PUBLICATION
Loss of growth hormone gene (gh1) in zebrafish arrests folliculogenesis in females and delays spermatogenesis in males
- Authors
- Hu, Z., Ai, N., Chen, W., Wong, Q.W., Ge, W.
- ID
- ZDB-PUB-190123-5
- Date
- 2019
- Source
- Endocrinology 160(3): 568-586 (Journal)
- Registered Authors
- Chen, Weiting, Ge, Wei, Hu, Zhe, Wong, Queenie
- Keywords
- none
- MeSH Terms
-
- Animals
- Female
- Growth Hormone/physiology*
- Male
- Mutagenesis, Site-Directed
- Ovarian Follicle/growth & development*
- Spermatogenesis*
- Zebrafish/genetics
- Zebrafish/growth & development*
- PubMed
- 30668682 Full text @ Endocrinology
Citation
Hu, Z., Ai, N., Chen, W., Wong, Q.W., Ge, W. (2019) Loss of growth hormone gene (gh1) in zebrafish arrests folliculogenesis in females and delays spermatogenesis in males. Endocrinology. 160(3):568-586.
Abstract
As a master hormone controlling growth and metabolism, growth hormone (GH) is also known to regulate reproduction. Studies in mammals have shown that mutations in GH or its receptor (GHR) not only result in retardation in body growth but also reproductive dysfunctions in both sexes. However, the roles of GH in reproduction of other vertebrates are poorly defined. In this study, we created two zebrafish GH (gh1) mutant lines using CRISPR/Cas9. The mutant developed normally up to 14 days post-fertilization (dpf); however, a high rate of mortality was observed afterwards in both lines, and only a small number of mutant fish could survive to adult stage. The body growth of the mutants was significantly retarded in both sexes in a gene dose-dependent manner compared to their wild type siblings. A severe dysfunction of gonadal development was observed in survived mutant females with ovarian folliculogenesis being arrested completely at primary growth stage until 100 dpf. Interestingly, the folliculogenesis in the mutant resumed after months of delay with certain number of follicles entering vitellogenic growth. As for male reproduction, although the spermatogenesis in mutant males seemed normal in adult, the GH-insufficient heterozygote showed an obvious delay of spermatogenesis (puberty onset) at early developmental stages. The adult mutant males could not breed with wild type females through natural spawning; however, the sperm isolated from the mutant testes could fertilize eggs through artificial fertilization. This study provides further genetic evidence for dependence of puberty onset on somatic growth but not age in fish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping