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991.
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994.
Deqiang Duanmu Charles Bachy Sebastian Sudek Chee-Hong Wong Valeria Jiménez Nathan C. Rockwell Shelley S. Martin Chew Yee Ngan Emily N. Reistetter Marijke J. van Baren Dana C. Price Chia-Lin Wei Adrian Reyes-Prieto J. Clark Lagarias Alexandra Z. Worden 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(44):15827-15832
995.
Temperature drives global patterns in forest biomass distribution in leaves,stems, and roots 总被引:1,自引:0,他引:1
Peter B. Reich Yunjian Luo John B. Bradford Hendrik Poorter Charles H. Perry Jacek Oleksyn 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(38):13721-13726
Whether the fraction of total forest biomass distributed in roots, stems, or leaves varies systematically across geographic gradients remains unknown despite its importance for understanding forest ecology and modeling global carbon cycles. It has been hypothesized that plants should maintain proportionally more biomass in the organ that acquires the most limiting resource. Accordingly, we hypothesize greater biomass distribution in roots and less in stems and foliage in increasingly arid climates and in colder environments at high latitudes. Such a strategy would increase uptake of soil water in dry conditions and of soil nutrients in cold soils, where they are at low supply and are less mobile. We use a large global biomass dataset (>6,200 forests from 61 countries, across a 40 °C gradient in mean annual temperature) to address these questions. Climate metrics involving temperature were better predictors of biomass partitioning than those involving moisture availability, because, surprisingly, fractional distribution of biomass to roots or foliage was unrelated to aridity. In contrast, in increasingly cold climates, the proportion of total forest biomass in roots was greater and in foliage was smaller for both angiosperm and gymnosperm forests. These findings support hypotheses about adaptive strategies of forest trees to temperature and provide biogeographically explicit relationships to improve ecosystem and earth system models. They also will allow, for the first time to our knowledge, representations of root carbon pools that consider biogeographic differences, which are useful for quantifying whole-ecosystem carbon stocks and cycles and for assessing the impact of climate change on forest carbon dynamics.After acquisition via photosynthesis (gross primary production), new plant carbon (C) is respired, transferred to mycorrhizal symbionts, exuded, or converted into new biomass (net primary production). The new biomass can be foliage, stems (including boles, branches, and bark), roots, or reproductive parts. The proportional allocation of new C to these four plant biomass pools, when combined with their turnover rates, results in the proportional distribution of standing biomass among these pools. Such processes can be influenced by plant size, resource supply, and/or climate (1–10). Although simple in concept, our understanding of these processes and our ability to quantify and predict them remain surprisingly rudimentary (3–13).The general lack of knowledge about C partitioning is important for a number of reasons, including its implications for the accuracy of global C cycle modeling and accounting. A recent study (11) concluded
different carbon partitioning schemes resulted in large variations in estimates of global woody carbon flux and storage, indicating that stand-level controls on carbon partitioning are not yet accurately represented in ecosystem models.Uncertainty about C partitioning in relation to biogeography and environmental effects is a particularly critical knowledge gap, because the direct and indirect influence of temperature or moisture availability on biomass partitioning could be important to growth, nutrient cycling, productivity, ecosystem fluxes, and other key plant and ecosystem processes (5, 7–10, 12). Additionally, uncertainty about belowground C allocation and biomass dynamics represents a major information gap that hampers efforts to estimate belowground C pools at continental to global scales (cf. 13 and 14).Some of the limited evidence available supports the hypothesis that under low temperatures both selection and phenotypic plasticity should promote a relatively greater fraction of forest biomass in roots (5, 7, 8, 12, 15–18), as a result of adaptation to low nutrient supply (7, 19–22) driven by low nutrient cycling rates and limited soil solution movement. Cold environments also are often periodically dry and exhibit low plant production (19–26). Belowground resource limitations obviously also rise with increasing shortage of rainfall relative to evaporative demand, which can influence biomass distribution as well (4, 5, 17). Uncertainties include whether there are differences across climate gradients in the fraction of gross primary production respired vs. converted into new biomass; how new biomass is partitioned to foliage, stems, and roots; what the turnover rates are for these different tissues; and what are the consequences of the biomass distribution in foliage, stem, and root. In this study we focus on the last uncertainty—biomass distributions in standing pools—which