Noduler augments infection induced cell proliferation through cross-talking with p38 MAPK signaling in wild silkworm, Antheraea mylitta 

Tuesday, November 12, 2013: 11:48 AM
Meeting Room 17 B (Austin Convention Center)
V Satyavathi Valluri , Laboratory of Molecular Genetics, Centre for DNA Fingerprinting and Diagnostics, Hyderabad, Andhra Pradesh, India
We previously identified a novel immune protein Noduler which binds specific bacterial components and elicit nodulation response in the wild silkworm, Antheraea mylitta. Upon bacterial infection, circulating hemocyte population increases significantly in the larval hemolymph resulting in the formation of melanized nodules around bacteria but the underlying signaling pathway is not known. Here, we report decrease in the circulating hemocyte population in the larval hemolymph and reduced phosphosphorylation of p38 mitogen activated protein kinase (MAPK) upon Noduler knockdown. Our result was further validated using immunofluorescence and Western blot analyses. Inhibition of p38 in the infected hemocytes cultured in vitro resulted in reduced cell proliferation and melanization. Based on our results, we show that Noduler is essential for the phosphorylation of p38. This is the first report implicating p38 signaling pathway in nodulation response in silkworms.
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