Abstract

N-linked glycosylation is a way of glycosylation for newly synthesized protein, which plays a key role in the maturation and transport of proteins. Glycoside hydrolases (GHs) are essential in this process, and are involved in processing of N-linked glycoproteins or degradation of carbohydrate structures. Here, we identified and characterized MoGls2 in Magnaporthe oryzae, which is a yeast glucosidase II homolog Gls2 and is required for trimming the final glucose in N-linked glycans and normal cell wall synthesis. Target deletion of MoGLS2 in M. oryzae resulted in a reduced mycelial growth, an increased conidial production, delayed conidial germination and loss the ability of sexual reproduction. Pathogenicity assays revealed that the ΔMogls2 mutant showed significantly decreased in virulence and infectious growth. Further studies showed that the mutant was less sensitive to salt and osmotic stress, and increased sensitivity to cell wall stresses. Additionally, the ΔMogls2 mutant showed a defect in cell wall integrity. Our results indicate that MoGls2 is a key protein for the growth and development of M. oryzae, involving in the regulation of asexual/sexual development, stress response, cell wall integrity and infectious growth.

Highlights

  • Rice blast, known as rice fever, is a devastating disease of rice caused by Magnaporthe oryzae, and has occurred in most rice-producing areas worldwide [1]

  • Transcription profile analysis of MoGLS2 during different developmental stages of M. oryzae showed that MoGLS2 was highly expressed during infection but not during conidiation when compared to the mycelial stage

  • The results showed that MoCOS1, MoHOX2 and MoSTUA were significantly up-regulated in the ΔMogls2 mutant (Fig 3C), indicating MoGls2 controls conidiation through negative regulating the expression of MoCOS1, MoHOX2 and MoSTUA in M. oryzae

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Summary

Introduction

Known as rice fever, is a devastating disease of rice caused by Magnaporthe oryzae, and has occurred in most rice-producing areas worldwide [1]. The disease can spread quickly and lead to 10–20% rice yield losses [1,2]. The fungal pathogen initiates infection by attachment of conidia to the plant surface and formed a dome shaped structure called an appressorium at the germ tube tip [3]. The mature appressorium generates huge turgor that forces invasive nail through rice epidermis into the interior of plant cells, causing diseases [4,5]. Identification and characterization of PLOS ONE | DOI:10.1371/journal.pone.0162243. Identification and characterization of PLOS ONE | DOI:10.1371/journal.pone.0162243 September 8, 2016

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