Rainfall seasonality dominates critical precipitation threshold for the Amazon forest in the LPJmL vegetation model.

Understanding the Amazon Rainforest's response to shifts in precipitation is paramount with regard to its sensitivity to climate change and deforestation. Studies using Dynamic Global Vegetation Models (DGVMs) typically only explore a range of socio-economically plausible pathways. In this study, we applied the state-of-the-art DGVM LPJmL to simulate the Amazon forest's response under idealized scenarios where precipitation is linearly decreased and subsequently increased between current levels and zero. Our results indicate a nonlinear but reversible relationship between vegetation Above Ground Biomass (AGB) and Mean Annual Precipitation (MAP), suggesting a threshold at a critical MAP value, below which vegetation biomass decline accelerates with decreasing MAP. We find that approaching this critical threshold is accompanied by critical slowing down, which can hence be expected to warn of accelerating biomass decline with decreasing rainfall. The critical precipitation threshold is lowest in the northwestern Amazon, whereas the eastern and southern regions may already be below their critical MAP thresholds. Overall, we identify the seasonality of precipitation and the potential evapotranspiration (PET) as the most important parameters determining the threshold value. While vegetation fires show little effect on the critical threshold and the biomass pattern in general, the ability of trees to adapt to water stress by investing in deep roots leads to increased biomass and a lower critical threshold in some areas in the eastern and southern Amazon where seasonality and PET are high. Our findings underscore the risk of Amazon forest degradation due to changes in the water cycle, and imply that regions that are currently characterized by higher water availability may exhibit heightened vulnerability to future drying.

Critical transitions in the Amazon forest system.

The possibility that the Amazon forest system could soon reach a tipping point, inducing large-scale collapse, has raised global concern1-3. For 65 million years, Amazonian forests remained relatively resilient to climatic variability. Now, the region is increasingly exposed to unprecedented stress from warming temperatures, extreme droughts, deforestation and fires, even in central and remote parts of the system1. Long existing feedbacks between the forest and environmental conditions are being replaced by novel feedbacks that modify ecosystem resilience, increasing the risk of critical transition. Here we analyse existing evidence for five major drivers of water stress on Amazonian forests, as well as potential critical thresholds of those drivers that, if crossed, could trigger local, regional or even biome-wide forest collapse. By combining spatial information on various disturbances, we estimate that by 2050, 10% to 47% of Amazonian forests will be exposed to compounding disturbances that may trigger unexpected ecosystem transitions and potentially exacerbate regional climate change. Using examples of disturbed forests across the Amazon, we identify the three most plausible ecosystem trajectories, involving different feedbacks and environmental conditions. We discuss how the inherent complexity of the Amazon adds uncertainty about future dynamics, but also reveals opportunities for action. Keeping the Amazon forest resilient in the Anthropocene will depend on a combination of local efforts to end deforestation and degradation and to expand restoration, with global efforts to stop greenhouse gas emissions.

A Novel Mechanism for SIRT1 Activators That Does Not Rely on the Chemical Moiety Immediately C-Terminal to the Acetyl-Lysine of the Substrate.

SIRT1, an NAD+-dependent deacetylase, catalyzes the deacetylation of proteins coupled with the breakdown of NAD+ into nicotinamide and 2'-O-acetyl-ADP-ribose (OAADPr). Selective SIRT1 activators have potential clinical applications in atherosclerosis, acute renal injury, and Alzheimer's disease. Here, we found that the activity of the potent SIRT1 activator CWR is independent of the acetylated substrate. It adopts a novel mechanism to promote SIRT1 activity by covalently bonding to the anomeric C1' carbon of the ribose ring in OAADPr. In addition, CWR is highly selective for SIRT1, with no effect on SIRT2, SIRT3, SIRT5, or SIRT6. The longer distance between the anomeric C1' carbon of the ribose ring in OAADPr and Arg274 of SIRT1 (a conserved residue among sirtuins) than that between the anomeric C1' carbon in OAADPr and the Arg of SIRT2, SIRT3, SIRT5, and SIRT6, should be responsible for the high selectivity of CWR for SIRT1. This was confirmed by site-directed mutagenesis of SIRT3. Consistent with the in vitro assays, the activator also reduced the acetylation levels of p53 in a concentration-dependent manner via SIRT1 in cells. Our study provides a new perspective for designing SIRT1 activators that does not rely on the chemical moiety immediately C-terminal to the acetyl-lysine of the substrate.