Abstract

Rice blast, known as rice “cancer”, is caused by Magnaporthe oryzae and is particularly serious in Asian and African rice regions. China is also a frequently occurring region of rice blast. Rice blast not only seriously threatens the yield and quality of rice but also affects food security in China. In M. oryzae, the Mst11-Mst7-Pmk1 MAPK signaling pathway mediates pathogenicity by regulating the formation of appressorium and the development of infection hyphae. Stomatal cytokinesis defective 2 (Scd2, also called Ral3 or Bem1) is a component of the Scd complex, which has been proven to be closely related to the MAPK signaling pathway. However, its biological roles in M. oryzae remain elusive. Here, we identified MoScd2, a homologous protein of Schizosaccharomyces pombe Scd2, and preliminarily revealed its role in the development of rice blast fungus. We found that MoScd2 was involved in colony growth, sporulation, spore morphology, spore germination, appressorium formation, turgor in appressoria, mobilization of glycogen from spores to appressoria and pathogenicity. The deletion of MoScd2 resulted in a reduction in Pmk1 and Mps1 phosphorylation levels. In addition, MoScd2 was confirmed to interact with MoMst50, which is a key component of the MAPK signaling pathway in M. oryzae. In summary, MoScd2 was involved in the MAPK signaling pathway of M. oryzae via interaction with MoMst50 to participate in the influence of pathogenicity. In addition, MoScd2 also influences M. oryzae pathogenicity by participating in autophagy.

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