Abstract

Mitochondria play key roles in cellular energy generation and lifespan of most eukaryotes. To understand the functions of four nuclear-encoded genes predicted to be related to the maintenance of mitochondrial morphology and function in Aspergillus nidulans, systematic characterization was carried out. The deletion and overexpression mutants of aodA, dnmA, mnSOD and pimA encoding alternative oxidase, dynamin related protein, manganese superoxide dismutase and Lon protease, respectively, were generated and examined for their growth, stress tolerances, respiration, autolysis, cell death, sterigmatocystin production, hyphal morphology and size, and mitochondrial superoxide production as well as development. Overall, genetic manipulation of these genes had less effect on cellular physiology and ageing in A. nidulans than that of their homologs in another fungus Podospora anserina with a well-characterized senescence. The observed interspecial phenotypic differences can be explained by the dissimilar intrinsic stabilities of the mitochondrial genomes in A. nidulans and P. anserina. Furthermore, the marginally altered phenotypes observed in A. nidulans mutants indicate the presence of effective compensatory mechanisms for the complex networks of mitochondrial defense and quality control. Importantly, these findings can be useful for developing novel platforms for heterologous protein production, or on new biocontrol and bioremediation technologies based on Aspergillus species.

Highlights

  • Fungal ageing and longevity are highly dependent on mitochondrial integrity and functions in both the yeast Saccharomyces cerevisiae and the filamentous fungus Podospora anserina[1,2,3,4]

  • A series of A. nidulans mutants were generated through the deletion and overexpression of nuclear-encoded genes that were shown to be directly involved in the maintenance of the integrity and function of mitochondria in other fungi, and a number of key physiological, morphological and developmental phenotypes of the mutants were analyzed

  • Fungal growth and stress sensitivities were hardly affected by the deletions and overexpressions of the mitochondrial function and morphology related genes and the phenotypic changes were rather sporadic (Fig. 1 and Supplementary Fig. S1)

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Summary

Introduction

Fungal ageing and longevity are highly dependent on mitochondrial integrity and functions in both the yeast Saccharomyces cerevisiae and the filamentous fungus Podospora anserina[1,2,3,4]. ROS are eliminated by an arsenal of antioxidative enzymes in fungal cells including superoxide dismutases, which convert superoxide to H2O2 These enzymes affect the mitochondrial ROS levels, mitochondrial stability, subsequent ageing and lifespan beneficially[12,13] the www.nature.com/scientificreports/. Overexpression of manganese superoxide dismutase encoded by PaSod[3] unexpectedly led to a reduced lifespan in P. anserina, and the deletion of the same gene increased the paraquat sensitivity but did not affect the peroxide tolerance and the lifespan of the fungus[14] These data warn us that the roles of ROS in lifespan and ageing may be controversial under certain conditions[4,14,15]. Overexpression of PaDnm[1] increased disintegration of mitochondria even in young cultures[18]

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