# miR-137 targets Myc to regulate growth during eye development

**Authors:** Radhika Padma, Manivannan Subramanian, Anuradha Venkatakrishnan Chimata, Arushi Rai, Sunanda Yogi, Anjali Sangeeth, Madhuri Kango-Singh, Amit Singh

PMC · DOI: 10.1242/dev.204373 · Development (Cambridge, England) · 2025-07-16

## TL;DR

The paper shows that miR-137 regulates eye development by targeting the Myc gene, which could help treat diseases involving Myc overactivity.

## Contribution

The study identifies miR-137 as a novel post-transcriptional regulator of Myc during eye development.

## Key findings

- miR-137 gain of function causes reduced eye size by downregulating eye development markers.
- Myc is confirmed as a target of miR-137, and Myc gain of function rescues miR-137-induced eye defects.
- miR-137 reduces tumor growth and Myc levels in a Drosophila tumor model.

## 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.

Summary: Identification and characterization of miR-137 as a post-transcriptional regulator of Myc that controls growth, offering insights into diseases such as neurodegenerative disorders and cancer, which are linked to Myc accumulation.

## Linked entities

- **Genes:** MIR137 (microRNA 137) [NCBI Gene 406928], MYC (MYC proto-oncogene, bHLH transcription factor) [NCBI Gene 4609], wg (Wnt family member 1 wingless) [NCBI Gene 692745], hth (Meis homeobox homothorax) [NCBI Gene 101737806], Ras85D (Ras oncogene at 85D) [NCBI Gene 41140]
- **Species:** Drosophila (taxon 7215)

## Full-text entities

- **Genes:** hth (homothorax) [NCBI Gene 41273] {aka 1323/07, 1422/04, CG17117, Dm-HTH, Dmel\CG17117, MEIS1}, mir-137 (mir-137 stem loop) [NCBI Gene 12798490] {aka 2R:11128979, CR33575, CR43012, Dmel\CR43012, Dmel_CR33575, dme-miR-137}, Myc (Myc) [NCBI Gene 31310] {aka CG10798, D-Myc, DM, DMYc, Diminutive, Dm}
- **Diseases:** neoplastic tumors (MESH:D009369), enlarged-eye (MESH:D006332)
- **Species:** Drosophila melanogaster (fruit fly, species) [taxon 7227]

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12338917/full.md

## References

126 references — full list in the complete paper: https://tomesphere.com/paper/PMC12338917/full.md

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Source: https://tomesphere.com/paper/PMC12338917