ArticleNucleic acids research2016
Alu repeats as transcriptional regulatory platforms in macrophage responses to M. tuberculosis infection.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
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- Discovering human transcription factor physical interactions with genetic variants, novel DNA motifs, and repetitive elements using enhanced yeast one-hybrid assays.Genome research · 2019Article
- Genome-wide analysis of polymerase III-transcribedGenome research · 2019Article
- Mycobacterium tuberculosis and macrophage nuclear receptors: What we do and don't know.Tuberculosis (Edinburgh, Scotland) · 2019Review
- Human Survival Motor Neuron genes generate a vast repertoire of circular RNAs.Nucleic acids research · 2019Article
- Macrophage nuclear receptors: Emerging key players in infectious diseases.PLoS pathogens · 2019Review
- Alveolar Macrophage Chromatin Is Modified to Orchestrate Host Response toFrontiers in genetics · 2019Article
- Identification and Classification of Differentially Expressed Genes and Network Meta-Analysis Reveals Potential Molecular Signatures Associated With Tuberculosis.Frontiers in genetics · 2019Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
To understand the epigenetic regulation of transcriptional response of macrophages during early-stage M. tuberculosis (Mtb) infection, we performed ChIPseq analysis of H3K4 monomethylation (H3K4me1), a marker of poised or active enhancers. De novo H3K4me1 peaks in infected cells were associated with genes implicated in host defenses and apoptosis. Our analysis revealed that 40% of de novo regions contained human/primate-specific Alu transposable elements, enriched in the AluJ and S subtypes. These contained several transcription factor binding sites, including those for members of the MEF2 and ATF families, and LXR and RAR nuclear receptors, all of which have been implicated in macrophage differentiation, survival, and responses to stress and infection. Combining bioinformatics, molecular genetics, and biochemical approaches, we linked genes adjacent to H3K4me1-associated Alu repeats to macrophage metabolic responses against Mtb infection. In particular, we show that LXRα signaling, which reduced Mtb viability 18-fold by altering cholesterol metabolism and enhancing macrophage apoptosis, can be initiated at response elements present in Alu repeats. These studies decipher the mechanism of early macrophage transcriptional responses to Mtb, highlighting the role of Alu element transposition in shaping human transcription programs during innate immunity.
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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.