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Cota, P. ; Saber, L. ; Taskin, D. ; Jing, C. ; Bastidas-Ponce, A. ; Vanheusden, M. ; Shahryari, A. ; Sterr, M. ; Burtscher, I. ; Bakhti, M. ; Lickert, H.

NEUROD2 function is dispensable for human pancreatic β cell specification.

Front. Endocrin. 14:1286590 (2023)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
INTRODUCTION: The molecular programs regulating human pancreatic endocrine cell induction and fate allocation are not well deciphered. Here, we investigated the spatiotemporal expression pattern and the function of the neurogenic differentiation factor 2 (NEUROD2) during human endocrinogenesis. METHODS: Using Crispr-Cas9 gene editing, we generated a reporter knock-in transcription factor (TF) knock-out human inducible pluripotent stem cell (iPSC) line in which the open reading frame of both NEUROD2 alleles are replaced by a nuclear histone 2B-Venus reporter (NEUROD2nVenus/nVenus). RESULTS: We identified a transient expression of NEUROD2 mRNA and its nuclear Venus reporter activity at the stage of human endocrine progenitor formation in an iPSC differentiation model. This expression profile is similar to what was previously reported in mice, uncovering an evolutionarily conserved gene expression pattern of NEUROD2 during endocrinogenesis. In vitro differentiation of the generated homozygous NEUROD2nVenus/nVenus iPSC line towards human endocrine lineages uncovered no significant impact upon the loss of NEUROD2 on endocrine cell induction. Moreover, analysis of endocrine cell specification revealed no striking changes in the generation of insulin-producing b cells and glucagon-secreting a cells upon lack of NEUROD2. DISCUSSION: Overall, our results suggest that NEUROD2 is expendable for human b cell formation in vitro.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Neurod2 ; Endocrine Cells ; Endocrinogenesis ; Ipsc Differentiation ; β Cells; Differentiation; Neurogenin3; System; Genes
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 1664-2392
e-ISSN 1664-2392
Zeitschrift Frontiers in Endocrinology
Quellenangaben Band: 14, Heft: , Seiten: , Artikelnummer: 1286590 Supplement: ,
Verlag Frontiers
Verlagsort Lausanne
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Regeneration Research (IDR)
POF Topic(s) 30201 - Metabolic Health
90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502300-001
G-501900-231
Förderungen DZD NEXT Young Talent Program
scholarship under the State Scholarship Fund by the China Scholarship Council
Helmholtz Research School for Diabetes (HRD) - Helmholtz Association - Initiative and Networking Fund (IVF)
German Center for Diabetes Research (DZD e.V.)
Helmholtz Portfolio Theme'Metabolic Dysfunction and Common Disease
Helmholtz Society
The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The work was supported by the Helmholtz Society, Helmholtz Portfolio Theme'Metabolic Dysfunction and Common Disease, and German Center f
DOI 10.3389/fendo.2023.1286590
WOS ID 001102677000001
Scopus ID 85176272022
PubMed ID 37955006
Erfassungsdatum 2023-11-28
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