Analysis of the role of α-arylphorin in the Heliothis virescens midgut response to Cry1Ac toxin from Bacillus thuringiensis

Homeostasis in the lepidopteran midgut epithelium is maintained by resident pluripotent stem cells that undergo asymmetrical division, whereby one daughter cell retains stem cell properties and the other daughter cell differentiates into either a mature columnar or goblet cell.  These new mature cells move apically to the luminal epithelial surface.  This stem cell-mediated mechanism of midgut regeneration is primarily observed during molting but it has also been observed following the loss of midgut epithelial integrity in Heliothis virescens larvae caused by ingestion of Cry1Ac toxin from the bacterium Bacillus thuringiensis.  Our previous work with in vitro models suggested that Cry1Ac intoxication induces secretion of α-arylphorin, which stimulates stem cell proliferation and differentiation.  Arylphorin, a hexameric storage protein, is synthesized and released by perivisceral fat body during molting, but there is growing evidence which indicates it is synthesized in the midgut epithelium, where it can more effectively mediate the H. virescens immune response to Cry toxin challenge.  In the current work, we present experimental data that further elucidates the mechanisms that mediate biochemical “cross-talk” between α-arylphorin and H. virescens midgut stem cells to control the regenerative response to Cry1Ac-induced midgut damage.