<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zambrano Siri RT</submitter><funding>Consejo Nacional de Investigaciones Científicas y Técnicas</funding><funding>Canada-Israel Industrial Research and Development Foundation</funding><funding>Agencia Nacional de Promoción de la Investigación, el Desarrollo Tecnológico y la Innovación</funding><funding>Agencia Nacional de Promoción Científica y Tecnológica</funding><pagination>e0343367</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12944795</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(2)</volume><pubmed_abstract>Trypanosoma cruzi, Trypanosoma brucei and Leishmania major, usually known as TriTryps, are the causal agents of animal and human sickness, and are characterized by having complex life cycles, alternating between a mammalian host and an insect vector. Their genes are organized in long transcriptional units that give rise to polycistronic transcripts which maturate into mRNA by a process known as trans-splicing. Among those genes, an important subset is composed of multi-copy genes, which play crucial roles in host invasion and immune evasion. Here, we predicted the most likely trans-splicing acceptor sites (TASs) for TriTryps and found that the average chromatin organization is very similar among them with a mild nucleosome depletion at the TASs, and the same layout is observed in most of the genome. A detailed examination of the nucleosome landscapes resulting from different levels of chromatin digestion in T. brucei shows that an MNase-sensitive complex is protecting the TASs, and it is at least partly composed of histones. Additionally, comparative analysis for single and multi-copy genes in T. cruzi revealed a differential chromatin structure at the TASs suggesting a novel mechanism to guarantee the fidelity of trans-splicing in trypanosomatids.</pubmed_abstract><journal>PloS one</journal><pubmed_title>Beyond the transcript: Chromatin implications in trans-splicing in Trypanosomatids.</pubmed_title><pmcid>PMC12944795</pmcid><funding_grant_id>IDRC-Project 109929</funding_grant_id><funding_grant_id>PICT Raíces 2019-4260</funding_grant_id><funding_grant_id>PICT 2020-00473</funding_grant_id><funding_grant_id>PIP-2021-2023-03073</funding_grant_id><funding_grant_id>PIBBA 2020-28720210100100CO</funding_grant_id><pubmed_authors>Beati P</pubmed_authors><pubmed_authors>Inchausti L</pubmed_authors><pubmed_authors>Smircich P</pubmed_authors><pubmed_authors>Alonso GD</pubmed_authors><pubmed_authors>Ocampo J</pubmed_authors><pubmed_authors>Zambrano Siri RT</pubmed_authors></additional><is_claimable>false</is_claimable><name>Beyond the transcript: Chromatin implications in trans-splicing in Trypanosomatids.</name><description>Trypanosoma cruzi, Trypanosoma brucei and Leishmania major, usually known as TriTryps, are the causal agents of animal and human sickness, and are characterized by having complex life cycles, alternating between a mammalian host and an insect vector. Their genes are organized in long transcriptional units that give rise to polycistronic transcripts which maturate into mRNA by a process known as trans-splicing. Among those genes, an important subset is composed of multi-copy genes, which play crucial roles in host invasion and immune evasion. Here, we predicted the most likely trans-splicing acceptor sites (TASs) for TriTryps and found that the average chromatin organization is very similar among them with a mild nucleosome depletion at the TASs, and the same layout is observed in most of the genome. A detailed examination of the nucleosome landscapes resulting from different levels of chromatin digestion in T. brucei shows that an MNase-sensitive complex is protecting the TASs, and it is at least partly composed of histones. Additionally, comparative analysis for single and multi-copy genes in T. cruzi revealed a differential chromatin structure at the TASs suggesting a novel mechanism to guarantee the fidelity of trans-splicing in trypanosomatids.</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026</publication><modification>2026-07-11T03:18:14.101Z</modification><creation>2026-07-11T03:12:06.859Z</creation></dates><accession>S-EPMC12944795</accession><cross_references><pubmed>41746921</pubmed><doi>10.1371/journal.pone.0343367</doi></cross_references></HashMap>