MoNOT3 Subunit Has Important Roles in Infection-Related Development and Stress Responses in Magnaporthe oryzae

Author:

Kim Youngmin12,Jo Miju13,An Sunmin13,Lee Yerim1,Choi Eu Ddeum1,Jeong Min-Hye1ORCID,Kim Ki-Tae1ORCID,Park Sook-Young1ORCID

Affiliation:

1. Department of Plant Medicine, Sunchon National University, Suncheon 57922, Republic of Korea

2. Fruit Research Institute, Jellanamdo Agricultural Research and Extension Servieces, Haenam 59021, Republic of Korea

3. Interdisciplinary Program in IT-Bio Convergence System (BK21 Plus), Sunchon National University, Suncheon 57922, Republic of Korea

Abstract

The multifunctional carbon catabolite repression negative on TATA-box-less complex (CCR4-NOT) is a multi-subunit complex present in all eukaryotes, including fungi. This complex plays an essential role in gene expression; however, a functional study of the CCR4-NOT complex in the rice blast fungus Magnaporthe oryzae has not been conducted. Seven genes encoding the putative CCR4-NOT complex were identified in the M. oryzae genome. Among these, a homologous gene, MoNOT3, was overexpressed during appressorium development in a previous study. Deletion of MoNOT3 in M. oryzae resulted in a significant reduction in hyphal growth, conidiation, abnormal septation in conidia, conidial germination, and appressorium formation compared to the wild-type. Transcriptional analyses suggest that the MoNOT3 gene affects conidiation and conidial morphology by regulating COS1 and COM1 in M. oryzae. Furthermore, Δmonot3 exhibited a lack of pathogenicity, both with and without wounding, which is attributable to deficiencies in the development of invasive growth in planta. This result was also observed in onion epidermal cells, which are non-host plants. In addition, the MoNOT3 gene was involved in cell wall stress responses and heat shock. Taken together, these observations suggest that the MoNOT3 gene is required for fungal infection-related cell development and stress responses in M. oryzae.

Funder

Sunchon National University Research Fund

Publisher

MDPI AG

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