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The integration of the HIV-1 genome into the host genome is an essential step in the life cycle of the virus and it plays a critical role in the expression, long-term persistence, and reactivation of HIV expression. To better understand the local genomic environment surrounding HIV-1 proviruses, we assessed the influence of non-canonical B-form DNA (non-B DNA) on the HIV-1 integration site selection. We showed that productively and latently infected cells exhibit different integration site biases towards non-B DNA motifs. We identified a correlation between the integration sites of the latent proviruses and non-B DNA features known to potently influence gene expression (e.g., cruciform, guanine-quadruplex (G4), triplex, and Z-DNA). The reactivation potential of latent proviruses with latency reversal agents also correlated with their proximity to specific non-B DNA motifs. The perturbation of G4 structures in vitro using G4 structure-destabilizing or -stabilizing ligands resulted in a significant reduction in integration within 100 base pairs of G4 motifs. The stabilization of G4 structures increased the integration within 300-500 base pairs from G4 motifs, increased integration near transcription start sites, and increased the proportion of latently infected cells. Moreover, we showed that host lens epithelium-derived growth factor (LEDGF)/p75 and cleavage and polyadenylation specificity factor 6 (CPSF6) influenced the distribution of integration sites near several non-B DNA motifs, especially G4 DNA. Our findings identify non-B DNA motifs as important factors that influence productive and latent HIV-1 integration and the reactivation potential of latent proviruses.
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http://dx.doi.org/10.3390/v14112494 | DOI Listing |
Genes (Basel)
August 2025
Division of Pharmacology and Toxicology, Dell Pediatric Research Institute, College of Pharmacy, The University of Texas at Austin, 1400 Barbara Jordan Boulevard, Austin, TX 78723, USA.
Repetitive DNA sequences are abundant in genomes and can adopt alternative DNA structures (i.e., non-B DNA).
View Article and Find Full Text PDFBiol Methods Protoc
August 2025
Département Génomes & Génétique, Institut Pasteur, Université de Paris, CNRS UMR 3525, 25 rue du Dr Roux, 75015, Paris, France.
DNA double-strand breaks (DSBs) represent critical events in genome integrity, arising from both endogenous cellular processes and exogenous factors. These breaks are implicated in various genomic aberrations and chromosomal rearrangements, leading to cancers and genetic disorders. Common and rare fragile sites, containing repetitive elements and non-B DNA structures, are particularly prone to breakage under replication stress, which play a pivotal role in cancer development and genetic diseases.
View Article and Find Full Text PDFMethods Mol Biol
August 2025
Department of Oncology, Dell Medical School, University of Texas at Austin, Austin, TX, USA.
Alternative DNA structures, such as Z-DNA, G-quadruplexes, and mirror repeats, have shown potential involvement in cancer etiology. NBBC (Non-B DNA Burden in Cancer) is a web-based tool designed for quantifying and analyzing non-B DNA motifs within a cancer context. Herein, we provide a step-by-step protocol for employing NBBC, starting with data input and proceeding through the quantification and normalization of non-B DNA motifs that result in calculation of non-B burden.
View Article and Find Full Text PDFChromosome Res
August 2025
Howard Hughes Medical Institute, Fred Hutch Cancer Center, 1100 Fairview Avenue N, Seattle, WA, 98109, USA.
The identification of CENPA, CENPB, and CENPC by Earnshaw and Rothfield 40 years ago has revealed the remarkable diversity and complexity of centromeres and confirmed most seed plants and animals have centromeres comprised of complex satellite arrays. The rapid evolution of centromeres and positive selection on CENPA and CENPC led to the centromere drive model, in which competition between tandem satellite arrays of differing size and centromere strength for inclusion in the egg of animals or megaspore of seed plants during female meiosis drives rapid evolution of centromeres and kinetochore proteins. Here we review recent work showing that non-B-form DNA structures in satellite centromeres make them sites of frequent replication fork stalling, and that repair of collapsed forks by break-induced replication rather than unequal sister chromatid exchange is likely the primary mode of satellite expansion and contraction, providing the variation in satellite copy number that is the raw material of centromere drive.
View Article and Find Full Text PDFInt J Mol Sci
July 2025
Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of Russian Academy of Sciences, Novosibirsk 630090, Russia.
The DNA of all living organisms is a common matrix for both replication and transcription processes. This sometimes leads to inevitable collisions between DNA replication and transcription machinery. There is plethora of evidence demonstrating that such collisions (or TRCs) are one of the most common and significant reasons for genomic instability.
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