The mitochondrial translocase of the inner membrane PaTim54 is involved in defense response and longevity in Podospora anserina
Autor: | Philippe Silar, Sylvain Brun, Alex Mercier, David Morais, Robert Debuchy, Colin Clairet |
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Přispěvatelé: | Laboratoire Interdisciplinaire des Energies de Demain (LIED (UMR_8236)), Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Intégrative de la Cellule (I2BC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Meiotic Recombination and Pairing (MRP), Département Biologie des Génomes (DBG), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Intégrative de la Cellule (I2BC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Universite Paris-Diderot intramural funding, BIOlogie et GEstion des Risques en agriculture (BIOGER), AgroParisTech-Institut National de la Recherche Agronomique (INRA), Différenciation sexuée et méiose chez les champignons (DSMC), Institut de génétique et microbiologie [Orsay] (IGM), Université Paris-Sud - Paris 11 (UP11)-Centre National de la Recherche Scientifique (CNRS) |
Rok vydání: | 2019 |
Předmět: |
Aging
Programmed cell death Hypha [SDV]Life Sciences [q-bio] Mutant Hyphae Mitochondrion Mitochondrial Membrane Transport Proteins Microbiology Podospora anserina Fungal Proteins Tim54 03 medical and health sciences Podospora Antibiosis Genetics Inner mitochondrial membrane 030304 developmental biology 0303 health sciences biology 030306 microbiology Fungi Hyphal Interference Hydrogen Peroxide biology.organism_classification Penicillium chrysogenum Mitochondria Cell biology Oxidative Stress Phenotype Mitochondrial Membranes Mutation Translocase of the inner membrane |
Zdroj: | Fungal Genetics and Biology Fungal Genetics and Biology, 2019, 132 (103257), pp.103257. ⟨10.1016/j.fgb.2019.103257⟩ Fungal Genetics and Biology, Elsevier, 2019, 132, pp.103257. ⟨10.1016/j.fgb.2019.103257⟩ Fungal Genetics and Biology, Elsevier, 2019, 132 (103257), pp.103257. ⟨10.1016/j.fgb.2019.103257⟩ |
ISSN: | 1087-1845 1096-0937 |
DOI: | 10.1016/j.fgb.2019.103257 |
Popis: | International audience; Fungi are very successful microorganisms capable of colonizing virtually any ecological niche where they must constantly cope with competitors including fungi, bacteria and nematodes. We have shown previously that the ascomycete Podopora anserina exhibits Hyphal Interference (HI), an antagonistic response triggered by direct contact of competing fungal hyphae. When challenged with Penicillium chrysogenum, P. anserina produces hydrogen peroxide at the confrontation and kills the hyphae of P. chrysogenum. Here, we report the characterization of the PDC2218 mutant affected in HI. When challenged with P. chrysogenum, the PDC2218 mutant produces a massive oxidative burst at the confrontation. However, this increased production of hydrogen peroxide is not correlated to increased cell death in P. chrysogenum. Hence, the oxidative burst and cell death in the challenger are uncoupled in PDC2218. The gene affected in PDC2218 is PaTim54, encoding the homologue of the budding yeast mitochondrial inner membrane import machinery component Tim54p. We show that PaTim54 is essential in P. anserina and that the phenotypes displayed by the PDC2218 mutant, renamed PaTim542218, are the consequence of a drastic reduction in the expression of PaTim54. Among these pleiotropic phenotypes, PDC2218-PaTim542218- displays increased lifespan, a phenotype in line with the observed mitochondrial defects in the mutant. |
Databáze: | OpenAIRE |
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