Difference between revisions of "Hamann 2022 J Fungi (Basel)"

Latest revision as of 12:28, 22 November 2022

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 • O2k-Network Lab: DE Frankfurt Osiewacz HD

Labels: MiParea: Respiration, Developmental biology

Organism: Fungi

Preparation: Intact cells Enzyme: Complex I

Pathway: CIV HRR: Oxygraph-2k

2022-11

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 {{Publication
-|title=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
+|title=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
 |info=J Fungi (Basel) 8:1015. [https://pubmed.ncbi.nlm.nih.gov/36294581 PMID: 36294581 Open Access]
 |authors=Hamann Andrea, Osiewacz Heinz D, Teichert Ines
 |year=2022
 |journal=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.
+|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
 |editor=[[Plangger M]]
+|mipnetlab=DE Frankfurt Osiewacz HD
 }}
 {{Labeling
-|area=Respiration
+|area=Respiration, Developmental biology
+|organism=Fungi
+|preparations=Intact cells
+|enzymes=Complex I
+|pathways=CIV
 |instruments=Oxygraph-2k
 |additional=2022-11
 }}