|WEI, WEI - Huazhong Agricultural University|
|ZHU, WENJUN - Huazhong Agricultural University|
|CHENG, JIASEN - Huazhong Agricultural University|
|XIE, JIATAO - Huazhong Agricultural University|
|JIANG, DAOHONG - Huazhong Agricultural University|
|LI, GUOQING - Huazhong Agricultural University|
|FU, YANPING - Huazhong Agricultural University|
Submitted to: Scientific Reports
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/24/2016
Publication Date: 4/12/2016
Citation: Wei, W., Zhu, W., Cheng, J., Xie, J., Jiang, D., Li, G., Chen, W., Fu, Y. 2016. Nox Complex signal and MAPK cascade pathway are cross-linked and essential for pathogenicity and conidiation of mycoparasite Coniothyrium minitans. Scientific Reports. 6:24325.
Interpretive Summary: Sclerotinia sclerotiorum is a devastating pathogen of many economically important crops such as cool season legumes. Management of Sclerotinia diseases is difficulty because of persistence of the pathogen in soil and lack of adequately resistant cultivars. Biological control using the mycoparasite Coniothyrium minitans is a promising option in integrated management of Sclerotinia diseases. C. minitans produces conidia for spreading and initiating infection and parasitization of Sclerotinia sclerotiorum. However, the molecular mechanisms of conidia production and mycoparasitism of C. minitans are not well understood. This study was aimed at understanding the role of NADPH oxidase (NOX) which generates reactive oxygen species in conidiation and parasitism. It was demonstrated that Nox complex signal and MAPK cascade pathway are cross-linked and essential for pathogenicity and the production of conidia of C. minitans. These findings will help understand and eventually improve efficacy of C. minitans in managing Sclerotinia diseases.
Technical Abstract: The NADPH oxidase complex of a sclerotial mycoparasite Coniothyrium minitans, an important biocontrol agent against crop diseases caused by Sclerotinia sclerotiorum, was identified and its functions involved in conidiation and mycoparasitism were studied. Gene knock-out and complementation experiments indicated that CmNox1, but not CmNox2, is necessary for conidiation and parasitism, and its expression could be significantly induced by its host. CmNox1 is regulated by CmRac1 which interacts with CmNoxR and interacts with CmSlt2, a homolog of Saccharomyces cerevisiae Slt2 encoding cell wall integrity-related MAP kinase. In 'CmNox1, CmSlt2-GFP fusion protein lost the ability to localize to the cell nucleus accurately. The defect of conidiation in 'CmRac1 could be partially restored by over-expressing CmSlt2, indicating that the CmSlt2 was a downstream regulatory factor of CmNox1 and was involved in conidiation and parasitism. The expressions of mycoparasitism-related genes CmPks1, Cmg1 and CH1 were all suppressed in the knock-out mutants of the genes in CmNox1-CmSlt2 signal pathway when cultivated either on PDA or on sclerotia. Therefore, our study infers that CmRac1-CmNoxR regulates CmNox1-CmSlt2 pathway in regulating conidiation and pathogenicity of C. minitans.