Skip to main content
. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Mech Ageing Dev. 2013 Dec 25;135:41–49. doi: 10.1016/j.mad.2013.12.002

Figure 1. Lack of Ntg1p prevents adaptive mtROS-mediated lifespan extension and elicits mild and conditional effects on respiration.

Figure 1

A. Chronological lifespan (CLS) analysis of wild-type DBY2006 and ntg1Δ following treatment with 50 μM menadione (MD) or ethanol (nt) during exponential growth. In all graphs, data points represent the average viability of three biological replicates and error bars represent the standard error of the mean. B. CLS of wild-type and ntg2Δ as in A. C. CLS of wild-type, tor1Δ, and ntg1Δ/tor1Δ. D. CLS of wild-type and ntg1Δ grown in 20% glucose (nt) or 0.5% glucose (CR). E-F. Analysis of mitochondrial oxygen consumption in wild-type DBY2006 and ntg1Δ strains during exponential growth (OD=0.5, E) and at day one of CLS (48 hours after inoculation, F). Oxygen consumption was measured as %O2/min/OD600, and the wild-type values were set to one. In all graphs, data points represent the mean of three biological replicates and error bars the SEM.