Abstract
African trypanosomes cause sleeping sickness in humans and nagana in cattle. These unicellular parasites are transmitted by the bloodsucking tsetse fly. In the mammalian host's circulation, proliferating slender stage cells differentiate into cell cycle-arrested stumpy stage cells when they reach high population densities. This stage transition is thought to fulfil two main functions: first, it auto-regulates the parasite load in the host; second, the stumpy stage is regarded as the only stage capable of successful vector transmission. Here, we show that proliferating slender stage trypanosomes express the mRNA and protein of a known stumpy stage marker, complete the complex life cycle in the fly as successfully as the stumpy stage, and require only a single parasite for productive infection. These findings suggest a reassessment of the traditional view of the trypanosome life cycle. They may also provide a solution to a long-lasting paradox, namely the successful transmission of parasites in chronic infections, despite low parasitemia.
Highlights
Trypanosomes are among the most successful parasites
Wholly 87 unexpectedly, slender stages proved at least as competent at infecting flies as stumpy stages. These findings suggest greater plasticity in the life cycle than supposed, prompting a reassessment of the current rigid view of the process. 91 92 Results 93 A single trypanosome is sufficient for infection of a tsetse fly
As the 3’UTR of the protein associated with differentiation 1 (PAD1) gene regulates the expression of pad1 (MacGregor and Matthews, 2012), cells expressing an NLS-GFP reporter fused to the 3' UTR of the PAD1 gene (GFP:PAD1UTR) will have GFP-positive nuclei when the PAD1 gene is active
Summary
Trypanosomes are among the most successful parasites. These flagellated protists infect all vertebrate classes, from fish to mammals, and can cause devastating diseases. The life cycle of T. brucei was initially elucidated more than a century ago As part of their life cycle, the trypanosomes undergo a full developmental program in the tsetse fly in order to become infective to the mammalian host (Koch, 1909b). This finding, made by Kleine in 1909, showed that transmission was not a purely mechanical event (Kleine, 1909). As early as 1912, Robertson suggested that the short, stumpy bloodstream trypanosomes represent the fly-infective stage (Robertson, 1912) While this assumption was questioned several times throughout the 20th century, the discovery of quorum sensing and SIF in the 1990s made it become generally accepted (Vassella et al, 1997). These findings suggest greater plasticity in the life cycle than supposed, prompting a reassessment of the current rigid view of the process. 91
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