<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang H</submitter><funding>University of Michigan</funding><funding>NEI NIH HHS</funding><funding>Midwest Eye-Banks</funding><funding>National Institutes of Health</funding><pagination>dev199484</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8917416</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>149(2)</volume><pubmed_abstract>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</pubmed_abstract><journal>Development (Cambridge, England)</journal><pubmed_title>Regulation of retinal amacrine cell generation by miR-216b and Foxn3.</pubmed_title><pmcid>PMC8917416</pmcid><funding_grant_id>R21 EY018707</funding_grant_id><funding_grant_id>R01EY024996</funding_grant_id><funding_grant_id>R01 EY024996</funding_grant_id><funding_grant_id>P30 EY007003</funding_grant_id><funding_grant_id>R21EY018707</funding_grant_id><pubmed_authors>Zhuang P</pubmed_authors><pubmed_authors>Meng F</pubmed_authors><pubmed_authors>Dai M</pubmed_authors><pubmed_authors>Turner DL</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Welchko RM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulation of retinal amacrine cell generation by miR-216b and Foxn3.</name><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</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan</publication><modification>2026-05-09T22:39:01.892Z</modification><creation>2025-02-19T03:27:14.949Z</creation></dates><accession>S-EPMC8917416</accession><cross_references><pubmed>34919141</pubmed><doi>10.1242/dev.199484</doi></cross_references></HashMap>