H. Kanuka, S.M. Brandt, D.S. Schneider. Microbioligy
and Immunology, Stanford University, Stanford, CA.
Malaria is a devastating public health menace, killing over one
million people every year and infecting about half a billion. The
malaria parasite, Plasmodium, has an intricate lifecycle in both its
vertebrate and insect hosts. We previously showed that the protozoan
Plasmodium gallinaceum, a close relative of the human malaria
parasite Plasmodium falciparum, can develop in the fruit fly
Drosophila melanogaster. To dissect this insect-parasite
relationship and to learn about factors governing an insect's
ability to act as a disease vector, we carried out a genetic screen
in Drosophila to identify mutations affecting these processes. We
screened for mutations that affect a fly's ability to support the
growth of Plasmodium gallinaceum by infecting flies with parasites
and then using real time reverse transcription PCR to determine the
parasite load in each strain. Here we focus on one of the mutants we
identified in which we can observe more Plasmodium growth than in
the wild type strain. We determined the mutated gene encodes a
putative cell-adhesion/recognition receptor protein. We will discuss
about some predicted functions of this gene product in relation to
Plasmodium growth in insect vector. |