ArticleEndocrinology2015
Two Zebrafish hsd3b Genes Are Distinct in Function, Expression, and Evolution.
Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
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- Direct male development in chromosomally ZZ zebrafish.Frontiers in cell and developmental biology · 2024Article
- Single-cell transcriptome reveals insights into the development and function of the zebrafish ovary.eLife · 2022Article
- Characterization of the Interrenal Gland and Sexual Traits Development inFrontiers in endocrinology · 2022Article
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- Neural innervation as a potential trigger of morphological color change and sexual dimorphism in cichlid fish.Scientific reports · 2020Article
- Hyperandrogenism in POMCa-deficient zebrafish enhances somatic growth without increasing adiposity.Journal of molecular cell biology · 2020Article
- Genetic Disruption of 21-Hydroxylase in Zebrafish Causes Interrenal Hyperplasia.Endocrinology · 2017Article
- Visualizing the Interrenal Steroidogenic Tissue and Its Vascular Microenvironment in Zebrafish.Journal of visualized experiments : JoVE · 2016Article
- Ferredoxin 1b (Fdx1b) Is the Essential Mitochondrial Redox Partner for Cortisol Biosynthesis in Zebrafish.Endocrinology · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
HSD3B catalyzes the synthesis of δ4 steroids such as progesterone in the adrenals and gonads. Individuals lacking HSD3B2 activity experience congenital adrenal hyperplasia with imbalanced steroid synthesis. To develop a zebrafish model of HSD3B deficiency, we characterized 2 zebrafish hsd3b genes. Our phylogenetic and conserved synteny analyses showed that the tandemly duplicated human HSD3B1 and HSD3B2 genes are coorthologs of zebrafish hsd3b1 on chromosome 9 (Dre9), whereas the gene called hsd3b2 resides on Dre20 in an ancestral chromosome segment, from which its ortholog was lost in the tetrapod lineage. Zebrafish hsd3b1(Dre 9) was expressed in adult gonads and headkidney, which contains interrenal glands, the zebrafish counterpart of the tetrapod adrenal. Knockdown of hsd3b1(Dre 9) caused the interrenal and anterior pituitary to expand and pigmentation to increase, resembling human HSD3B2 deficiency. The zebrafish hsd3b2(Dre 20) gene was expressed in zebrafish early embryos as maternal transcripts that disappeared 1 day after fertilization. Morpholino inactivation of hsd3b2(Dre 20) led to embryo elongation, which was rescued by the injection of hsd3b2 mRNA. Thus, zebrafish hsd3b2(Dre 20) evolved independently of hsd3b1(Dre 9) with a morphogenetic function during early embryogenesis. Zebrafish hsd3b1(Dre 9), on the contrary, functions like mammalian HSD3B2, whose deficiency leads to congenital adrenal hyperplasia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.