Deletion of the <i>Prdm3</i> Gene Causes a Neuronal Differentiation Deficiency in P19 Cells
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 <i...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2020-09-01
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| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/21/19/7192 |
| Summary: | 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 <i>Prdm3</i> in neurogenesis and the mechanisms regulating its expression. We found that <i>Prdm3</i> mRNA expression was induced during neurogenesis and that <i>Prdm3</i> gene knockout caused premature neuronal differentiation of the P19 cells and enhanced the growth of non-neuronal cells. Interestingly, we found that <i>Gata6</i> expression was also significantly upregulated during neurogenesis. We further studied the regulatory mechanism of <i>Prdm3</i> expression. To determine the role of GATA6 in the regulation of <i>Prdm3</i> mRNA expression, we used a luciferase-based reporter assay and found that <i>Gata6</i> overexpression significantly increased the activity of the <i>Prdm3</i> promoter. Finally, the combination of retinoic acid receptors <i>α</i> and <i>β</i>, along with <i>Gata6</i> 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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| ISSN: | 1661-6596 1422-0067 |