ArticlePloS one2013
Sterile alpha motif containing 7 (samd7) is a novel crx-regulated transcriptional repressor in the retina.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Pathogenic variants inGenome research · 2024Article
- Mutations in SAMD7 cause autosomal-recessive macular dystrophy with or without cone dysfunction.American journal of human genetics · 2024Article
- Transcription factor interactions explain the context-dependent activity of CRX binding sites.PLoS computational biology · 2024Article
- Pathogenic variants in Crx have distinct cis-regulatory effects on enhancers and silencers in photoreceptors.bioRxiv : the preprint server for biology · 2023Article
- Single-cell RNA sequencing of the retina in a model of retinitis pigmentosa reveals early responses to degeneration in rods and cones.BMC biology · 2022Article
- Depletion of miR-96 Delays, But Does Not Arrest, Photoreceptor Development in Mice.Investigative ophthalmology & visual science · 2022Article
- Article
- Epigenetic regulation of retinal development.Epigenetics & chromatin · 2021Review
- Functional Annotations of Single-Nucleotide Polymorphism (SNP)-Based and Gene-Based Genome-Wide Association Studies Show Genes Affecting Keratitis Susceptibility.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Transcriptional profiling of murine retinas undergoing semi-synchronous cone photoreceptor differentiation.Developmental biology · 2019Article
- Samd7 is a cell type-specific PRC1 component essential for establishing retinal rod photoreceptor identity.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- A challenge to the striking genotypic heterogeneity of retinitis pigmentosa: a better understanding of the pathophysiology using the newest genetic strategies.Eye (London, England) · 2016Review
- Identification of the Photoreceptor Transcriptional Co-Repressor SAMD11 as Novel Cause of Autosomal Recessive Retinitis Pigmentosa.Scientific reports · 2016Article
- Autosomal recessive retinitis pigmentosa with homozygous rhodopsin mutation E150K and non-coding cis-regulatory variants in CRX-binding regions of SAMD7.Scientific reports · 2016Article
- Early-onset autosomal recessive cerebellar ataxia associated with retinal dystrophy: new human hotfoot phenotype caused by homozygous GRID2 deletion.Genetics in medicine : official journal of the American College of Medical Genetics · 2015Article
- Comparison of two methods used to culture and purify rat retinal Müller cells.International journal of ophthalmology · 2013Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inherited retinal diseases are mainly caused by mutations in genes that are highly expressed in photoreceptors of the retina. The majority of these genes is under the control of the transcription factor Cone rod homeobox (Crx), that acts as a master transcription factor in photoreceptors. Using a genome-wide chromatin immunoprecipitation dataset that highlights all potential in vivo targets of Crx, we have identified a novel sterile alpha motif (SAM) domain containing protein, Samd7. mRNA Expression of Samd7 was confined to the late postnatal and adult mouse retina as well as the pineal gland. Using immunohistochemistry and Western blot, we could detect Samd7 protein in the outer nuclear layer of adult mouse retina. Ectopic over-expression in HEK293 cells demonstrated that Samd7 resides in the cytoplasm as well as the nucleus. In vitro electroporation of fluorescent reporters into living mouse retinal cultures revealed that transcription of the Samd7 gene depends on evolutionary conserved Crx motifs located in the first intron enhancer. Moreover, Crx knock-down with shRNA strongly reduced Samd7 reporter activity and endogenous Samd7 protein, indicating that Crx is required for retinal expression of Samd7. Finally, using co-transfections in luciferase reporter assays we found that Samd7 interferes with Crx-dependent transcription. Samd7 suppressed luciferase activity from a reporter plasmid with five Crx consensus repeats in a dose dependent manner and reduced Crx-mediated transactivation of regulatory sequences in the retinoschisin gene and the Samd7 gene itself. Taken together, we have identified a novel retinal SAM domain protein, Samd7, which could act as a transcriptional repressor involved in fine-tuning of Crx-regulated gene expression.
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