PUBLICATION
KCTD10 is critical for heart and blood vessel development of zebrafish
- Authors
- Hu, X., Gan, S., Xie, G., Li, L., Chen, C., Ding, X., Han, M., Xiang, S., Zhang, J.
- ID
- ZDB-PUB-140513-196
- Date
- 2014
- Source
- Acta biochimica et biophysica Sinica 46: 377-86 (Journal)
- Registered Authors
- Li, Li
- Keywords
- KCTD10, PDIP1, blood vessel, heart, zebrafish
- MeSH Terms
-
- RNA, Messenger/genetics
- Zebrafish
- Molecular Sequence Data
- Heart/embryology*
- Sequence Homology, Amino Acid
- Animals
- Amino Acid Sequence
- DNA Primers
- Base Sequence
- Computational Biology
- Blood Vessels/embryology*
- Gene Expression Profiling
- Potassium Channels, Voltage-Gated/chemistry
- Potassium Channels, Voltage-Gated/genetics
- Potassium Channels, Voltage-Gated/physiology*
- PubMed
- 24705121 Full text @ Acta. Biochim. Biophys. Sin (Shanghai)
Citation
Hu, X., Gan, S., Xie, G., Li, L., Chen, C., Ding, X., Han, M., Xiang, S., Zhang, J. (2014) KCTD10 is critical for heart and blood vessel development of zebrafish. Acta biochimica et biophysica Sinica. 46:377-86.
Abstract
KCTD10 is a member of the PDIP1 family, which is highly conserved during evolution, sharing a lot of similarities among human, mouse, and zebrafish. Recently, zebrafish KCTD13 has been identified to play an important role in the early development of brain and autism. However, the specific function of KCTD10 remains to be elucidated. In this study, experiments were carried out to determine the expression pattern of zebrafish KCTD10 mRNA during embryonic development. It was found that KCTD10 is a maternal gene and KCTD10 is of great importance in the shaping of heart and blood vessels. Our data provide direct clues that knockdown of KCTD10 resulted in severe pericardial edema and loss of heart formation indicated by morphological observation and crucial heart markers like amhc, vmhc, and cmlc2. The heart defect caused by KCTD10 is linked to RhoA and PCNA. Flk-1 staining revealed that intersomitic vessels were lost in the trunk, although angioblasts could migrate to the midline. These findings could be helpful to better understand the determinants responsible for the heart and blood vessel defects.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping