Abstract
Biomphalaria glabrata snails that display either resistant or susceptible phenotypes to the parasitic trematode, Schistosoma mansoni provide an invaluable resource towards elucidating the molecular basis of the snail-host/schistosome relationship. Previously, we showed that induction of stress genes either after heat-shock or parasite infection was a major feature distinguishing juvenile susceptible snails from their resistant counterparts. In order to examine this apparent association between heat stress and snail susceptibility, we investigated the effect of temperature modulation in the resistant snail stock, BS-90. Here, we show that, incubated for up to 4 hrs at 32°C prior to infection, these resistant snails became susceptible to infection, i.e. shedding cercariae at 5 weeks post exposure (PE) while unstressed resistant snails, as expected, remained resistant. This suggests that susceptibility to infection by this resistant snail phenotype is temperature-sensitive (ts). Additionally, resistant snails treated with the Hsp 90 specific inhibitor, geldanamycin (GA) after heat stress, were no longer susceptible to infection, retaining their resistant phenotype. Consistently, susceptible snail phenotypes treated with 100 mM GA before parasite exposure also remained uninfected. These results provide direct evidence for the induction of stress genes (heat shock proteins; Hsp 70, Hsp 90 and the reverse transcriptase [RT] domain of the nimbus non-LTR retrotransposon) in B. glabrata susceptibility to S. mansoni infection and characterize the resistant BS-90 snails as a temperature-sensitive phenotype. This study of reversing snail susceptibility phenotypes to S. mansoni provides an opportunity to directly track molecular pathway(s) that underlie the B. glabrata snail's ability to either sustain or destroy the S. mansoni parasite.
Highlights
Schistosomes are parasitic trematodes that cause the chronic debilitating disease schistosomiasis, a neglected tropical disease that persists in over 70 countries of the developing world
To rule out any possibility that the amplicons detected in lanes 1 to 4 might have originated from genomic DNA contamination in RNA preparations utilized for first strand cDNA synthesis, control reactions performed without reverse transcriptase (2M-MLVRT) in the first stand reaction were utilized for PCR amplifications (Fig. 1A, lanes 5 to 8)
We have shown that upregulation of stress-related transcripts, such as those examined in this study, Hsp 70, Hsp 90 and RT in the B. glabrata snail host, soon after infection, plays an important role in their susceptibility to S. mansoni
Summary
Schistosomes are parasitic trematodes that cause the chronic debilitating disease schistosomiasis, a neglected tropical disease that persists in over 70 countries of the developing world. The relative ease of maintaining B. glabrata in the laboratory has enabled it to become the host/pathogen model system of choice in which studies aimed at elucidating the molecular basis of snail/ schistosome interactions are being conducted. Using pedigree snail stocks with varying susceptibility phenotypes, a strong genetic basis was shown to exist for the susceptibility of B. glabrata to S. mansoni [4]. In adult B. glabrata, resistance to S. mansoni has been shown to be a dominant single-gene trait that is inherited by simple Mendelian genetics. Genetics of resistance has been shown to be a complex trait, involving 5 to 6 genes each with multiple alleles. Genetics of susceptibility to the parasite either in juvenile or adult snails has been shown to be multi-genic [5]
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