The Immediate Responses to Irradiation from Imaginal Discs and Hemocytes of Larval Manduca sexta.

Saturday, October 29, 2011
Hall 1-2 (San Jose Convention Center)
Silva Nicholas, BS , Biology, San Francisco State University, San Francisco , CA
Sayed Miry, BS , Biology, San Francisco State University, San Francisco , CA
Megumi Fuse, PhD , Biology, San Francisco State University, San Francisco , CA
Many organisms have the ability to regenerate tissue after extensive damage through a cascade of intracellular events. In the fruitfly Drosophila melanogaster, clusters of progenitor cells known as imaginal discs differentiate into adult structures such as wings and eyes, which show an astounding regenerative capacity after damage. This regeneration results in local and systemic responses as the tissues are repaired, presumably through interactions with the endocrine system. Research suggests that the delay is due to potential blood-borne factors secreted by the damaged imaginal discs. However, due to limited hemolymph (blood) volume in the fruitfly, the physiological mechanisms involved are still unclear. In order to investigate potential blood-borne factors we introduced an alternative insect model with greater hemolymph volume, namely, Manduca sexta. In the current study, we monitored apoptosis in the imaginal discs using Tunel and hemocyte population changes from the hemolymph using flow cytometry, after x-ray irradiation. Our results validate the work in D. melanogaster, where selective damage to imaginal disc following irradiation was noted by increased apoptosis in the imaginal discs. Additionally, several changes in hemocyte populations were noted, including changes in size, morphology, and population density. This data suggests that M. sexta is a strong complementary model to D. melanogaster due to the selective damage at imaginal disc resulting from x-ray irradiation. Moreover, the responses seen in the hemolymph have not yet been described in D. melanogaster, which lead us to hypothesize that the imaginal discs and hemocytes may mediate the delay in development during repair.