Benchmark Forecasts for Climate Change

We assessed three important criteria of forecastability—simplicity, certainty, and variability. Climate is complex due to many causal variables and their variable interactions. There is uncertainty about causes, effects, and data. Using evidence-based (scientific) forecasting principles, we determined that a naïve no change extrapolation method was the appropriate benchmark. To be useful to policy makers, a proposed forecasting method would have to provide forecasts that were substantially more accurate than the benchmark. We calculated benchmark forecasts against the UK Met Office Hadley Centre\u27s annual average thermometer data from 1850 through 2007. For 20- and 50-year horizons the mean absolute errors were 0.18°C and 0.24°C. The accuracy of forecasts from our naïve model is such that even perfect forecasts would be unlikely to help policy makers. We nevertheless evaluated the Intergovernmental Panel on Climate Change\u27s 1992 forecast of 0.03°C-per-year temperature increases. The small sample of errors from ex ante forecasts for 1992 through 2008 was practically indistinguishable from the naïve benchmark errors. To get a larger sample and evidence on longer horizons we backcast successively from 1974 to 1850. Averaged over all horizons, IPCC errors were more than seventimes greater than errors from the benchmark. Relative errors were larger for longer backcast horizons

UV-B perceived by the UVR8 photoreceptor inhibits plant thermomorphogenesis

Small increases in ambient temperature can elicit striking effects on plant architecture, collectively termed thermomorphogenesis [1]. In Arabidopsis thaliana, these include marked stem elongation and leaf elevation, responses that have been predicted to enhance leaf cooling [ 2, 3, 4 and 5]. Thermomorphogenesis requires increased auxin biosynthesis, mediated by the bHLH transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) [ 6, 7 and 8], and enhanced stability of the auxin co-receptor TIR1, involving HEAT SHOCK PROTEIN 90 (HSP90) [9]. High-temperature-mediated hypocotyl elongation additionally involves localized changes in auxin metabolism, mediated by the indole-3-acetic acid (IAA)-amido synthetase Gretchen Hagen 3 (GH3).17 [10]. Here we show that ultraviolet-B light (UV-B) perceived by the photoreceptor UV RESISTANCE LOCUS 8 (UVR8) [11] strongly attenuates thermomorphogenesis via multiple mechanisms inhibiting PIF4 activity. Suppression of thermomorphogenesis involves UVR8 and CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1)-mediated repression of PIF4 transcript accumulation, reducing PIF4 abundance. UV-B also stabilizes the bHLH protein LONG HYPOCOTYL IN FAR RED (HFR1), which can bind to and inhibit PIF4 function. Collectively, our results demonstrate complex crosstalk between UV-B and high-temperature signaling. As plants grown in sunlight would most likely experience concomitant elevations in UV-B and ambient temperature, elucidating how these pathways are integrated is of key importance to the understanding of plant development in natural environments