ArticleNature communications2022
Maternal SMCHD1 regulates Hox gene expression and patterning in the mouse embryo.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Meta-analysis of endometrial transcriptome data reveals novel molecular targets for recurrent implantation failure.Journal of assisted reproduction and genetics · 2024Pooled it
- SMCHD1 loss re-wires MYOD1 enhancer nexuses and chromatin accessibility landscapes in muscle cells.bioRxiv : the preprint server for biology · 2026Article
- Phylogenomic analysis of Cervidae provides insights into antler origin and evolution.Zoological research · 2026Article
- Identification of novel vertebral development factors through UK Biobank candidate gene search and body imaging analysis.Communications biology · 2025Article
- SMCHD1 maintains heterochromatin, genome compartments and epigenome landscape in human myoblasts.Nature communications · 2025Article
- Polycomb function in early mouse development.Cell death and differentiation · 2025Review
- SMCHD1 has separable roles in chromatin architecture and gene silencing that could be targeted in disease.Nature communications · 2023Article
- SMCHD1 and LRIF1 converge at the FSHD-associated D4Z4 repeat and LRIF1 promoter yet display different modes of action.Communications biology · 2023Article
- Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation.Epigenetics & chromatin · 2022Article
- HOX epimutations driven by maternal SMCHD1/LRIF1 haploinsufficiency trigger homeotic transformations in genetically wildtype offspring.Nature communications · 2022Article
Corrections and comments
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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
Parents transmit genetic and epigenetic information to their offspring. Maternal effect genes regulate the offspring epigenome to ensure normal development. Here we report that the epigenetic regulator SMCHD1 has a maternal effect on Hox gene expression and skeletal patterning. Maternal SMCHD1, present in the oocyte and preimplantation embryo, prevents precocious activation of Hox genes post-implantation. Without maternal SMCHD1, highly penetrant posterior homeotic transformations occur in the embryo. Hox genes are decorated with Polycomb marks H2AK119ub and H3K27me3 from the oocyte throughout early embryonic development; however, loss of maternal SMCHD1 does not deplete these marks. Therefore, we propose maternal SMCHD1 acts downstream of Polycomb marks to establish a chromatin state necessary for persistent epigenetic silencing and appropriate Hox gene expression later in the developing embryo. This is a striking role for maternal SMCHD1 in long-lived epigenetic effects impacting offspring phenotype.
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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.