ArticleNucleic acids research2026
Genome-wide mapping of replication stress response factors reveals the management of polycistronic transcription, replication initiation, and responses to replication stress in Leishmania.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- ATR, a DNA damage kinase, modulates DNA replication timing in Leishmania major.PLoS genetics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Exposed single-stranded DNA (ssDNA) accumulating at stalled or collapsed replication forks (RFs) can trigger the replication stress response (RSR) to prevent genome instability. Leishmania are parasitic eukaryotes whose plastic genomes facilitate rapid adaptations under stress, with intrinsic replication stress (RS) implicated as a source. Little is known about the Leishmania RSR. Here, we reveal the global dynamics of the RSR in Leishmania major by performing ChIP-seq, focusing on two key RSR proteins, γH2A and RPA1, in the absence and presence of RS. We show that common RS 'hotspots' coincide with DNA replication initiation and transcription termination in Leishmania. When replication is stalled, RSR factors accumulate at early S-phase origins, with a signal pattern reminiscent of bidirectional RF progression. Under chronic RS conditions, increased accumulation of RSR factors emerges at wider sites of transcription initiation, suggesting Leishmania may possess compensatory strategies to limit the effects of RS and ensure DNA replication completion under stress. In contrast, chronic RS enhances RSR factor accumulation at transcription termination sites, highlighting these regions as RS 'hotspots' in Leishmania. Lastly, variations in replication protein A (RPA) dynamics in Ataxia Telangiectasia and Rad3 Related (ATR)-deficient cells uncover crucial roles of this kinase in managing polycistronic transcription and DNA replication, particularly under RS, in Leishmania.
Indexed as
Identifiers
What OpenQuestion holds
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.