Cellular Respiration Defect Makes Sac Fungi Infertile


Sordaria macrospora is a model system for studying the development of fruiting bodies in sac fungi, called filamentous ascomycetes. Using conventional mutagenesis, over 100 developmental mutants were generated for this fungus in the 1990s.

Assistant Professor Dr. Ines Teichert from the General and Molecular Botany Group of the Department of Biology and Biotechnology at Ruhr University in Bochum, Germany, in cooperation with Dr. Andrea Hamann and Professor Heinz D. Osiewacz from the Goethe University Frankfurt, studied such a mutant: unlike the wild-type strain, the so-called pro34 mutant does not form mature fruiting bodies and sexual spores, and additionally has a slower growth rate. Using genome sequencing, the researchers identified a major gap in a gene, which they named pro34. In the wild-type strain, this gene is affected by RNA editing during fruiting body formation; this means that a new variant of RNA and protein is generated at this stage, which may have a specific function.

Compensation of a fault consumes energy

But what is the function of PRO34 in the first place? “Thanks to fluorescence microscopy, we succeeded in localizing PRO34 in the mitochondria,” explains Ines Teichert. These cell organelles contain the respiratory chain, a series of protein complexes that, to put it simply, help generate energy in the form of adenosine triphosphate (ATP). In the mutant, one of these complexes is missing. The mutant is nonetheless viable; indeed, fungi as well as plants have various alternative pathways in the mitochondrial respiratory chain to compensate for these defects. “However, this compensation is insufficient to cover the high energy demand during the formation of the fruiting body, and thus the mutant remains sterile”, explains Ines Teichert.

A surprising finding was that the so-called alternative oxidase (AOX) is also activated in the pro34 mutant. “According to previous findings, AOX generally compensates for other defects and must therefore perform additional functions”, specifies Ines Teichert. The authors speculate on a protective function of AOX against oxidative stress, since a defect in the mitochondrial respiratory chain leads to an increased formation of oxygenated radicals. “An explanation could also be that AOX helps in the assembly of certain mitochondrial complexes,” the authors believe. “Therefore, the pro34 mutant is an excellent starting point for further analyses.”

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Materials provided by Ruhr-University of Bochum. Original written by Meike Drießen. Note: Content may be edited for style and length.


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