ArticleBMC genomics2009
Histone acetylations mark origins of polycistronic transcription in Leishmania major.
Article in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 152 citations in OpenAlex.
- Transcription Start Regions in PTU-intergenic regions drive cell cycle-dependent transcriptional activation events inMicrobiology spectrum · 2026Article
- Genome-wide mapping of replication stress response factors reveals the management of polycistronic transcription, replication initiation, and responses to replication stress in Leishmania.Nucleic acids research · 2026Article
- Histone post-translational modifications of Leishmania braziliensis.Scientific data · 2025Article
- Epigenetic landscape of Leishmania-host interactions.Epigenomics · 2025Review
- RNA synthesis inMicrobiology spectrum · 2025Article
- Trypanosomatid histones: the building blocks of the epigenetic code of highly divergent eukaryotes.The Biochemical journal · 2025Review
- Histone H3 K4 trimethylation occurs mainly at the origins of polycistronic transcription in the genome of Leishmania infantum promastigotes and intracellular amastigotes.BMC genomics · 2025Article
- R-loops acted on by RNase H1 influence DNA replication timing and genome stability in Leishmania.Nature communications · 2025Article
- Mono-allelic epigenetic regulation of polycistronic transcription initiation by RNA polymerase II inmBio · 2025Article
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- Non-coding RNAs as emerging players inFrontiers in cellular and infection microbiology · 2025Article
- Characterization of Tau95 led to the identification of a four-subunit TFIIIC complex in trypanosomatid parasites.Applied microbiology and biotechnology · 2024Article
- Analyses of the essential C82 subunit uncovered some differences in RNA polymerase III transcription betweenParasitology · 2024Article
- Protein phosphatase PP1 regulation of RNA polymerase II transcription termination and allelic exclusion of VSG genes in trypanosomes.Nucleic acids research · 2024Article
- Leishmania PNUTS discriminates between PP1 catalytic subunits through an RVxF-ΦΦ-F motif and polymorphisms in the PP1 C-tail and catalytic domain.The Journal of biological chemistry · 2023Article
- Bromodomain Factor 5 as a Target for Antileishmanial Drug Discovery.ACS infectious diseases · 2023Article
- Knockout of protein phosphatase 1 in Leishmania major reveals its role during RNA polymerase II transcription termination.Nucleic acids research · 2023Article
- Advances in Protozoan Epigenetic Targets and Their Inhibitors for the Development of New Potential Drugs.Pharmaceuticals (Basel, Switzerland) · 2023Review
- The paradigm of intracellular parasite survival and drug resistance in leishmanial parasite through genome plasticity and epigenetics: Perception and future perspective.Frontiers in cellular and infection microbiology · 2023Review
- Localization of Epigenetic Markers inPathogens (Basel, Switzerland) · 2022Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMany components of the RNA polymerase II transcription machinery have been identified in kinetoplastid protozoa, but they diverge substantially from other eukaryotes. Furthermore, protein-coding genes in these organisms lack individual transcriptional regulation, since they are transcribed as long polycistronic units. The transcription initiation sites are assumed to lie within the 'divergent strand-switch' regions at the junction between opposing polycistronic gene clusters. However, the mechanism by which Kinetoplastidae initiate transcription is unclear, and promoter sequences are undefined.
resultsThe chromosomal location of TATA-binding protein (TBP or TRF4), Small Nuclear Activating Protein complex (SNAP50), and H3 histones were assessed in Leishmania major using microarrays hybridized with DNA obtained through chromatin immunoprecipitation (ChIP-chip). The TBP and SNAP50 binding patterns were almost identical and high intensity peaks were associated with tRNAs and snRNAs. Only 184 peaks of acetylated H3 histone were found in the entire genome, with substantially higher intensity in rapidly-dividing cells than stationary-phase. The majority of the acetylated H3 peaks were found at divergent strand-switch regions, but some occurred at chromosome ends and within polycistronic gene clusters. Almost all these peaks were associated with lower intensity peaks of TBP/SNAP50 binding a few kilobases upstream, evidence that they represent transcription initiation sites.
conclusionThe first genome-wide maps of DNA-binding protein occupancy in a kinetoplastid organism suggest that H3 histones at the origins of polycistronic transcription of protein-coding genes are acetylated. Global regulation of transcription initiation may be achieved by modifying the acetylation state of these origins.
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