TAF1 is needed for the proliferation and maturation of thyroid follicle cells via Notch signaling.
Am J Physiol Endocrinol Metab
; 326(6): E832-E841, 2024 Jun 01.
Article
em En
| MEDLINE
| ID: mdl-38656129
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 mutation TATA-box binding protein associated Factor 1 (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.NEW & NOTEWORTHY In our study, we obtained a novel zebrafish line with thyroid dysgenesis (TD) and identified the candidate pathogenetic mutation TATA-box binding protein associated Factor 1 (taf1). Further researches revealed that taf1 was required for thyroid follicular cells by binding to the NOTCH1 promoter region. Our findings revealed a novel role of TAF1 in thyroid morphogenesis.
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Base de dados:
MEDLINE
Assunto principal:
Glândula Tireoide
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Peixe-Zebra
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Transdução de Sinais
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Fatores Associados à Proteína de Ligação a TATA
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Fator de Transcrição TFIID
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Proliferação de Células
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article