%0 Journal Article %T Evidence that low endocytic activity is not directly responsible for human serum resistance in the insect form of African trypanosomes %A Senthil KA Natesan %A Lori Peacock %A Ka Leung %A Wendy Gibson %A Mark C Field %J BMC Research Notes %D 2010 %I BioMed Central %R 10.1186/1756-0500-3-63 %X Using a well-characterized procyclic parasite with augmented endocytic flux mediated via TbRab5A overexpression, we found that insect stage parasites were able to grow both in the presence of trypanosome lytic factor (TLF) provided in human serum, and also in tsetse flies. Additionally, by placing blood stage parasites in restricted glucose medium, we observed that enlargement of the flagellar pocket, a key morphology associated with defective endocytosis, manifests in parallel with loss of cellular ATP levels.These observations suggest that a high rate of endocytosis per se is insufficient to render insect form parasites sensitive to TLF or tsetse-derived trypanocidal factors. However, the data do suggest that endocytosis is energetically burdensome, as endocytic activity is rapidly compromised on energy depletion in bloodstream stages. Hence an important aspect of endocytic modulation in the nutrient-poor tsetse midgut is likely energetic conservation.Trypanosoma brucei is the causative agent of African sleeping sickness in humans and similar disease in sylvatic and domestic animals [1] and is transmitted by tsetse flies (genus Glossina). The life cycle involves several proliferative stages, two of which are readily grown in laboratory culture, bloodstream form (BSF) and procyclic form (PCF). The BSF is well known for its ability to evade the adaptive immune response of the mammalian host by antigenic variation. Endocytosis is developmentally regulated in trypanosomes and at least ten-fold up-regulated in BSFs compared to PCFs [2]. Nutrient uptake is a major function of endocytosis for all life stages, but the increased endocytic activity in BSFs potentially also offers protection against the mammalian immune system by efficient recycling of the variant surface glycoprotein (VSG) coat and rapid capping and internalization of anti-VSG antibody [3-5]. However, it is unclear if there is a similar defensive role associated with endocytosis in PCFs, or an adequate expl %U http://www.biomedcentral.com/1756-0500/3/63