ArticleCell reports2021
Correct dosage of X chromosome transcription is controlled by a nuclear pore component.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Transcription initiation drives dosage compensation establishment and maintenance in maleScience advances · 2026Article
- Sex Chromosome Dosage Compensation in Insects.Insects · 2025Review
- Fission yeast essential nuclear pore protein Nup211 regulates the expression of genes involved in cytokinesis.PloS one · 2024Article
- Nuclear transport proteins: structure, function, and disease relevance.Signal transduction and targeted therapy · 2023Review
- You are who your friends are-nuclear pore proteins as components of chromatin-binding complexes.FEBS letters · 2023Review
- Dosage Compensation inInternational journal of molecular sciences · 2022Review
- ZC3HC1 is a structural element of the nuclear basket effecting interlinkage of TPR polypeptides.Molecular biology of the cell · 2022Article
- Article
- Using Single Molecule RNA FISH to Determine Nuclear Export and Transcription Phenotypes in Drosophila Tissues.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Review
- Modulation of Global Gene Expression by Aneuploidy and CNV of Dosage Sensitive Regulatory Genes.Genes · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Dosage compensation in Drosophila melanogaster involves a 2-fold transcriptional upregulation of the male X chromosome, which relies on the X-chromosome-binding males-specific lethal (MSL) complex. However, how such 2-fold precision is accomplished remains unclear. Here, we show that a nuclear pore component, Mtor, is involved in setting the correct levels of transcription from the male X chromosome. Using larval tissues, we demonstrate that the depletion of Mtor results in selective upregulation at MSL targets of the male X, beyond the required 2-fold. Mtor and MSL components interact genetically, and depletion of Mtor can rescue the male lethality phenotype of MSL components. Using RNA fluorescence in situ hybridization (FISH) analysis and nascent transcript sequencing, we find that the effect of Mtor is not due to defects in mRNA export but occurs at the level of nascent transcription. These findings demonstrate a physiological role for Mtor in the process of dosage compensation, as a transcriptional attenuator of X chromosome gene expression.
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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.