PUBLICATION
Loss of the adaptor protein Sh3bgrl initiates ovarian fibrosis in zebrafish
- Authors
- Jin, Z., Wang, D., Lv, H., Wu, B., Li, Z., Guo, X., Wang, H., Yang, S.
- ID
- ZDB-PUB-230913-52
- Date
- 2023
- Source
- FEBS letters 597(21): 2643-2655 (Journal)
- Registered Authors
- Yang, Shulan
- Keywords
- ECM, POI, ovarian fibrosis, sh3bgrl, zebrafish
- MeSH Terms
-
- Adaptor Proteins, Signal Transducing*/genetics
- Animals
- Female
- Fibrosis
- Ovary*
- Zebrafish*/genetics
- PubMed
- 37698355 Full text @ FEBS Lett.
Citation
Jin, Z., Wang, D., Lv, H., Wu, B., Li, Z., Guo, X., Wang, H., Yang, S. (2023) Loss of the adaptor protein Sh3bgrl initiates ovarian fibrosis in zebrafish. FEBS letters. 597(21):2643-2655.
Abstract
Ovarian fibrosis is a reproduction obstacle leading to female infertility in vertebrates, but the cause underlying the cellular events is unclear. Here, we found that the small adaptor protein SH3-domain-binding glutamate-rich protein like (Sh3bgrl) plays an important role in female reproduction in zebrafish. Two sh3bgrl mutant alleles that result in sh3bgrl depletion contributes to female spawning inability. Comparative transcriptome analysis revealed that sh3bgrl knockout mechanistically causes the upregulation of genes associated with extracellular matrix (ECM) and fiber generation in the zebrafish ovary. Consequently, extra ECM or fibers accumulate and are deposited in the ovary, resulting in eventual spawning inability. Our findings thus provide insights into understanding the underlying mechanism of infertility by ovarian fibrosis and provide a novel and valuable model to study female reproduction abnormality.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping