Caenorhabditis elegans homologue of Fam210 is required for oogenesis and reproduction
| Autor: | Jing Kang, Wei-Jun Yang, Jianzhi Zhao, Hengda Zhou, Caiyong Chen, Yongtian Chen, Suhong Xu, Fengxiu Sun |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Erythrocytes
education ved/biology.organism_classification_rank.species Oxidative phosphorylation Mitochondrion Bone and Bones Germline Vulva Mitochondrial Proteins 03 medical and health sciences Oogenesis 0302 clinical medicine Mitochondrial unfolded protein response Genetics Animals Humans Caenorhabditis elegans Caenorhabditis elegans Proteins Model organism Molecular Biology Beta oxidation 030304 developmental biology 0303 health sciences biology ved/biology Reproduction biology.organism_classification humanities Mitochondria Cell biology Intestines Citric acid cycle Germ Cells Unfolded Protein Response Female 030217 neurology & neurosurgery Signal Transduction Transcription Factors |
| Zdroj: | Journal of Genetics and Genomics. 47:694-704 |
| ISSN: | 1673-8527 |
| DOI: | 10.1016/j.jgg.2020.10.008 |
| Popis: | Mitochondria are the central hub for many metabolic processes, including the citric acid cycle, oxidative phosphorylation, and fatty acid oxidation. Recent studies have identified a new mitochondrial protein family, Fam210, that regulates bone metabolism and red cell development in vertebrates. The model organism Caenorhabditis elegans has a Fam210 gene, y56a3a.22, but it lacks both bones and red blood cells. In this study, we report that Y56A3A.22 plays a crucial role in regulating mitochondrial protein homeostasis and reproduction. The nematode y56a3a.22 is expressed in various tissues, including the intestine, muscle, hypodermis, and germline, and its encoded protein is predominantly localized in mitochondria. y56a3a.22 deletion mutants are sterile owing to impaired oogenesis. Loss of Y56A3A.22 induced mitochondrial unfolded protein response (UPRmt), which is mediated through the ATFS-1-dependent pathway, in tissues such as the intestine, germline, hypodermis, and vulval muscle. We further show that infertility and UPRmt induces by Y56A3A.22 deficiency are not attributed to systemic iron deficiency. Together, our study reveals an important role of Y56A3A.22 in regulating mitochondrial protein homeostasis and oogenesis and provides a new genetic tool for exploring the mechanisms regulating mitochondrial metabolism and reproduction as well as the fundamental role of the Fam210 family. |
| Databáze: | OpenAIRE |
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