Hamann 2022 J Fungi (Basel)

Hamann A, Osiewacz HD, Teichert I (2022) Sordaria macrospora sterile mutant pro34 is impaired in respiratory complex I assembly. https://doi.org/10.3390/jof8101015

» J Fungi (Basel) 8:1015. PMID: 36294581 Open Access

Hamann Andrea,  Osiewacz Heinz D,  Teichert Ines (2022) J Fungi (Basel)

Abstract: The formation of fruiting bodies is a highly regulated process that requires the coordinated formation of different cell types. By analyzing developmental mutants, many developmental factors have already been identified. Yet, a complete understanding of fruiting body formation is still lacking. In this study, we analyzed developmental mutant pro34 of the filamentous ascomycete Sordaria macrospora. Genome sequencing revealed a deletion in the pro34 gene encoding a putative mitochondrial complex I assembly factor homologous to Neurospora crassa CIA84. We show that PRO34 is required for fast vegetative growth, fruiting body and ascospore formation. The pro34 transcript undergoes adenosine to inosine editing, a process correlated with sexual development in fruiting body-forming ascomycetes. Fluorescence microscopy and western blot analysis showed that PRO34 is a mitochondrial protein, and blue-native PAGE revealed that the pro34 mutant lacks mitochondrial complex I. Inhibitor experiments revealed that pro34 respires via complexes III and IV, but also shows induction of alternative oxidase, a shunt pathway to bypass complexes III and IV. We discuss the hypothesis that alternative oxidase is induced to prevent retrograde electron transport to complex I intermediates, thereby protecting from oxidative stress. • Keywords: RNA editing, Alternative oxidase (AOX), Ascospore formation, Cytochrome c oxidase (COX), Fruiting body formation, Mitochondrial complex I assembly, Mitochondrial respiration • Bioblast editor: Plangger M

Labels: MiParea: Respiration 

HRR: Oxygraph-2k 

2022-11