ArticleThe EMBO journal2021
RIF1 and KAP1 differentially regulate the choice of inactive versus active X chromosomes.
Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Xist in X chromosome inactivation: mechanisms and disease relevance.Cell communication and signaling : CCS · 2025Review
- RIF1 controls replication timing in early mouse embryos independently of lamina-associated nuclear organization.Developmental cell · 2025Article
- RIF1 integrates DNA repair and transcriptional requirements during the establishment of humoral immune responses.Nature communications · 2025Article
- Establishment and maintenance of random monoallelic expression.Development (Cambridge, England) · 2024Review
- Orchestrating Asymmetric Expression: Mechanisms behindEpigenomes · 2024Review
- RIF1 regulates early replication timing in murine B cells.Nature communications · 2023Article
- Regulatory principles and mechanisms governing the onset of random X-chromosome inactivation.Current opinion in genetics & development · 2023Review
- Review
- RIF1 and KAP1 differentially regulate the choice of inactive versus active X chromosomes.The EMBO journal · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The onset of random X chromosome inactivation in mouse requires the switch from a symmetric to an asymmetric state, where the identities of the future inactive and active X chromosomes are assigned. This process is known as X chromosome choice. Here, we show that RIF1 and KAP1 are two fundamental factors for the definition of this transcriptional asymmetry. We found that at the onset of differentiation of mouse embryonic stem cells (mESCs), biallelic up-regulation of the long non-coding RNA Tsix weakens the symmetric association of RIF1 with the Xist promoter. The Xist allele maintaining the association with RIF1 goes on to up-regulate Xist RNA expression in a RIF1-dependent manner. Conversely, the promoter that loses RIF1 gains binding of KAP1, and KAP1 is required for the increase in Tsix levels preceding the choice. We propose that the mutual exclusion of Tsix and RIF1, and of RIF1 and KAP1, at the Xist promoters establish a self-sustaining loop that transforms an initially stochastic event into a stably inherited asymmetric X-chromosome state.
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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.