Characterising a novel protein that influences longevity in C. elegans
Timothy Chalmers (1), Myung Jin Kang (1), David Sinclair (1, 2) and Lindsay Wu (1)
School of Medical Sciences, UNSW Sydney, New South Wales, Australia
Paul F Glenn Laboratories for the Biological Mechanisms of Aging, Harvard Medical School, Boston MA, United States
Transposable elements are characterised by an ability to shift location throughout the genome, through either a “cut and paste” or “copy and paste” mechanism. These “cut and paste” elements, or DNA transposons, have previously been supposed to work autonomously within one cell. Previous work, conducted in the Laboratory for Ageing Research, UNSW, uncovered that the uncharacterised putative DNA transposon C09B7.2 mediates longevity in the small roundworm Caenorhabditis elegans (C. elegans). Remarkably this protein exhibits a predicted N-terminal signal peptide, suggesting secretion and non-cell-autonomous transposon activity. Transfection of the mammalian cell line, CHO-K1, with the protein coding region of C09B7.2, results in the presence of C09B7.2 protein in both the cell lysates and media, although absence of a robust negative control leaves definitive secretion, and hence cell-non-autonomous activity, incomplete. Further, we present the generation and confirmation of a novel C09B7.2 overexpression transgenic mutant in C.elegans, inducible by thermal stress. Label-free proteomic analysis for this transgenic mutant suggest a role for C09B7.2 in upregulating DNA binding and transcription pathways. Elucidating the function of C09B7.2 as a potential transposable element remains to be confirmed.