The Genome of the Kinetoplastid Parasite, <i>Leishmania major</i>

TLDR

Leishmania species cause a spectrum of human diseases in tropical and subtropical regions of the world. Leishmania major’s genes are organized into long, strand‑specific, polycistronic clusters lacking general transcription factors, indicating distinct RNA polymerase II transcription mechanisms from other eukaryotes, though chromatin remodeling is possible. Sequencing the 36‑chromosome, 32.8‑Mb haploid genome of Leishmania major revealed 8,272 protein‑coding genes (36 % with putative function), 911 RNA genes, and 39 pseudogenes, including host‑pathogen interaction genes, surface glycoconjugate synthesis machinery, and abundant RNA‑binding proteins indicative of active posttranscriptional regulation.

Abstract

Leishmania species cause a spectrum of human diseases in tropical and subtropical regions of the world. We have sequenced the 36 chromosomes of the 32.8-megabase haploid genome of Leishmania major (Friedlin strain) and predict 911 RNA genes, 39 pseudogenes, and 8272 protein-coding genes, of which 36% can be ascribed a putative function. These include genes involved in host-pathogen interactions, such as proteolytic enzymes, and extensive machinery for synthesis of complex surface glycoconjugates. The organization of protein-coding genes into long, strand-specific, polycistronic clusters and lack of general transcription factors in the L. major, Trypanosoma brucei, and Trypanosoma cruzi (Tritryp) genomes suggest that the mechanisms regulating RNA polymerase II-directed transcription are distinct from those operating in other eukaryotes, although the trypanosomatids appear capable of chromatin remodeling. Abundant RNA-binding proteins are encoded in the Tritryp genomes, consistent with active posttranscriptional regulation of gene expression.