<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Faria J</submitter><funding>European Research Council</funding><funding>Medical Research Council</funding><funding>Wellcome Trust</funding><pagination>289-300</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7610597</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>6(3)</volume><pubmed_abstract>Highly selective gene expression is a key requirement for antigenic variation in several pathogens, allowing evasion of host immune responses and maintenance of persistent infections&lt;sup>1&lt;/sup>. African trypanosomes-parasites that cause lethal diseases in humans and livestock-employ an antigenic variation mechanism that involves monogenic antigen expression from a pool of >2,600 antigen-coding genes&lt;sup>2&lt;/sup>. In other eukaryotes, the expression of individual genes can be enhanced by mechanisms involving the juxtaposition of otherwise distal chromosomal loci in the three-dimensional nuclear space&lt;sup>3-5&lt;/sup>. However, trypanosomes lack classical enhancer sequences or regulated transcription initiation&lt;sup>6,7&lt;/sup>. In this context, it has remained unclear how genome architecture cont</pubmed_abstract><journal>Nature microbiology</journal><pubmed_title>Spatial integration of transcription and splicing in a dedicated compartment sustains monogenic antigen expression in African trypanosomes.</pubmed_title><pmcid>PMC7610597</pmcid><funding_grant_id>100320/Z/12/Z</funding_grant_id><funding_grant_id>100320</funding_grant_id><funding_grant_id>MR/K015869/1</funding_grant_id><funding_grant_id>715466</funding_grant_id><funding_grant_id>203134/Z/16/Z</funding_grant_id><pubmed_authors>Luzak V</pubmed_authors><pubmed_authors>Hutchinson S</pubmed_authors><pubmed_authors>Muller LSM</pubmed_authors><pubmed_authors>Faria J</pubmed_authors><pubmed_authors>Glover L</pubmed_authors><pubmed_authors>Horn D</pubmed_authors><pubmed_authors>Brink BG</pubmed_authors><pubmed_authors>Siegel TN</pubmed_authors></additional><is_claimable>false</is_claimable><name>Spatial integration of transcription and splicing in a dedicated compartment sustains monogenic antigen expression in African trypanosomes.</name><description>Highly selective gene expression is a key requirement for antigenic variation in several pathogens, allowing evasion of host immune responses and maintenance of persistent infections&lt;sup>1&lt;/sup>. African trypanosomes-parasites that cause lethal diseases in humans and livestock-employ an antigenic variation mechanism that involves monogenic antigen expression from a pool of >2,600 antigen-coding genes&lt;sup>2&lt;/sup>. In other eukaryotes, the expression of individual genes can be enhanced by mechanisms involving the juxtaposition of otherwise distal chromosomal loci in the three-dimensional nuclear space&lt;sup>3-5&lt;/sup>. However, trypanosomes lack classical enhancer sequences or regulated transcription initiation&lt;sup>6,7&lt;/sup>. In this context, it has remained unclear how genome architecture cont</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2026-05-09T08:25:41.664Z</modification><creation>2022-02-10T19:23:10.481Z</creation></dates><accession>S-EPMC7610597</accession><cross_references><pubmed>33432154</pubmed><doi>10.1038/s41564-020-00833-4</doi></cross_references></HashMap>