ArticleGenetics2025
The TRIM-NHL RNA-binding protein MEI-P26 modulates the size of Drosophila Type I neuroblast lineages.
Article in Genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The RNA-binding activity of theRNA biology · 2026Article
- RNA-binding is the essential biological function of thebioRxiv : the preprint server for biology · 2026Article
- miR-10-3p, but not miR-1006-3p, regulatesmicroPublication biology · 2026Article
- Divergent functions of the RNA-binding protein, Mei-P26 in germline and somatic lineages ofFrontiers in cell and developmental biology · 2026Article
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Authors and funding
3 authors.
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Abstract
The Drosophila TRIM-NHL RNA-binding protein (RBP), MEI-P26, has previously been shown to suppress tumor formation in the germline. Here we show that, in the Drosophila larval central brain, cell-type-specific expression of MEI-P26 plays a vital role in regulating neural development. MEI-P26 and another TRIM-NHL RBP, Brain tumor (BRAT), have distinct expression patterns in Type I neuroblast (NB) lineages: While both proteins are expressed in NBs, BRAT is expressed in ganglion mother cells (GMCs) but not neurons, whereas MEI-P26 is expressed in neurons but not GMCs. Knockdown of MEI-P26 leads to re-expression of the stem cell marker Deadpan (DPN) and over-production of neurons. In contrast, ectopically expressed MEI-P26 reduces NB lineage size by repressing division of GMCs, resulting in reduced neuron production. We show that MEI-P26 positively regulates expression of Prospero (PROS), a transcription factor that is known to repress cell cycle-related genes. Ectopic expression of PROS phenocopies ectopic expression of MEI-P26. In both cases, Cyclin B (CYCB) expression is downregulated. Importantly, knockdown of PROS in the context of ectopic MEI-P26 rescues the neural lineage. Based on these results, we conclude that MEI-P26 functions to prevent over-production of neurons by promoting production of PROS which, in turn, downregulates cell division.
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