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Deng, Y. Z.

Publications and source records attributed to Deng, Y. Z..

2 recordsLinked to original sources

Fungal auxin is a quorum-based modulator of blast disease severity

Auxin is an important phytohormone regulating plant growth and development, and can also be produced by microbial pathogens including the rice-blast fungus Magnaporthe oryzae. However, the detailed biosynthesis pathway, biological function(s), and cellular distribution of such fungal auxin in M. oryzae remain largely unknown. Here, we report a sequential accumulation of intrinsic auxin in the three conidial cells, the infection structure (appressorium), and the invasive hyphae in M. oryzae. Such fungus-derived auxin was also secreted out and perceived by the host plants. A mitochondria-associated Indole-3-pyruvate decarboxylase, Ipd1, is essential for auxin/Indole-3-acetic acid biosynthesis in M. oryzae. The ipd1{Delta} was defective in pathogenicity whereas overexpression of IPD1 led to enhanced virulence in rice. Chemical inhibition of fungal IAA biosynthesis, or its increase via external supplementation decreased or increased the severity of blast disease, respectively, in a dose-dependent manner. Furthermore, the IAA produced and secreted by M. oryzae governed the incidence and severity of blast disease in a quorum-dependent manner. Appressorium formation, conidial cell death critical for appressorium function, and the transcription of infection-related genes, MPG1 and INV1, directly correlated with cell density and/or IAA levels within the conidial population at the early stages of pathogenic development. Overall, our study revealed that the severity of blast disease is regulated via quorum sensing with intrinsic IAA serving as an associated signal transducer in rice blast.

microbiology↗

Ferroptosis contributes to developmental cell death in rice blast

We identified that ferroptosis, an iron-dependent non-apoptotic cell death process, occurs in the rice blast fungus Magnaporthe oryzae, and plays a key role in infection-related development therein. Ferroptosis in the blast fungus was confirmed based on the four basic criteria. We confirmed the dependence of ferroptosis on ferric ions, and optimized C11-BODIPY581/591 as a key sensor for subcellular detection and quantification of lipid peroxides that mediate ferroptotic cell death during the pathogenic growth phase of M. oryzae. In addition, we uncovered an important regulatory function for reduced glutathione and the NADPH oxidases in generating/modulating the superoxide moieties for ferroptotic cell death in Magnaporthe. Ferroptosis was found to be necessary for the specific developmental cell death in conidia during appressorium maturation in rice blast. Such ferroptotic cell death initiated first in the terminal cell and progressed sequentially to the entire conidium. Chelation of iron or chemical inhibition of ferroptosis caused conidial cells to remain viable and led to strong defects in host invasion by M. oryzae. Precocious induction of ferroptosis in a blast-susceptible rice cultivar led to resistance against M. oryzae invasion. Interestingly, ferroptosis and autophagy were found to play inter-reliant or codependent roles in contributing to such precise cell death in M. oryzae conidia during pathogenic differentiation. Our study provides significant molecular insights into understanding the role of developmental cell death and iron homeostasis in infection-associated morphogenesis and in fungus-plant interaction in the blast pathosystem.

cell biology↗