Abstract

The regulation of gene expression in trypanosomes is unique. In the absence of transcriptional control at the level of initiation, a subset of Trypanosoma brucei genes form post-transcriptional regulons in which mRNAs are co-regulated in response to differentiation signals.See research articles http://www.biomedcentral.com/1471-2164/10/427, http://www.biomedcentral.com/1471-2164/10/482 and http://www.biomedcentral.com/1471-2164/10/495.

Highlights

  • The kinetoplastid parasites diverged early in the eukaryotic branch of life and several of their members are responsible for some of the great scourges of humanity, including sleeping sickness, Chagas disease and leishmaniasis

  • The ‘TriTryp’ (Leishmania species, T. brucei and T. cruzi) genomes are organized into large gene clusters that are constitutively co-transcribed by RNA polymerase II (Pol II)

  • Recent chromatin immunoprecipitation and sequencing (ChIP-seq) experiments examining the genome-wide distribution of chromatin components in T. brucei showed that the seemingly unregulated transcription of trypanosomes is directed by histone post-translational modifications, indicating the important role that chromatin modifications play in polycistronic transcription initiation and termination [9]

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Summary

Introduction

The kinetoplastid parasites diverged early in the eukaryotic branch of life and several of their members are responsible for some of the great scourges of humanity, including sleeping sickness (caused by Trypanosoma brucei), Chagas disease (caused by Trypanosoma cruzi) and leishmaniasis (caused by Leishmania species). Coordinated post-transcriptional regulation of T. brucei mRNAs during differentiation. Genes in T. brucei are organized into long polycistronic clusters that are co-transcribed by RNA polymerase II (Pol II) to yield polycistronic pre-mRNAs, which are processed by trans-splicing (addition of a capped spliced leader RNA of 39 nucleotides to the 5' terminus of transcripts) and 3'-polyadenylation to generate mature mRNAs. Transcription initiates from divergent strand-switch regions (SSRs) and terminates at convergent SSRs, where tRNA genes are often located ( they can be present at non-SSRs).

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