ArticleNature communications2023
Buffering of transcription rate by mRNA half-life is a conserved feature of Rett syndrome models.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 12 citations in OpenAlex.
- P-glycoprotein 1 as a shared target for resensitizing drug-resistant tumor cells and preventing fibronectin-driven metastasis.Theranostics · 2026Article
- Exploring the complexity of MECP2 function in Rett syndrome.Nature reviews. Neuroscience · 2025Review
- RVINN: a flexible modeling for inferring dynamic transcriptional and post-transcriptional regulation using physics-informed neural networks.Bioinformatics (Oxford, England) · 2025Article
- Zebrafish mecp2 null-mutation increases anxiety and cortisol levels but no change in adult social preference and larval chemically-induced hyperlocomotion.BMC neuroscience · 2025Article
- Gene-specific transcript buffering revealed by perturbation of coactivator complexes.Science advances · 2025Article
- Transcriptomic Evidence Reveals the Dysfunctional Mechanism of Synaptic Plasticity Control in ASD.Genes · 2024Article
- Buffering of transcription rate by mRNA half-life is a conserved feature of Rett syndrome models.Nature communications · 2023Article
- Transcriptional buffering and 3'UTR lengthening are shaped during human neurodevelopment by shifts in mRNA stability and microRNA load.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Transcriptional changes in Rett syndrome (RTT) are assumed to directly correlate with steady-state mRNA levels, but limited evidence in mice suggests that changes in transcription can be compensated by post-transcriptional regulation. We measure transcription rate and mRNA half-life changes in RTT patient neurons using RATEseq, and re-interpret nuclear and whole-cell RNAseq from Mecp2 mice. Genes are dysregulated by changing transcription rate or half-life and are buffered when both change. We utilized classifier models to predict the direction of transcription rate changes and find that combined frequencies of three dinucleotides are better predictors than CA and CG. MicroRNA and RNA-binding Protein (RBP) motifs are enriched in 3'UTRs of genes with half-life changes. Nuclear RBP motifs are enriched on buffered genes with increased transcription rate. We identify post-transcriptional mechanisms in humans and mice that alter half-life or buffer transcription rate changes when a transcriptional modulator gene is mutated in a neurodevelopmental disorder.
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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.