PUBLICATION
TAF1 is needed for the proliferation and maturation of thyroid follicle cells via Notch signaling
- Authors
- Zhang, C., Yang, L., Zhang, H., Wu, F., Zhang, Y., Zhang, K., Wu, C., Li, R., Dong, M., Zhao, S., Song, H.
- ID
- ZDB-PUB-240425-4
- Date
- 2024
- Source
- American journal of physiology. Endocrinology and metabolism 326(6): E832-E841 (Journal)
- Registered Authors
- Dong, Mei, Song, Huai-Dong, Wu, Fengyao, Zhao, Shuangxia
- Keywords
- Notch signaling, Positional cloning, TATA-box binding protein associated Factor 1, Thyroid development, Zebrafish
- MeSH Terms
-
- Animals
- Cell Proliferation*/genetics
- Histone Acetyltransferases
- Humans
- Receptor, Notch1/genetics
- Receptor, Notch1/metabolism
- Signal Transduction*/genetics
- TATA-Binding Protein Associated Factors*/genetics
- TATA-Binding Protein Associated Factors*/metabolism
- Thyroid Dysgenesis/genetics
- Thyroid Dysgenesis/metabolism
- Thyroid Gland*/metabolism
- Transcription Factor TFIID*/genetics
- Transcription Factor TFIID*/metabolism
- Zebrafish*/genetics
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 38656129 Full text @ Am. J. Physiol. Endocrinol. Metab.
Citation
Zhang, C., Yang, L., Zhang, H., Wu, F., Zhang, Y., Zhang, K., Wu, C., Li, R., Dong, M., Zhao, S., Song, H. (2024) TAF1 is needed for the proliferation and maturation of thyroid follicle cells via Notch signaling. American journal of physiology. Endocrinology and metabolism. 326(6):E832-E841.
Abstract
Thyroid dysgenesis (TD) is the common pathogenic mechanism of congenital hypothyroidism (CH). In addition, known pathogenic genes are limited to those that are directly involved in thyroid development. To identify additional candidate pathogenetic genes, we performed forward genetic screening for TD in zebrafish, followed by positional cloning. The candidate gene was confirmed in vitro using the Nthy-ori 3.1 cell line and in vivo using a zebrafish model organism. We obtained a novel zebrafish line with thyroid dysgenesis and identified the candidate pathogenetic gene taf1 by positional cloning. Further molecular studies revealed that taf1 was needed for the proliferation of thyroid follicular cells by binding to the NOTCH1 promoter region. Knockdown of TAF1 impaired the proliferation and maturation of thyroid cells, thereby leading to thyroid dysplasia. This study showed that TAF1 promoted Notch signaling and that this association played a pivotal role in thyroid development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping