ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
The TRIM-NHL protein Brat promotes axon maintenance by repressing src64B expression.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- The making of the Drosophila mushroom body.Frontiers in physiology · 2023Review
- Drosophila Netrin-B controls mushroom body axon extension and regulates courtship-associated learning and memory of a Drosophila fragile X syndrome model.Molecular brain · 2019Article
- A Novel Mutation in Brain Tumor Causes Both Neural Over-Proliferation and Neurodegeneration in AdultG3 (Bethesda, Md.) · 2018Article
- Review
- Brain Tumor promotes axon growth across the midline through interactions with the microtubule stabilizing protein Apc2.PLoS genetics · 2018Article
- Combinatorial control of messenger RNAs by Pumilio, Nanos and Brain Tumor Proteins.RNA biology · 2017Article
- Exploring Potential Germline-Associated Roles of the TRIM-NHL Protein NHL-2 Through RNAi Screening.G3 (Bethesda, Md.) · 2017Article
- Proliferation control in neural stem and progenitor cells.Nature reviews. Neuroscience · 2015Review
- Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The morphology and the connectivity of neuronal structures formed during early development must be actively maintained as the brain matures. Although impaired axon stability is associated with the progression of various neurological diseases, relatively little is known about the factors controlling this process. We identified Brain tumor (Brat), a conserved member of the TRIM-NHL family of proteins, as a new regulator of axon maintenance in Drosophila CNS. Brat function is dispensable for the initial growth of Mushroom Body axons, but is required for the stabilization of axon bundles. We found that Brat represses the translation of src64B, an upstream regulator of a conserved Rho-dependent pathway previously shown to promote axon retraction. Furthermore, brat phenotypes are phenocopied by src64B overexpression, and partially suppressed by reducing the levels of src64B or components of the Rho pathway, suggesting that brat promotes axon maintenance by downregulating the levels of Src64B. Finally, Brat regulates brain connectivity via its NHL domain, but independently of its previously described partners Nanos, Pumilio, and d4EHP. Thus, our results uncover a novel post-transcriptional regulatory mechanism that controls the maintenance of neuronal architecture by tuning the levels of a conserved rho-dependent signaling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.