Related Experiment Video
Updated: May 23, 2025
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A Possible Zebrafish Model of Polycystic Kidney Disease: Knockdown of wnt5a Causes Cysts in Zebrafish Kidneys
Published on: December 2, 2014
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gdf11 is required for pronephros/cloaca development through targeting TGF-β signaling
Xinning Tian1,2, Wantao Yao1,2, Jin Tan1,2
1Department of Cardiology, the Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, China.
Scientific Reports
|March 7, 2025
Summary
Growth differentiation factor 11 (Gdf11) is crucial for kidney and cloaca development. Disrupting Gdf11 impairs these organs, highlighting the transforming growth factor-beta (TGF-β) pathway
Area of Science:
- Developmental Biology
- Renal Physiology
- Molecular Biology
Background:
- Kidney congenital abnormalities impair renal function.
- Gdf11, a TGF-β family member, is linked to renal abnormalities.
- Gdf11's role in kidney and cloaca organogenesis is unclear.
Purpose of the Study:
- To elucidate the molecular and cellular roles of Gdf11 in kidney and cloaca development.
- To investigate the involvement of the TGF-β pathway in Gdf11-mediated organogenesis.
Main Methods:
- Utilized zebrafish models for gdf11 deletion and knockdown.
- Employed TGF-β small molecule activators for rescue experiments.
- Analyzed pronephros and cloaca formation defects.
Main Results:
- gdf11 deletion/knockdown significantly disrupted pronephros and cloaca formation in zebrafish.
- The TGF-β pathway was identified as acting downstream of Gdf11.
- TGF-β activator partially rescued developmental defects in gdf11 mutants.
Conclusions:
- Gdf11 is critical for pronephros and cloaca development via TGF-β signaling.
- This study offers new insights into renal and cloaca developmental diseases.
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