Expression data from single embryonic chick retinal cells
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ABSTRACT:
ORGANISM(S): Gallus gallus
PROVIDER: GSE87663 | GEO | 2017/05/09
SECONDARY ACCESSION(S): PRJNA345503
REPOSITORIES: GEO
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Project description:The chicken embryo (Gallus gallus) is a classic model system for studying developmental biology. During chick development, embryonic day 8 (E8) retina are packed with multipotent neuronal precursors on the cusp of differentiation into all retinal cell types. By E18 the retina is nearly fully mature with all major retinal cell types differentiated and expressing cell type-specific genes. Whole retina were harvested from embryonic day 8 (E8), E16, and E18 developing chicken embryos. Whole cornea were also collected from E18 embryos as a reference tissue. Duplicates were obtained for each time point and total RNA was extracted from samples using a Qiagen AllPrep Mini Kit. To characterize differential gene expression in these tissues, Illumina stranded TrueSeq RNA-Seq libraries were prepared from total RNA and 125 PE sequencing reads were obtained. These data will be used to characterize retina-specific patters of gene expression as well as global changes in gene expression between critical developmental time points in the chicken retina.
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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.
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