ArticleHuman molecular genetics2013
The genome-defence gene Tex19.1 suppresses LINE-1 retrotransposons in the placenta and prevents intra-uterine growth retardation in mice.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Transposable element regulation in mammalian germ cells and other contexts: multilayered repression, fertility, and regulated activation.Epigenomics · 2026Review
- Increased mtDNA mutation frequency in oocytes causes epigenetic alterations and embryonic defects.National science review · 2022Article
- Review
- In silico modeling of the interaction between TEX19 and LIRE1, and analysis of TEX19 gene missense SNPs.Molecular genetics & genomic medicine · 2021Article
- Developmental genome-wide DNA methylation asymmetry between mouse placenta and embryo.Epigenetics · 2020Article
- Tex19.1 inhibits the N-end rule pathway and maintains acetylated SMC3 cohesin and sister chromatid cohesion in oocytes.The Journal of cell biology · 2020Article
- A potential new mechanism for pregnancy loss: considering the role of LINE-1 retrotransposons in early spontaneous miscarriage.Reproductive biology and endocrinology : RB&E · 2020Review
- Meiotic gene activation in somatic and germ cell tumours.Andrology · 2019Review
- Article
- Intrauterine growth retardation-associated syncytin b hypermethylation in maternal rat blood revealed by DNA methylation array analysis.Pediatric research · 2017Article
- Article
- DNA Methylation Divergence and Tissue Specialization in the Developing Mouse Placenta.Molecular biology and evolution · 2017Article
- Tex19.1 promotes Spo11-dependent meiotic recombination in mouse spermatocytes.PLoS genetics · 2017Article
- Human germ/stem cell-specific gene TEX19 influences cancer cell proliferation and cancer prognosis.Molecular cancer · 2017Article
- The impact of transposable elements on mammalian development.Development (Cambridge, England) · 2016Review
- Placental Hypomethylation Is More Pronounced in Genomic Loci Devoid of Retroelements.G3 (Bethesda, Md.) · 2016Article
- Transposable elements in the mammalian embryo: pioneers surviving through stealth and service.Genome biology · 2016Review
- DAZL and CPEB1 regulate mRNA translation synergistically during oocyte maturation.Journal of cell science · 2016Article
- Restricting retrotransposons: a review.Mobile DNA · 2016Review
- Tex19 and Sectm1 concordant molecular phylogenies support co-evolution of both eutherian-specific genes.BMC evolutionary biology · 2015Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
DNA methylation plays an important role in suppressing retrotransposon activity in mammalian genomes, yet there are stages of mammalian development where global hypomethylation puts the genome at risk of retrotransposition-mediated genetic instability. Hypomethylated primordial germ cells appear to limit this risk by expressing a cohort of retrotransposon-suppressing genome-defence genes whose silencing depends on promoter DNA methylation. Here, we investigate whether similar mechanisms operate in hypomethylated trophectoderm-derived components of the mammalian placenta to couple expression of genome-defence genes to the potential for retrotransposon activity. We show that the hypomethylated state of the mouse placenta results in activation of only one of the hypomethylation-sensitive germline genome-defence genes: Tex19.1. Tex19.1 appears to play an important role in placenta function as Tex19.1(-/-) mouse embryos exhibit intra-uterine growth retardation and have small placentas due to a reduction in the number of spongiotrophoblast, glycogen trophoblast and sinusoidal trophoblast giant cells. Furthermore, we show that retrotransposon mRNAs are derepressed in Tex19.1(-/-) placentas and that protein encoded by the LINE-1 retrotransposon is upregulated in hypomethylated trophectoderm-derived cells that normally express Tex19.1. This study suggests that post-transcriptional genome-defence mechanisms are operating in the placenta to protect the hypomethylated cells in this tissue from retrotransposons and suggests that imbalances between retrotransposon activity and genome-defence mechanisms could contribute to placenta dysfunction and disease.
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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.