Deoxyribonucleic (DNA) methylation is one of the widespread epigenetic modifications of genomic DNA, and has been postulated to be a predisposing influence on disease onset and infections. The ability to quantify differences in DNA methylation between the genomes of normal vs.stressed Biomphalaria glabrata would help to profile changes potentially linked to resistance to Schistosoma mansoni infection. Thus, this study sought to measure differences in cytosine DNA methylation of various B. glabrata tissues responding over time to either biological or physiological stresses (S. mansoni exposure vs. heat shock). Here, this study measured DNA methylation at the B. glabrataheat shock protein 70 (Bg-hsp 70) intragenic regionto profile the regions methylome with a simple and cost-effective method. The study found DNA hypomethylation of the Bg-hsp 70 region occurs in the snails in response to both stressors; heat shock and parasite exposure, however, overall DNA hypomethylation after heat shock was similar among the tissues examined. In contrast, DNA methylation remained suppressed for up to 5 h when snails were responding to stress from parasite exposure. In parasite exposed snails, the levels of Bg-hsp 70 methylation in whole body, head foot and ovotestis decreased from 30 min to 2 h, and the reduction persisted in the hepatopancreas for up to 5 h. The DNA hypomethylation of the Bg-hsp 70 intragenic region correlated negatively with the level of Bg-hsp 70 mRNA in infected snails but not in thermally stressed snails. From this study results, the study conclude that the hepatopancreas is the most active host organs in terms of differential DNA methylation events following parasite infection. Also, from these data the study postulate that different epigenetic mechanisms underlie, Bg-hsp70 gene regulation in this snails while responding to stress due either to parasite exposure or heat shock.
Key words: DNA methylation, invertebrate, Biomphalaria glabrata, epigenome, Schistosoma manson iinfection, thermal stress.
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