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. 2018 Aug 9;12(8):e0006552.
doi: 10.1371/journal.pntd.0006552. eCollection 2018 Aug.

The snail Biomphalaria glabrata as a model to interrogate the molecular basis of complex human diseases

Joanna M Bridger  1 , Paul J Brindley  2   3 , Matty Knight  2   3   4
Affiliations

The snail Biomphalaria glabrata as a model to interrogate the molecular basis of complex human diseases

Joanna M Bridger et al. PLoS Negl Trop Dis. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. The movement of specific gene loci in Biomphalaria glabrata cell nuclei upon an exposure to miracidia of Schistosoma mansoni.
Panels a and b display nuclei that have been extracted from tissues of snails before (a) and after (b) an exposure to schistosome miracidia (c). The blue fluorescent dye DAPI is used to delineate the nuclei as it intercalates into DNA and the Hsp70 gene loci (green), visualized with a fluorescent dye, after nuclei have been fixed and subjected to FISH, employing specific complimentary probes that bind exclusively to the gene of interest. Panel d is a cartoon representing the movement of gene loci seen after the stimulus of the infection. The white arrows represent the directed and active movement of the gene loci to transcription factories (red stars), with consequent up-regulation (yellow arrows). Scale bar 5 μm. FISH, fluorescence in situ hybridization; Hsp, heat shock protein.
Fig 2
Fig 2. qPCR analysis shows that piwi RNA is differentially regulated in S. mansoni infected in B. glabrata snails depending on their susceptibility phenotypes as follows: Panel A, resistant BS-90 stock; B, susceptible NMRI stock; and C, susceptible BB02 stock.
qPCR was performed as previously reported by Ittiprasert and colleagues (2009) with the following primers: 5′-GTCACACCTACCAGCTACAATG and 3′-GGTTCCCTGCCAGTTGAAATA. NMRI, Naval Medical Research Institute.
Fig 3
Fig 3. Working model with siglec-like–mediated signal transduction in Biomphalaria glabrata cells following stimulation by metabolites (hormone/peptides?) secreted by the schistosome miracidium during infection.
We hypothesize that snail Hsp70 communicates with snail cell surface siglecs to mediate suppression of innate immune responses that, in turn, facilitates productive infection in susceptible genotypes of the snail. By contrast, siglec paralogues in resistant genotypes of the snail fail to transmit Hsp70 amplified signaling, and productive parasitism fails to be supported. Hsp, heat shock protein; siglecs, sialic acid-binding immunoglobulin like lectins.
See this image and copyright information in PMC

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