Plant Science
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Vegetative growth and conidiation of M. oryzae strains in CM medium. (A) Colony morphology on CM plates for 6 days at 28°C with 12 h light and dark alternation. (B) Development of conidia on conidiophores on CM. (C) Statistical analysis of the vegetative growth rate of the tested strain on CM plates. (D) Statistical analysis of the number of conidia on CM plates. Asterisks in each data column indicate significant differences at p < 0.05.
Source publication
The rice blast disease, caused by the fungus Magnaporthe oryzae, is a significant agricultural problem that adversely impacts rice production and food security. Understanding the precise molecular pathways involved in the interaction between the pathogen and its host is crucial for developing effective disease management strategies. This study exam...
Citations
... Once inside the plant, the fungus rapidly expands and grows as hyphae within the plant tissues spreading from plant cell to plant cell, resulting in the formation of necrotic lesions in 3 to 5 days [6]. On the surface of these lesions, the fungus produces new conidia, which can lead to secondary infections on the same plant or spread to adjacent plants [7]. This cycle continues as conidia are released into the environment, particularly in wet conditions, further promoting the spread of the disease over larger areas [8]. ...
Unique genes refer to genes specific to a particular organism and play crucial roles in the biological functions, evolutionary processes, and adaptations to external environments. However, the roles of unique genes in plant pathogenic fungi remain largely unexplored. In this study, we identified a novel unique gene in the rice blast fungus Magnaporthe oryzae, named MoUNG (M. oryzae unique gene), through T-DNA insertion mutagenesis. The disruption of the MoUNG promoter region in the T-DNA insertion mutant (T30-104) led to an almost loss of MoUNG expression. MoUNG has no functional domains and lacks homologues in other organism. It is highly expressed during the early-infection stage between 16 and 32 h post-inoculation (HPI), in contrast to its expression in mycelia and at the later infection stage of 48 HPI. Notably, attempts to knock out MoUNG were unsuccessful, so we examined the T30-104 mutant and found it showed significantly reduced growth, conidiation, and pathogenicity. Introducing the full-length MoUNG with its promoter into T30-104 restored these phenotypic defects. Additionally, subcellular localization assays revealed that MoUNG exhibits a dot-like distribution within the cytoplasm of mycelium, conidium, appressorium, and invasive hypha. Furthermore, knock-down of MoUNG produced results similar to those observed with the insertion mutation. In conclusion, we identified a novel unique gene MoUNG in M. oryzae and demonstrated its involvement in growth, conidiation, and pathogenicity.
