Developmental dynamics of mitochondrial mRNA abundance and editing reveal roles for temperature and the differentiation-repressive kinase RDK1 in cytochrome oxidase subunit II mRNA editing

mBio. 2023 Oct 31;14(5):e0185423. doi: 10.1128/mbio.01854-23. Epub 2023 Oct 5.

Abstract

Trypanosoma brucei is the unicellular parasite that causes African sleeping sickness and nagana disease in livestock. The parasite has a complex life cycle consisting of several developmental forms in the human and tsetse fly insect vector. Both the mammalian and insect hosts provide different nutritional environments, so T. brucei must adapt its metabolism to promote its survival and to complete its life cycle. As T. brucei is transmitted from the human host to the fly, the parasite must regulate its mitochondrial gene expression through a process called uridine insertion/deletion editing to achieve mRNAs capable of being translated into functional respiratory chain proteins required for energy production in the insect host. Therefore, it is essential to understand the mechanisms by which T. brucei regulates mitochondrial gene expression during transmission from the mammalian host to the insect vector.

Keywords: RNA editing; Trypanosoma brucei; developmental regulation; differentiation.

MeSH terms

  • Animals
  • Electron Transport Complex IV / genetics
  • Electron Transport Complex IV / metabolism
  • Humans
  • Mammals / metabolism
  • Protozoan Proteins / genetics
  • Protozoan Proteins / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Temperature
  • Trypanosoma brucei brucei* / metabolism
  • Trypanosomiasis, African*
  • Tsetse Flies* / parasitology

Substances

  • Electron Transport Complex IV
  • RNA, Messenger
  • Protozoan Proteins