Regulation of retinal amacrine cell generation by miR-216b and Foxn3 [miRNA-seq Ptf1a]
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ABSTRACT:
PROVIDER: PRJNA697989 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13586177.fastq.gz | Fastqsanger.gz | |||
| SRR13586178.fastq.gz | Fastqsanger.gz | |||
| SRR13586179.fastq.gz | Fastqsanger.gz | |||
| SRR13586180.fastq.gz | Fastqsanger.gz | |||
| SRR13586181.fastq.gz | Fastqsanger.gz |
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Project description:The mammalian retina contains a complex mixture of different types of neurons. We find that the microRNA miR-216b is preferentially expressed in postmitotic retinal amacrine cells in the mouse retina, and expression of miR-216a/b and miR-217 in the retina depend in part on Ptf1a, a transcription factor required for amacrine cell differentiation. Surprisingly, ectopic expression of miR-216b, or the related miR-216a, can direct the formation of additional amacrine cells in the developing retina. In addition, we observe the loss of bipolar neurons in the retina after miR-216b expression. We identify the mRNA for the transcriptional regulator Foxn3 as a retinal target of miR-216b by Argonaute PAR-CLIP and reporter analysis. Inhibition of Foxn3 in the postnatal developing retina by RNAi also increases the formation of amacrine cells and reduces bipolar cell formation, while overexpression of Foxn3 inhibits amacrine cell formation prior to the expression of Ptf1a. Disruption of Foxn3 by CRISPR in embryonic retinal explants also reduces amacrine cell formation. Co-expression of Foxn3 partially reverses the effects of ectopic miR-216b on retinal cell type formation. Our results identify Foxn3 as a novel regulator of interneuron formation in the developing retina and suggest that miR-216b likely regulates expression of Foxn3 and other genes in amacrine cells.
2021-12-22 | GSE165831 | GEO
Project description:The mammalian retina contains a complex mixture of different types of neurons. We find that the microRNA miR-216b is preferentially expressed in postmitotic retinal amacrine cells in the mouse retina, and expression of miR-216a/b and miR-217 in the retina depend in part on Ptf1a, a transcription factor required for amacrine cell differentiation. Surprisingly, ectopic expression of miR-216b, or the related miR-216a, can direct the formation of additional amacrine cells in the developing retina. In addition, we observe the loss of bipolar neurons in the retina after miR-216b expression. We identify the mRNA for the transcriptional regulator Foxn3 as a retinal target of miR-216b by Argonaute PAR-CLIP and reporter analysis. Inhibition of Foxn3 in the postnatal developing retina by RNAi also increases the formation of amacrine cells and reduces bipolar cell formation, while overexpression of Foxn3 inhibits amacrine cell formation prior to the expression of Ptf1a. Disruption of Foxn3 by CRISPR in embryonic retinal explants also reduces amacrine cell formation. Co-expression of Foxn3 partially reverses the effects of ectopic miR-216b on retinal cell type formation. Our results identify Foxn3 as a novel regulator of interneuron formation in the developing retina and suggest that miR-216b likely regulates expression of Foxn3 and other genes in amacrine cells.
2021-12-22 | GSE165827 | GEO
Project description:The mammalian retina contains a complex mixture of different types of neurons. We find that the microRNA miR-216b is preferentially expressed in postmitotic retinal amacrine cells in the mouse retina, and expression of miR-216a/b and miR-217 in the retina depend in part on Ptf1a, a transcription factor required for amacrine cell differentiation. Surprisingly, ectopic expression of miR-216b, or the related miR-216a, can direct the formation of additional amacrine cells in the developing retina. In addition, we observe the loss of bipolar neurons in the retina after miR-216b expression. We identify the mRNA for the transcriptional regulator Foxn3 as a retinal target of miR-216b by Argonaute PAR-CLIP and reporter analysis. Inhibition of Foxn3 in the postnatal developing retina by RNAi also increases the formation of amacrine cells and reduces bipolar cell formation, while overexpression of Foxn3 inhibits amacrine cell formation prior to the expression of Ptf1a. Disruption of Foxn3 by CRISPR in embryonic retinal explants also reduces amacrine cell formation. Co-expression of Foxn3 partially reverses the effects of ectopic miR-216b on retinal cell type formation. Our results identify Foxn3 as a novel regulator of interneuron formation in the developing retina and suggest that miR-216b likely regulates expression of Foxn3 and other genes in amacrine cells.
