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Trypanosoma brucei has been a subject of ardent scrutiny since it was shown at the turn of the 20th century to be the causative agent of human African trypanosomiasis, then known as sleeping sickness, and Nagana in cattle. Technological advances that began around the start of the 21st century allowed T. brucei to emerge as a bona fide model organism, with an effective and versatile genetic toolkit that facilitates molecular dissection of these fascinating parasites [1]. Other technological advances emerging at the same time allowed biologists to construct a consensual eukaryotic tree of life [2]. This tree (Fig 1) supported T. brucei and related euglenozoans forming their own major clade (Discoba), only distantly related to supergroups like Opisthokonta, which encompasses fungi and animals, and Archaeplastida, which contains land plants. This means that, far from being primitive eukaryotes, trypanosomes have evolved independently of any other model organism for over an eon. Thus, T. brucei and its ilk are not just intrinsically interesting parasites but also attractive models for investigating the evolution of fundamental molecular and cellular biology of eukaryotes from a detached perspective. We have recently delved into the evolutionary cell biology (ECB) of the ancient mitochondrial contact site and cristae organization system (MICOS) protein complex in T. brucei to better understand how it contributes to the architecture of an ancient organelle, the mitochondrion [3,4].

A parasite’s take on the evolutionary cell biology of MICOS