Caenorhabditis elegans homologue of Fam210 is required for oogenesis and reproduction

Jing Kang; Hengda Zhou; Fengxiu Sun; Yongtian Chen; Jianzhi Zhao; Wei-Jun Yang; Suhong Xu; Caiyong Chen

doi:10.1016/j.jgg.2020.10.008

Volume 47 Issue 11

Nov. 2020

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Caenorhabditis elegans homologue of Fam210 is required for oogenesis and reproduction

doi: 10.1016/j.jgg.2020.10.008

a
MOE Key Laboratory of Biosystems Homeostasis and Protection, College of Life Sciences, Zhejiang University, Hangzhou 310058, China
b
Center for Stem Cell and Regenerative Medicine and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China

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Corresponding author: E-mail address: chency@zju.edu.cn (Caiyong Chen)
Publish Date: 2020-11-25

Abstract

Abstract

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 (UPR^mt), 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 UPR^mt 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.
- Oogenesis,
- Iron metabolism,
- Mitochondrial protein homeostasis,
- Ferritin,
- Reproduction

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