2021-12-22 | GSE165830 | GEO
Project description:Regulation of retinal amacrine cell generation by miR-216b and Foxn3
| PRJNA697987 | ENA
Project description:Regulation of retinal amacrine cell generation by miR-216b and Foxn3 [PAR-CLIP]
| PRJNA697981 | ENA
Project description:Regulation of retinal amacrine cell generation by miR-216b and Foxn3 [miRNA-seq P0]
| PRJNA697990 | ENA
Project description:The mammalian retina contains a complex mixture of different types of neurons. We find that microRNA miR-216b is preferentially expressed in postmitotic retinal amacrine cells in the mouse retina, and expression of miR-216a/b and miR-217 in retina depend in part on Ptf1a, a transcription factor required for amacrine cell differentiation. Surprisingly, ectopic expression of miR-216b directed the formation of additional amacrine cells and reduced bipolar neurons in the developing retina. We identify the Foxn3 mRNA as a retinal target of miR-216b by Argonaute PAR-CLIP and reporter analysis. Inhibition of Foxn3, a transcription factor, in the postnatal developing retina by RNAi increased the formation of amacrine cells and reduced bipolar cell formation. Foxn3 disruption by CRISPR in embryonic retinal explants also increased amacrine cell formation, whereas Foxn3 overexpression inhibited amacrine cell formation prior to Ptf1a expression. Co-expression of Foxn3 partially reversed the effects of ectopic miR-216b on retinal cell formation. Our results identify Foxn3 as a novel regulator of interneuron formation in the developing retina and suggest that miR-216b likely regulates Foxn3 and other genes in amacrine cells.
| S-EPMC8917416 | biostudies-literature
Project description:Analysis of retinas from mice with a targeted disruption of the Foxn3 gene revealed additional displaced amacrine interneurons and additional retinal astrocytes in the inner plexiform layer and in the ganglion cell layer. The forkhead transcription factor Foxn3 is a transcriptional repressor. Numerous genes linked to cilia structure or assembly were upregulated in embryonic retinas without Foxn3, including Foxj1, a forkhead transcription factor required for motile cilia. Ectopic primary cilia were observed on bipolar and amacrine interneurons in postnatal retinas without Foxn3. CUT&RUN analysis revealed that many upregulated retinal genes were bound by the Foxn3 and Rfx3 proteins. A short hydrophobic motif shared by Foxj1, Foxn4, and Foxn3 proteins was found to be required for association with the Rfx3 protein and for transcriptional repression by Foxn3, as well as for full transcriptional activation by Foxn4 with Rfx3. AlphaFold 3 predicts an interaction between the hydrophobic motif and the Rfx3 dimerization domain. Mutations in Rfx3 at the predicted interaction site disrupted association of Rfx3 with Foxn3 or Foxn4. These results reveal a new layer of transcriptional regulation of genes required for cilia, with Foxn3 functioning as a repressor of cilia genes and limiting primary cilia formation in the developing retina.
2025-09-04 | GSE306960 | GEO
Project description:Analysis of retinas from mice with a targeted disruption of the Foxn3 gene revealed additional displaced amacrine interneurons and additional retinal astrocytes in the inner plexiform layer and in the ganglion cell layer. The forkhead transcription factor Foxn3 is a transcriptional repressor. Numerous genes linked to cilia structure or assembly were upregulated in embryonic retinas without Foxn3, including Foxj1, a forkhead transcription factor required for motile cilia. Ectopic primary cilia were observed on bipolar and amacrine interneurons in postnatal retinas without Foxn3. CUT&RUN analysis revealed that many upregulated retinal genes were bound by the Foxn3 and Rfx3 proteins. A short hydrophobic motif shared by Foxj1, Foxn4, and Foxn3 proteins was found to be required for association with the Rfx3 protein and for transcriptional repression by Foxn3, as well as for full transcriptional activation by Foxn4 with Rfx3. AlphaFold 3 predicts an interaction between the hydrophobic motif and the Rfx3 dimerization domain. Mutations in Rfx3 at the predicted interaction site disrupted association of Rfx3 with Foxn3 or Foxn4. These results reveal a new layer of transcriptional regulation of genes required for cilia, with Foxn3 functioning as a repressor of cilia genes and limiting primary cilia formation in the developing retina.
2025-09-04 | GSE306964 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-12-22 | GSE165832 | GEO