title: Cellular homeostasis in fungi: impact on the aging process.
abstract: Cellular quality control pathways are needed for maintaining the biological function of organisms. If these pathways become compromised, the results are usually highly detrimental. Functional impairments of cell components can lead to diseases and in extreme cases to organismal death. Dysfunction of cells can be induced by a number of toxic by-products that are formed during metabolic activity, like reactive oxygen and nitrogen species, for example. A key source of reactive oxygen species (ROS) are the organelles of oxidative phosphorylation, mitochondria. Therefore mitochondrial function is also directly affected by ROS, especially if there is a compromised ROS-scavenging capacity. Biological systems therefore depend on several lines of defence to counteract the toxic effects of ROS and other damaging agents. The first level is active at the molecular level and consists of various proteases that bind and degrade abnormally modified and / or aggregated mitochondrial proteins. The second level is concerned with maintaining the quality of whole mitochondria. Among the pathways of this level are mitochondrial dynamics and autophagy (mitophagy). Mitochondrial dynamics describes the time-dependent fusion and fission of mitochondria. It is argued that this kind of organellar dynamics has the power to restore the function of impaired organelles by content mixing with intact organelles. If the first and second lines of defence against damage fail and mitochondria become damaged too severely, there is the option to remove affected cells before they can elicit more damage to their surrounding environment by apoptosis. This form of programmed cell death is strictly regulated by a complex network of interacting components and can be divided into mitochondria-dependent and mitochondria-independent modes of action. In this review we give an overview on various biological quality control systems in fungi (yeasts and filamentous fungi) with an emphasis on autophagy (mitophagy) and apoptosis and how these pathways allow fungal organisms to maintain a balanced cellular homeostasis.
authors.affiliation: Faculty of Biosciences, Institute of Molecular Biosciences and Cluster of Excellence Macromolecular Complexes, Johann Wolfgang Goethe University, 60438, Frankfurt/Main, Germany, c.scheckhuber@googlemail.com.
authors.forename: Christian Q
authors.initials: CQ
authors.lastname: Scheckhuber
authors.forename: Andrea
authors.initials: A
authors.lastname: Hamann
authors.forename: Diana
authors.initials: D
authors.lastname: Brust
authors.forename: Heinz D
authors.initials: HD
authors.lastname: Osiewacz
mesh_terms: D000375:Aging / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D017209:Apoptosis; D001343:Autophagy; D020169:Caspases / Q000235:genetics / Q000378:metabolism; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism; D005658:Fungi / Q000235:genetics / Q000254:growth & development / Q000378:metabolism*; D006706:Homeostasis; D008136:Longevity; D050296:Microbial Viability; D063306:Mitophagy; D015398:Signal Transduction; D013997:Time Factors
chemical_list: D005656:Fungal Proteins; D020169:Caspases