ena-STUDY-UNIVERSITY OF OXFORD-29-11-2018-09:42:54:514-530
RNA-seq data and analysis (from the side of the insect) in a Drosophila-Herpetomonas interaction model.
Dipteran insects transmit diseases to humans, often in the form of trypanosomatid parasites. To accelerate research in more difficult contexts of dipteran-parasite relationships, we studied the interaction of the model dipteran Drosophila melanogaster and its natural trypanosomatid Herpetomonas muscarum. Parasite infection reduced fecundity but not lifespan in NF-?B/Relish-deficient flies. Gene expression analysis implicated the two NF-?B pathways Toll and Imd as well as STAT signalling. Tissue specific knockdown of key components of these pathways in enterocytes (ECs) and intestinal progenitor cells influenced initial numbers, infection dynamics and time of clearance. Herpetomonas triggered STAT activation and proliferation of Intestinal Stem Cells (ISCs). Loss of Relish suppressed the latter, resulting in increased parasite numbers and delayed clearance. Finally, loss of Toll signalling decreased EC numbers and enabled parasite persistence. This network of signalling may represent a general mechanism of the dipteran early response to trypanosomatids, crucial for parasite establishment and therefore transmission.
Dipteran insects transmit diseases to humans, often in the form of trypanosomatid parasites. To accelerate research in more difficult contexts of dipteran-parasite relationships, we studied the interaction of the model dipteran Drosophila melanogaster and its natural trypanosomatid Herpetomonas muscarum. Parasite infection reduced fecundity but not lifespan in NF-?B/Relish-deficient flies. Gene expression analysis implicated the two NF-?B pathways Toll and Imd as well as STAT signalling. Tissue specific knockdown of key components of these pathways in enterocytes (ECs) and intestinal progenitor cells influenced initial numbers, infection dynamics and time of clearance. Herpetomonas triggered STAT activation and proliferation of Intestinal Stem Cells (ISCs). Loss of Relish suppressed the latter, resulting in increased parasite numbers and delayed clearance. Finally, loss of Toll signalling decreased EC numbers and enabled parasite persistence. This network of signalling may represent a general mechanism of the dipteran early response to trypanosomatids, crucial for parasite establishment and therefore transmission.