AUTHOR=Dang Yuejia , Wei Yi , Batool Wajjiha , Sun Xicen , Li Xiaoqian , Zhang Shi-Hong 

TITLE=Contribution of the Mitochondrial Carbonic Anhydrase (MoCA1) to Conidiogenesis and Pathogenesis in Magnaporthe oryzae

JOURNAL=Frontiers in Microbiology

VOLUME=13

YEAR=2022

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2022.845570

DOI=10.3389/fmicb.2022.845570

ISSN=1664-302X

ABSTRACT=<p>The interconversion of CO<sub>2</sub> and HCO<sub>3</sub><sup>−</sup> catalyzed by carbonic anhydrases (CAs) is a fundamental biochemical process in organisms. During mammalian–pathogen interaction, both host and pathogen CAs play vital roles in resistance and pathogenesis; during planta–pathogen interaction, however, plant CAs function in host resistance but whether pathogen CAs are involved in pathogenesis is unknown. Here, we biologically characterized the <italic>Magnaporthe oryzae</italic> CA (MoCA1). Through detecting the DsRED-tagged proteins, we observed the fusion MoCA1 in the mitochondria of <italic>M. oryzae</italic>. Together with the measurement of CA activity, we confirmed that MoCA1 is a mitochondrial zinc-binding <italic>CA</italic>. <italic>MoCA1</italic> expression, upregulated with H<sub>2</sub>O<sub>2</sub> or NaHCO<sub>3</sub> treatment, also showed a drastic upregulation during conidiogenesis and pathogenesis. When <italic>MoCA1</italic> was deleted, the mutant Δ<italic>MoCA1</italic> was defective in conidiophore development and pathogenicity. 3,3′-Diaminobenzidine (DAB) staining indicated that more H<sub>2</sub>O<sub>2</sub> accumulated in Δ<italic>MoCA1</italic>; accordingly, <italic>ATPase</italic> genes were downregulated and ATP content decreased in Δ<italic>MoCA1</italic>. Summarily, our data proved the involvement of the mitochondrial <italic>MoCA1</italic> in conidiogenesis and pathogenesis in the rice blast fungus. Considering the previously reported HCO<sub>3</sub><sup>−</sup> transporter MoAE4, we propose that <italic>MoCA1</italic> in cooperation with <italic>MoAE4</italic> constitutes a HCO<sub>3</sub><sup>−</sup> homeostasis-mediated disease pathway, in which <italic>MoCA1</italic> and <italic>MoAE4</italic> can be a drug target for disease control.</p>