ArticleGenetics1998
Evidence for 3' untranslated region-dependent autoregulation of the Drosophila gene encoding the neuronal nuclear RNA-binding protein ELAV.
Article in Genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 53 citations in OpenAlex.
- The E3 ligase MEX3B forms a tripartite complex withOpen biology · 2025Article
- Targeting HuR-Vav3 mRNA interaction prevents Pseudomonas aeruginosa adhesion to the cystic fibrosis airway epithelium.JCI insight · 2023Article
- Cup is essential forRNA biology · 2023Article
- ALS-related FUS mutations alter axon growth in motoneurons and affect HuD/ELAVL4 and FMRP activity.Communications biology · 2021Article
- Landscape and evolution of tissue-specific alternative polyadenylation across Drosophila species.Genome biology · 2017Article
- Promiscuity in post-transcriptional control of gene expression: Drosophila sex-lethal and its regulatory partnerships.FEBS letters · 2017Review
- Sxl-Dependent, tra/tra2-Independent Alternative Splicing of the Drosophila melanogaster X-Linked Gene found in neurons.G3 (Bethesda, Md.) · 2015Article
- Concentration and Localization of Coexpressed ELAV/Hu Proteins Control Specificity of mRNA Processing.Molecular and cellular biology · 2015Article
- Advancing the functional utility of PAR-CLIP by quantifying background binding to mRNAs and lncRNAs.Genome biology · 2014Article
- Emerging complexity of the HuD/ELAVl4 gene; implications for neuronal development, function, and dysfunction.RNA (New York, N.Y.) · 2013Review
- ELAV mediates 3' UTR extension in the Drosophila nervous system.Genes & development · 2012Article
- Characterization of multiple exon 1 variants in mammalian HuD mRNA and neuron-specific transcriptional control via neurogenin 2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- RNA-binding protein HuR autoregulates its expression by promoting alternative polyadenylation site usage.Nucleic acids research · 2012Article
- Neural-specific elongation of 3' UTRs during Drosophila development.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- ELAV-mediated 3'-end processing of ewg transcripts is evolutionarily conserved despite sequence degeneration of the ELAV-binding site.Genetics · 2011Article
- Deciphering the role of RNA-binding proteins in the post-transcriptional control of gene expression.Briefings in functional genomics · 2010Review
- Novel recognition motifs and biological functions of the RNA-binding protein HuD revealed by genome-wide identification of its targets.Nucleic acids research · 2010Article
- The third RNA recognition motif of Drosophila ELAV protein has a role in multimerization.Nucleic acids research · 2008Article
- Neuronal ELAV proteins enhance mRNA stability by a PKCalpha-dependent pathway.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Shared RNA-binding sites for interacting members of the Drosophila ELAV family of neuronal proteins.Nucleic acids research · 2005Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Drosophila locus embryonic lethal abnormal visual system (elav) encodes a nuclear RNA-binding protein essential for normal neuronal differentiation and maintenance of neurons. ELAV is thought to play its role by binding to RNAs produced by other genes necessary for neuronal differentiation and consequently to affect their metabolism by an as yet unknown mechanism. ELAV structural homologues have been identified in a wide range of organisms, including humans, indicating an important conserved role for the protein. Analysis of elav germline transformants presented here shows that one copy of elav minigenes lacking a complete 3' untranslated region (3' UTR) rescues null mutations at elav, but that two copies are lethal. Additional in vivo experiments demonstrate that elav expression is regulated through the 3' UTR of the gene and indicate that this level of regulation is dependent upon ELAV itself. Because ELAV is an RNA-binding protein, the simplest model to account for these findings is that ELAV binds to the 3' UTR of its own RNA to autoregulate its expression. I discuss the implications of these results for normal elav function.
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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.