Abstract

SummaryMetabolic switching and rewiring play a dynamic role in programmed cell differentiation. Many pathogenic microbes need to survive in nutrient-deficient conditions and use the glyoxylate cycle, an anaplerotic pathway of the tricarboxylic acid cycle, to produce carbohydrates. The plant pathogenic fungus Magnaporthe oryzae (Pyricularia oryzae) has a unique chitin deacetylase, Cbp1. The spatiotemporal activity of this protein is required for modification of the M. oryzae wall and for cell differentiation into the specialized infection structure (appressorium). Here we show that acetic acid, another product released by the Cbp1-catalyzed conversion of chitin into chitosan, induces appressorium formation. An extremely low concentration (fM) of acetic acid restored cell differentiation in a Δcbp1 mutant possibly through the glyoxylate cycle.

Highlights

  • All living organisms and their individual cells must respond and adapt to various environmental changes

  • Many pathogenic microbes need to survive in nutrient-deficient conditions and use the glyoxylate cycle, an anaplerotic pathway of the tricarboxylic acid cycle, to produce carbohydrates

  • We focused on acetic acid, which is another product released by the Cbp1-catalyzed conversion of chitin into chitosan, as a candidate for the upstream factor of signal transduction for infection-specific cell differentiation

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Summary

Introduction

All living organisms and their individual cells must respond and adapt to various environmental changes. The glyoxylate cycle is an anaplerotic pathway of the tricarboxylic acid (TCA) cycle and has a unique two-step metabolic bypass pathway using isocitrate lyase (Icl) and malate synthase (Mls) (Figure S1). Succinate is used in gluconeogenesis via the TCA cycle This bypass is reported to be essential for the virulence of many pathogenic microbes (Lorenz and Fink, 2001; McKinney et al, 2000; Idnurm and Howlett, 2002; Wang et al, 2003; Dunn et al, 2009). Metabolic switching in nutrient-deficient environments is dependent on changes in the nutrient source (Nakatsukasa et al, 2015), but its mechanism remains poorly understood

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