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    Home > Biochemistry News > Biotechnology News > Defects in cellular respiration lead to cystic infertility

    Defects in cellular respiration lead to cystic infertility

    • Last Update: 2022-11-15
    • Source: Internet
    • Author: User
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    The macrospora Sordaria macrospora is a model system
    for studying the development of fruiting bodies of cystic fungi (Ascomyces filamentous).
    In the 90s of the 20th century, using traditional mutagenesis techniques, this fungus produced more than 100 developmental mutants
    .

    Dr.
    Ines Teichert, assistant professor in the General and Molecular Botany Group at the Department of Biology and Biotechnology at the Ruhr University Bohin, Germany, in collaboration with Dr.
    Andrea Hamann and Prof.
    Heinz D.
    Osiewacz of Goethe University Frankfurt, Germany, have been studying a mutant that, unlike wild-type strains, the so-called pro34 mutant does not form mature fruiting bodies and sex spores and grows slower
    .
    Through genome sequencing, the researchers found a major gap in a gene, which they named Pro34
    .
    In wild-type strains, the gene is affected by RNA editing during fruiting body formation; This means that a new variant of RNA and protein is produced at this time, and it may have a specific function
    .

    Compensating for defects requires energy consumption

    But what exactly is the function of the PRO34?" Using fluorescence microscopy, we successfully localized PRO34 in mitochondria," explains Ines Teichert
    .
    These organelles contain the respiratory chain, a series of protein complexes that, simply, help produce energy
    in the form of adenosine triphosphate (ATP).
    In the mutant, one of the complexes is
    missing.
    The mutant is still alive; This is because fungi, like plants, have various alternative pathways in the mitochondrial respiratory chain to compensate for these deficiencies
    .
    "However, this compensation is not sufficient to cover the high energy demands during fruiting body formation, so the mutant remains sterile," Ines Teichert said
    .

    A surprising finding was that so-called alternative oxidase (AOX) was similarly activated
    in the pro34 mutant.
    Ines Teichert noted: "Based on previous findings, AOX can often compensate for other deficiencies and therefore have to perform additional functions
    .
    " The authors speculate about AOX's protective function against oxidative stress, as defects in the mitochondrial respiratory chain lead to increased
    formation of oxygen free radicals.
    "One explanation may be that AOX contributes to the assembly of certain mitochondrial complexes," the authors argue.

    Therefore, the PRO34 mutant is an excellent starting point
    for subsequent analysis.

    Journal Reference:

    1. Andrea Hamann, Heinz D.
      Osiewacz, Ines Teichert.
      Sordaria macrospora Sterile Mutant pro34 Is Impaired in Respiratory Complex I Assembly.
      Journal of Fungi, 2022; 8 (10): 1015 DOI: 10.
      3390/jof8101015

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