Deletion of the Gene Causes a Neuronal Differentiation Deficiency in P19 Cells

Overview

Journal Int J Mol Sci

Publisher MDPI

Specialties Biochemistry
Chemistry
Molecular Biology

Date 2020 Oct 2

PMID 33003409

Citations 6

Authors

Pawel Leszczynski

Magdalena Smiech

Aamir Salam Teeli

Effi Haque

Robert Viger

Hidesato Ogawa

Mariusz Pierzchala

Hiroaki Taniguchi

Affiliations

Soon will be listed here.

Abstract

PRDM (PRDI-BF1 (positive regulatory domain I-binding factor 1) and RIZ1 (retinoblastoma protein-interacting zinc finger gene 1) homologous domain-containing) transcription factors are a group of proteins that have a significant impact on organ development. In our study, we assessed the role of in neurogenesis and the mechanisms regulating its expression. We found that mRNA expression was induced during neurogenesis and that gene knockout caused premature neuronal differentiation of the P19 cells and enhanced the growth of non-neuronal cells. Interestingly, we found that expression was also significantly upregulated during neurogenesis. We further studied the regulatory mechanism of expression. To determine the role of GATA6 in the regulation of mRNA expression, we used a luciferase-based reporter assay and found that overexpression significantly increased the activity of the promoter. Finally, the combination of retinoic acid receptors and , along with overexpression, further increased the activity of the luciferase reporter. Taken together, our results suggest that in the P19 cells, PRDM3 contributed to neurogenesis and its expression was stimulated by the synergism between GATA6 and the retinoic acid signaling pathway.

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