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Interannual variability of African rainfall impacts local and global communities, but its past behavior and response in future climate projections are poorly understood. This is primarily due to short instrumental records and a lack of long high-resolution palaeoclimate proxy records. Here we present an annually resolved 91,000 year Early Pleistocene record of hydroclimate from the early hominin-bearing Makapansgat Valley, South Africa. Changes in speleothem annual band thickness are dominated by precession over four consecutive orbital cycles with strong millennial-scale periodicity. The frequency of interannual variability (2.0–6.5 yr oscillations) does not change systematically, yet its amplitude is modulated by the orbital forcing. These long-term characteristics of interannual variability are reproduced with transient climate model simulations of water balance for South Africa from the Late Pleistocene to Recent. Based on these results, we suggest that the frequency of interannual variations in southern African rainfall is likely to be stable under anthropogenic warming, but that the size of year-to-year variations may increase. We see an orbitally forced increase in the amplitude of interannual climate variability between 1.8 Ma and 1.7 Ma coincident with the first evidence for the Acheulean stone tool technology.

Erratum : Aging Cell (2006) 5:4, 359-359. VS is in the laboratory of Neurobiologie des processus adaptatifs from 2003; We have studied the mechanisms underlying nonpathological age-related neuronal cell death. Fifty per cent of neurons in the rat enteric nervous system are lost between 12 and 18 months of age in ad libitum (AL) fed rats. Caloric restriction (CR) protects almost entirely against this neuron loss. Using the ROS-sensitive dyes, dihydrorhodamine (DHR) and 2-[6-(4'-hydroxy)phenoxy-3H-xanthen-3-on-9-yl]benzoic acid (HPF) in vitro, we show that the onset of cell death is linked with elevated intraneuronal levels of reactive oxygen species (ROS). Treatment with the neurotrophic factors NT3 and GDNF enhances neuronal antioxidant defence in CR rats at 12-15 months and 24 months but not in adult or aged AL-fed animals. To examine the link between elevated ROS and neuronal cell death, we assessed apoptotic cell death following in vitro treatment with the redox-cycling drug, menadione. Menadione fails to increase apoptosis in 6-month neurons. However, in 12-15mAL fed rats, when age-related cell death begins, menadione induces a 7- to 15-fold increase in the proportion of apoptotic neurons. CR protects age-matched neurons against ROS-induced apoptosis. Treatment with neurotrophic factors, in particular GDNF, rescues neurons from menadione-induced cell death, but only in 12-15mCR animals. We hypothesize that CR enhances antioxidant defence through neurotrophic factor signalling, thereby reducing age-related increases in neuronal ROS levels and in ROS-induced cell death.