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. 2013 Nov 22;13(1):165–174. doi: 10.1111/acel.12171

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© 2013 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Protection from Aβ-mediated proteotoxicity by NT219. (A) CL2006 worms were cultivated on EV bacteria and treated with either 600 μm NT219 or the vehicle on days 1 and 2 of adulthood. The worms were placed on plates which supplemented daily with NT219 or the vehicle. Rates of paralysis were scored daily from day 3 to day 12 of adulthood. NT219 significantly reduced the rate of paralysis within the worm population (triangles) compared with the control group (black circles). daf-2 RNAi (open squares) provides more efficient protection compared with NT219. (B) Four independent repeats of the experiment described in A. (C) The knockdown of daf-16 (open circles) or hsf-1 (diamonds) by RNAi completely abolished the protective effect of NT219. (D) Similarly to daf-2 RNAi, NT219 treatment resulted in Aβ hyperaggregation as revealed by WB analysis of high-speed supernatants of CL2006 worms which were treated with the vehicle (Ve), NT219 or with daf-2 RNAi. (E) Immunofluorescence using an Aβ antibody indicates that IIS reduction by either NT219 or daf-2 RNAi leads to the accumulation of Aβ in the center of the worm.