ArticleProceedings of the National Academy of Sciences of the United States of America2007
Repression of Six3 by a corepressor regulates rhodopsin expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 65 citations in OpenAlex.
- Variant-to-gene mapping identifiesbioRxiv : the preprint server for biology · 2026Article
- SIX3 as a Regulator of Development and Disease.Journal of developmental biology · 2026Review
- Deletion of the homeodomain gene Six3 from kisspeptin neurons causes subfertility in female mice.Molecular and cellular endocrinology · 2022Article
- Ciliary photoreceptors in sea urchin larvae indicate pan-deuterostome cell type conservation.BMC biology · 2021Article
- The SIX Family of Transcription Factors: Common Themes Integrating Developmental and Cancer Biology.Frontiers in cell and developmental biology · 2021Review
- The Nucleosome Remodelling and Deacetylation complex suppresses transcriptional noise during lineage commitment.The EMBO journal · 2019Article
- NuRD subunit MTA1 interacts with the DNA non-homologous end joining Ku complex in cancer cells.RSC advances · 2018Article
- The Homeotic Protein SIX3 Suppresses Carcinogenesis and Metastasis through Recruiting the LSD1/NuRD(MTA3) Complex.Theranostics · 2018Article
- Review
- Article
- Article
- A trans-Regulatory Code for the Forebrain Expression of Six3.2 in the Medaka Fish.The Journal of biological chemistry · 2015Article
- The nucleosome remodeling and deacetylase complex in development and disease.Translational research : the journal of laboratory and clinical medicine · 2015Review
- Physiological functions of MTA family of proteins.Cancer metastasis reviews · 2014Review
- MTA1--a stress response protein: a master regulator of gene expression and cancer cell behavior.Cancer metastasis reviews · 2014Review
- Impact of histone deacetylase 1 and metastasis-associated gene 1 expression in esophageal carcinogenesis.Oncology letters · 2014Article
- Estrogen receptor coregulators and pioneer factors: the orchestrators of mammary gland cell fate and development.Frontiers in cell and developmental biology · 2014Review
- Loss of E-cadherin promotes prostate cancer metastasis via upregulation of metastasis-associated gene 1 expression.Oncology letters · 2012Article
- Sertoli cell-specific expression of metastasis-associated protein 2 (MTA2) is required for transcriptional regulation of the follicle-stimulating hormone receptor (FSHR) gene during spermatogenesis.The Journal of biological chemistry · 2012Article
- Metastasis-associated protein 1 drives tumor cell migration and invasion through transcriptional repression of RING finger protein 144A.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Here, we provide gain-of-function, loss-of function, and molecular evidence supporting genetic interactions between metastasis associated protein 1 (MTA1) and Six3 and between Six3 and rhodopsin. We discovered that MTA1 physically interacts with the Six3 chromatin in a histone deacetylase-dependent manner, leading to transcriptional suppression of the Six3 gene. MTA1 is also a Six3-interacting corepressor that contributes to a self-negative regulation of Six3 transcription by Six3. In contrast, deletion of the MTA1 alleles in murine embryonic fibroblasts or its knockdown in rat retinal ganglion cells stimulates Six3 expression. MTA1 inactivation in the MTA1-null mice results in an elevated Six3 level and proliferation of the retina cells with no obvious abnormities in eye formation. However, unexpectedly, we discovered an enhanced recruitment of Six3 to the rhodopsin chromatin in retina from the MTA1-null mice; Six3's homeodomain interacts with specific DNA elements in the rhodopsin promoter to stimulate its transcription, resulting in increased rhodopsin expression. Further, in holoprosencephaly patients, Six3 protein with a naturally occurring deletion mutation in the helix 3 of the homeodomain does not bind to rhodopsin DNA or stimulate rhodopsin transcription, implying a potential defective rhodopsin pathway in the affected holoprosencephaly patients. Further Six3 cooperates with Crx or NRL in stimulating transcription from the rhodopsin-luc. These findings reveal a previously unrecognized role for the MTA1 as an upstream modifier of Six3 and indicate that Six3 is a direct stimulator of rhodopsin expression, thus revealing a putative role for the MTA1/Six3/rhodopsin pathway in vertebrate eye.
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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.