{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Padma R"],"funding":["University of Dayton","NEI NIH HHS","Knights Templar Eye Foundation","National Institutes of Health","NIH HHS"],"pagination":["dev204373"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12338917"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["152(14)"],"pubmed_abstract":["During development, regulation of gene expression is key to cellular homeostasis. Gene expression regulation by non-coding RNAs involves the prevention of mRNA accumulation or the inhibition of translation of their target gene. In a forward-genetic screen to identify the microRNA involved in the growth and patterning of the Drosophila eye, we identified the highly conserved miR-137. Gain of function of miR-137 results in a reduced-eye phenotype by downregulating retinal determination and differentiation markers, and by upregulating negative regulators of eye development, such as Wingless (Wg) and Homothorax (Hth). Loss of function of miR-137 results in an enlarged-eye phenotype. Using bioinformatics and genetic approaches, we identified the oncogene Myc as the target of miR-137. Gain of function of Myc can rescue the reduced-eye phenotype of miR-137 gain of function, and vice versa. We tested the role of miR-137 in regulating Myc levels in the RasV12;scribRNAi, a tumor model of oncogenic cooperation that results in neoplastic tumors. Gain of function of miR-137 in the RasV12;scribRNAi background significantly reduced tumor phenotype as well as Myc levels in the eye. Our studies highlight miR-137 as a post-transcriptional regulator of Myc and a promising therapeutic target for diseases associated with Myc accumulation."],"journal":["Development (Cambridge, England)"],"pubmed_title":["miR-137 targets Myc to regulate growth during eye development."],"pmcid":["PMC12338917"],"funding_grant_id":["R01 EY032959","1RO1EY032959-01","KTEF-411281","2024-29"],"pubmed_authors":["Yogi S","Sangeeth A","Padma R","Subramanian M","Rai A","Singh A","Kango-Singh M","Chimata AV"],"additional_accession":[]},"is_claimable":false,"name":"miR-137 targets Myc to regulate growth during eye development.","description":"During development, regulation of gene expression is key to cellular homeostasis. Gene expression regulation by non-coding RNAs involves the prevention of mRNA accumulation or the inhibition of translation of their target gene. In a forward-genetic screen to identify the microRNA involved in the growth and patterning of the Drosophila eye, we identified the highly conserved miR-137. Gain of function of miR-137 results in a reduced-eye phenotype by downregulating retinal determination and differentiation markers, and by upregulating negative regulators of eye development, such as Wingless (Wg) and Homothorax (Hth). Loss of function of miR-137 results in an enlarged-eye phenotype. Using bioinformatics and genetic approaches, we identified the oncogene Myc as the target of miR-137. Gain of function of Myc can rescue the reduced-eye phenotype of miR-137 gain of function, and vice versa. We tested the role of miR-137 in regulating Myc levels in the RasV12;scribRNAi, a tumor model of oncogenic cooperation that results in neoplastic tumors. Gain of function of miR-137 in the RasV12;scribRNAi background significantly reduced tumor phenotype as well as Myc levels in the eye. Our studies highlight miR-137 as a post-transcriptional regulator of Myc and a promising therapeutic target for diseases associated with Myc accumulation.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-05-04T15:24:39.495Z","creation":"2026-04-07T20:38:38.039Z"},"accession":"S-EPMC12338917","cross_references":{"pubmed":["40554764"],"doi":["10.1242/dev.204373"]}}