Accumulating evidence highlights increased mortality risks for trees during severe drought, particularly under warmer temperatures and increasing vapour pressure deficit (VPD). Resulting forest die-off events have severe consequences for ecosystem services, biophysical and biogeochemical land-atmosphere processes. Despite advances in monitoring, modelling and experimental studies of the causes and consequences of tree death from individual tree to ecosystem and global scale, a general mechanistic understanding and realistic predictions of drought mortality under future climate conditions are still lacking. We update a global tree mortality map and present a roadmap to a more holistic understanding of forest mortality across scales. We highlight priority research frontiers that promote: (1) new avenues for research on key tree ecophysiological responses to drought; (2) scaling from the tree/plot level to the ecosystem and region; (3) improvements of mortality risk predictions based on both empirical and mechanistic insights; and (4) a global monitoring network of forest mortality. In light of recent and anticipated large forest die-off events such a research agenda is timely and needed to achieve scientific understanding for realistic predictions of drought-induced tree mortality. The implementation of a sustainable network will require support by stakeholders and political authorities at the international level.
SummaryUpward transport of CO 2 via the transpiration stream from belowground to aboveground tissues occurs in tree stems. Despite potentially important implications for our understanding of plant physiology, the fate of internally transported CO 2 derived from autotrophic respiratory processes remains unclear.We infused a 13 CO 2 -labeled aqueous solution into the base of 7-yr-old field-grown eastern cottonwood (Populus deltoides) trees to investigate the effect of xylem-transported CO 2 derived from the root system on aboveground carbon assimilation and CO 2 efflux. The 13 C label was transported internally and detected throughout the tree. Up to 17% of the infused label was assimilated, while the remainder diffused to the atmosphere via stem and branch efflux. The largest amount of assimilated 13 C was found in branch woody tissues, while only a small quantity was assimilated in the foliage. Petioles were more highly enriched in 13 C than other leaf tissues.Our results confirm a recycling pathway for respired CO 2 and indicate that internal transport of CO 2 from the root system may confound the interpretation of efflux-based estimates of woody tissue respiration and patterns of carbohydrate allocation.
Understanding which species are able to recover from drought, under what conditions, and the mechanistic processes involved, will facilitate predictions of plant mortality in response to global change. In response to drought, some species die because of embolism-induced hydraulic failure, whilst others are able to avoid mortality and recover, following rehydration. Several tree species have evolved strategies to avoid embolism, whereas others tolerate high embolism rates but can recover their hydraulic functioning upon drought relief. Here, we focus on structures and processes that might allow some plants to recover from drought stress via embolism reversal. We provide insights into how embolism repair may have evolved, anatomical and physiological features that facilitate this process, and describe possible trade-offs and related costs. Recent controversies on methods used for estimating embolism formation/repair are also discussed, providing some methodological suggestions. Although controversial, embolism repair processes are apparently based on the activity of phloem and ray/axial parenchyma. The mechanism is energetically demanding, and the costs to plants include metabolism and transport of soluble sugars, water and inorganic ions. We propose that embolism repair should be considered as a possible component of a 'hydraulic efficiency-safety' spectrum. We also advance a framework for vegetation models, describing how vulnerability curves may change in hydrodynamic model formulations for plants that recover from embolism.
See also the Commentary by Cernusak and Cheesman
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