دورية أكاديمية

GLIS3 regulates transcription of thyroid hormone biosynthetic genes in coordination with other thyroid transcription factors

التفاصيل البيبلوغرافية
العنوان: GLIS3 regulates transcription of thyroid hormone biosynthetic genes in coordination with other thyroid transcription factors
المؤلفون: Hong Soon Kang, Sara A. Grimm, Raja Jothi, Pilar Santisteban, Anton M. Jetten
المصدر: Cell & Bioscience, Vol 13, Iss 1, Pp 1-18 (2023)
بيانات النشر: BMC, 2023.
سنة النشر: 2023
المجموعة: LCC:Biotechnology
LCC:Biology (General)
LCC:Biochemistry
مصطلحات موضوعية: GLIS3, NKX2.1, PAX8, FOXE1, Gene transcription, Thyroid follicular cells, Biotechnology, TP248.13-248.65, Biology (General), QH301-705.5, Biochemistry, QD415-436
الوصف: Abstract Background Loss of the transcription factor GLI-Similar 3 (GLIS3) function causes congenital hypothyroidism (CH) in both humans and mice due to decreased expression of several thyroid hormone (TH) biosynthetic genes in thyroid follicular cells. Whether and to what extent, GLIS3 regulates thyroid gene transcription in coordination with other thyroid transcriptional factors (TFs), such as PAX8, NKX2.1 and FOXE1, is poorly understood. Methods PAX8, NKX2.1, and FOXE1 ChIP-Seq analysis with mouse thyroid glands and rat thyrocyte PCCl3 cells was performed and compared to that of GLIS3 to analyze the co-regulation of gene transcription in thyroid follicular cells by these TFs. Results Analysis of the PAX8, NKX2.1, and FOXE1 cistromes identified extensive overlaps between these TF binding loci and those of GLIS3 indicating that GLIS3 shares many of the same regulatory regions with PAX8, NKX2.1, and FOXE1, particularly in genes associated with TH biosynthesis, induced by thyroid stimulating hormone (TSH), and suppressed in Glis3KO thyroid glands, including Slc5a5 (Nis), Slc26a4, Cdh16, and Adm2. ChIP-QPCR analysis showed that loss of GLIS3 did not significantly affect PAX8 or NKX2.1 binding and did not cause major alterations in H3K4me3 and H3K27me3 epigenetic signals. Conclusions Our study indicates that GLIS3 regulates transcription of TH biosynthetic and TSH-inducible genes in thyroid follicular cells in coordination with PAX8, NKX2.1, and FOXE1 by binding within the same regulatory hub. GLIS3 does not cause major changes in chromatin structure at these common regulatory regions. GLIS3 may induce transcriptional activation by enhancing the interaction of these regulatory regions with other enhancers and/or RNA Polymerase II (Pol II) complexes.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2045-3701
Relation: https://doaj.org/toc/2045-3701
DOI: 10.1186/s13578-023-00979-8
URL الوصول: https://doaj.org/article/00d726bfdce14c65b8344d1a622b9f7c
رقم الأكسشن: edsdoj.00d726bfdce14c65b8344d1a622b9f7c
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:20453701
DOI:10.1186/s13578-023-00979-8