The mitochondrial localized CISD-3.1/CISD-3.2 proteins are required to maintain normal germline structure and function in Caenorhabditis elegans
| Autor: | Pamela A. Padilla, Ron Mittler, Luhua Song, Chipo F. Gray, Skylar D. King |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Iron-Sulfur Proteins
Embryology Nematoda Physiology Mutant Apoptosis Mitochondrion medicine.disease_cause Biochemistry Germline Animal Cells Medicine and Health Sciences Homeostasis Caenorhabditis elegans Energy-Producing Organelles Mutation Multidisciplinary biology Cell Death Eukaryota Animal Models Cell biology Mitochondria Experimental Organism Systems Cell Processes OVA Medicine Cellular Structures and Organelles Cellular Types Anatomy Genital Anatomy Research Article Programmed cell death Protein family Imaging Techniques Science Bioenergetics Research and Analysis Methods Mitochondrial Proteins Model Organisms Oxygen homeostasis Fluorescence Imaging medicine Animals Gonads Caenorhabditis elegans Proteins Embryos Organisms Reproductive System Biology and Life Sciences Cell Biology biology.organism_classification Invertebrates Germ Cells Oocytes Animal Studies Caenorhabditis Physiological Processes Zoology Developmental Biology |
| Zdroj: | PLoS ONE, Vol 16, Iss 2, p e0245174 (2021) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | Reproductive organs and developing tissues have high energy demands that require metabolic functions primarily supported by mitochondria function. The highly conserved CISD/NEET iron-sulfur (Fe-S) protein family regulates iron and reactive oxygen homeostasis, both of which are important for mitochondrial function. Disruption of iron and reactive oxygen homeostasis typically leads to detrimental effects. In humans, CISD dysfunction is associated with human health issues including Wolfram syndrome 2. UsingC.elegans, we previously determined that thecisd-1,cisd-3.1andcisd-3.2have an overlapping role in the regulation of physiological germline apoptosis through the canonical programmed cell death pathway. Here, we isolated thecisd-3.2(pnIs68)mutant that resulted in physiological and fitness defects including germline abnormalities that are associated with abnormal stem cell niche and disrupted formation of bivalent chromosomes. Thecisd-3.2(pnIs68)mutation led to complete disruption of thecisd-3.2gene expression and a decrease in expression of genetically intactcisd-1andcisd-3.1genes suggesting an indirect impact of thecisd-3.2(pnIs68)allele. The CISD-3.2 and CISD-3.1 proteins localize to the mitochondria in many tissues throughout development. Thecisd-3.2(pnIs68)mutant displays phenotypes associated with mitochondrial dysfunction, including disruption of the mitochondrial network within the germline. These results further support the idea that the CISD protein family is required for mitochondrial function that supports important functions in animals including overall fitness and germline viability. |
| Databáze: | OpenAIRE |
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