ArticleMechanisms of development
Split ends antagonizes the Notch and potentiates the EGFR signaling pathways during Drosophila eye development.
Article in Mechanisms of development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Genomic and transcriptomic evaluation of primary and recurrent luminal B-like breast cancer.ESMO open · 2026Article
- Spen and Nito prevent dedifferentiation of intermediate progenitors by maintaining Notch target expression in stem cells at low levels.Cell reports · 2026Article
- Article
- O-GlcNAc transferase congenital disorder of glycosylation (OGT-CDG): Potential mechanistic targets revealed by evaluating the OGT interactome.The Journal of biological chemistry · 2024Review
- Pan-cancer analysis identifies SPEN mutation as a predictive biomarker with the efficacy of immunotherapy.BMC cancer · 2023Article
- SPOC domain proteins in health and disease.Genes & development · 2023Review
- SPEN haploinsufficiency causes a neurodevelopmental disorder overlapping proximal 1p36 deletion syndrome with an episignature of X chromosomes in females.American journal of human genetics · 2021Article
- Spen modulates lipid droplet content in adult Drosophila glial cells and protects against paraquat toxicity.Scientific reports · 2020Article
- Transcriptomic and proteomic signatures of stemness and differentiation in the colon crypt.Communications biology · 2020Article
- Multiple loci linked to inversions are associated with eye size variation in species of the Drosophila virilis phylad.Scientific reports · 2020Article
- The evolution of transcriptional repressors in the Notch signaling pathway: a computational analysis.Hereditas · 2019Article
- Spen limits intestinal stem cell self-renewal.PLoS genetics · 2018Article
- An autonomous metabolic role for Spen.PLoS genetics · 2017Article
- Article
- A phospho-dependent mechanism involving NCoR and KMT2D controls a permissive chromatin state at Notch target genes.Nucleic acids research · 2016Article
- spenito is required for sex determination in Drosophila melanogaster.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The transcriptional corepressor SMRTER influences both Notch and ecdysone signaling during Drosophila development.Biology open · 2012Article
- Structural and functional analysis of the repressor complex in the Notch signaling pathway of Drosophila melanogaster.Molecular biology of the cell · 2011Article
- Kaposi's sarcoma-associated herpesvirus ORF57 interacts with cellular RNA export cofactors RBM15 and OTT3 to promote expression of viral ORF59.Journal of virology · 2011Article
- The RNA-binding motif protein 15B (RBM15B/OTT3) acts as cofactor of the nuclear export receptor NXF1.The Journal of biological chemistry · 2009Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The Notch and Epidermal Growth Factor Receptor (EGFR) signaling pathways interact cooperatively and antagonistically to regulate many aspects of Drosophila development, including the eye. How output from these two signaling networks is fine-tuned to achieve the precise balance needed for specific inductive interactions and patterning events remains an open and important question. Previously, we reported that the gene split ends (spen) functions within or parallel to the EGFR pathway during midline glial cell development in the embryonic central nervous system. Here, we report that the cellular defects caused by loss of spen function in the developing eye imaginal disc place spen as both an antagonist of the Notch pathway and a positive contributor to EGFR signaling during retinal cell differentiation. Specifically, loss of spen results in broadened expression of Scabrous, ectopic activation of Notch signaling, and a corresponding reduction in Atonal expression at the morphogenetic furrow. Consistent with Spen's role in antagonizing Notch signaling, reduction of spen levels is sufficient to suppress Notch-dependent phenotypes. At least in part due to loss of Spen-dependent down-regulation of Notch signaling, loss of spen also dampens EGFR signaling as evidenced by reduced activity of MAP kinase (MAPK). This reduced MAPK activity in turn leads to a failure to limit expression of the EGFR pathway antagonist and the ETS-domain transcriptional repressor Yan and to a corresponding loss of cell fate specification in spen mutant ommatidia. We propose that Spen plays a role in modulating output from the Notch and EGFR pathways to ensure appropriate patterning during eye development.
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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.