ArticleCell cycle (Georgetown, Tex.)2015
Destabilization of pluripotency in the absence of Mad2l2.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- PRDM14 extinction enables the initiation of trophoblast stem cell formation.Cellular and molecular life sciences : CMLS · 2024Article
- REV7: a small but mighty regulator of genome maintenance and cancer development.Frontiers in oncology · 2024Review
- Alternative polyadenylation and dynamic 3' UTR length is associated with polysome recruitment throughout the cardiomyogenic differentiation of hESCs.Frontiers in molecular biosciences · 2024Article
- Zfp296 knockout enhances chromatin accessibility and induces a unique state of pluripotency in embryonic stem cells.Communications biology · 2023Article
- REV7: Jack of many trades.Trends in cell biology · 2021Review
- The Perlman syndrome DIS3L2 exoribonuclease safeguards endoplasmic reticulum-targeted mRNA translation and calcium ion homeostasis.Nature communications · 2020Article
- Unraveling 3'-end RNA uridylation at nucleotide resolution.Methods (San Diego, Calif.) · 2019Review
- MAD2L2 inhibits colorectal cancer growth by promoting NCOA3 ubiquitination and degradation.Molecular oncology · 2018Article
- SPRINT: an SNP-free toolkit for identifying RNA editing sites.Bioinformatics (Oxford, England) · 2017Article
- MAD2L2 Promotes Open Chromatin in Embryonic Stem Cells and Derepresses the Dppa3 Locus.Stem cell reports · 2017Article
- Identification of the first small-molecule inhibitor of the REV7 DNA repair protein interaction.Bioorganic & medicinal chemistry · 2016Article
- Dis3l2-Mediated Decay Is a Quality Control Pathway for Noncoding RNAs.Cell reports · 2016Article
- The multifaceted roles of the HORMA domain in cellular signaling.The Journal of cell biology · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The induction and maintenance of pluripotency requires the expression of several core factors at appropriate levels (Oct4, Sox2, Klf4, Prdm14). A subset of these proteins (Oct4, Sox2, Prdm14) also plays crucial roles for the establishment of primordial germ cells (PGCs). Here we demonstrate that the Mad2l2 (MAD2B, Rev7) gene product is not only required by PGCs, but also by pluripotent embryonic stem cells (ESCs), depending on the growth conditions. Mad2l2(-/-) ESCs were unstable in LIF/serum medium, and differentiated into primitive endoderm. However, they could be stably propagated using small molecule inhibitors of MAPK signaling. Several components of the MAPK cascade were up- or downregulated even in undifferentiated Mad2l2(-/-) ESCs. Global levels of repressive histone H3 variants were increased in mutant ESCs, and the epigenetic signatures on pluripotency-, primitive endoderm-, and MAPK-related loci differed. Thus, H3K9me2 repressed the Nanog promoter, while the promoter of Gata4 lost H3K27me3 and became de-repressed in LIF/serum condition. Promoters associated with genes involved in MAPK signaling also showed misregulation of these histone marks. Such epigenetic modifications could be indirect consequences of mutating Mad2l2. However, our previous observations suggested the histone methyltransferases as direct (G9a) or indirect (Ezh2) targets of Mad2l2. In effect, the intricate balance necessary for pluripotency becomes perturbed in the absence of Mad2l2.
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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.