is a direct consequence of new biomass allocation and subsequent turnover rate. Following optimal partitioning theory (1–4), we posit that the fraction of total forest biomass in roots should increase and in foliage should decrease when belowground resources are scarce.We use a large dataset based on more than 6,200 observations of forest stands in 61 countries (Tables S1–S3 and Fig. 1) to test the following hypotheses: (i) with increasing temperature, proportional biomass distribution (i.e., fraction of total biomass) should decrease in roots and increase in foliage; (ii) with increasing water shortage (estimated by an index of rainfall to evaporative demand), proportional biomass distribution should increase in roots and decrease in foliage; and (iii) gymnosperm and angiosperm forests should follow similar patterns. The dataset comprises data entries for individual stands including total foliage mass per hectare (Mfol), total stem mass per hectare (Mstem), total root mass per hectare (Mroot), and, where available, total mass per hectare (Mtot = Mfol + Mstem + Mroot). Forests were either naturally regenerated or plantations. Stands were classified as gymnosperm or angiosperm based on whichever represented a greater fraction of basal area or biomass; almost all native forests were of mixed species.Open in a separate windowFig. 1.Map showing location of all stands in the assembled database (see Tables S1 and S2 for additional information specific to those with root, foliage, and stem biomass data or with foliage and stem biomass data) across color-coded ranges of MAT.The sampled forests varied widely in age (from 3–400 y) and size (with Mtot ranging from near zero to 300 Mg/ha). Differences in biomass (which we refer to as size) reflect differences in productivity, density, and especially the range of ages of sampled stands. Because tree-size scaling is allometric (3, 4, 7, 9), we use an allometric approach to account for size-related changes in biomass partitioning in examining broad biogeographic patterns. Forests with high biomass have larger trees on average than forests with low biomass (given that tree density typically is lower in the former), so the forest size allometry characterized herein likely has its roots at the individual tree scale, but our analyses use stand Mtot, not individual tree biomass. We also examine biogeographic differences in the fraction of Mtot in foliage (Ffol), stem (Fstem), and root (Froot).The term “allocation” has been used historically to describe both the onward distribution, or flux, of newly acquired substances (usually C or biomass) to different plant functions and differences in how those pools are distributed at any point in time. To minimize confusion about these different measures. we hereafter use the term “allocation” along with “new biomass” or “new C” only to indicate the former and discuss either the proportion of biomass or the fraction of biomass distributed in foliage, stems, or roots to indicate the latter.The sampled forests varied widely geographically and in mean annual temperature (MAT) (from −13 to 29 °C) and mean annual precipitation (MAP) (from 20–420 cm) (Tables S1 and S2 and Fig. 1). Because a number of seasonal and annual climatic factors covary, it is difficult to ascertain which are responsible for the observed patterns (Materials and Methods and SI Materials and Methods). Because MAP is strongly correlated with MAT and is not a good global measure of water availability, we used an aridity index, the ratio of MAP to annual potential evapotranspiration (MAP/PET) (27) as a measure of relative water availability. MAP/PET ranged from <0.5 in cold, high-latitude zones to >3 in temperate and tropical rainforests. The forests ranged from sea level to >4,000 m elevation, with the large majority at <1,000 m elevation. More sampled forests were from Asia and Europe than other continents, and more were boreal and temperate than tropical. Thus, inferences from these data are likely to be most reliable across the gradient from subtropical to cold boreal forests. 相似文献
996.
Younghee Kim Valeria Tarallo Nagaraj Kerur Tetsuhiro Yasuma Bradley D. Gelfand Ana Bastos-Carvalho Yoshio Hirano Reo Yasuma Takeshi Mizutani Benjamin J. Fowler Shengjian Li Hiroki Kaneko Sasha Bogdanovich Balamurali K. Ambati David R. Hinton William W. Hauswirth Razqallah Hakem Charles Wright Jayakrishna Ambati 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(45):16082-16087
997.
Jillian R. Hufgard Jenna L.N. Sprowles Emily M. Pitzer Sheryl E. Koch Min Jiang Qin Wang Xiang Zhang Jacek Biesiada Jack Rubinstein Alvaro Puga Michael T. Williams Charles V. Vorhees 《Journal of applied toxicology : JAT》2019,39(4):603-621
Polychlorinated biphenyls (PCBs) are toxic environmental pollutants. Humans are exposed to PCB mixtures via contaminated food or water. PCB exposure causes adverse effects in adults and after exposure in utero. PCB toxicity depends on the congener mixture and CYP1A2 gene activity. For coplanar PCBs, toxicity depends on ligand affinity for the aryl hydrocarbon receptor (AHR). Previously, we found that perinatal exposure of mice to a three‐coplanar/five‐noncoplanar PCB mixture induced deficits in novel object recognition and trial failures in the Morris water maze in Cyp1a2?/?::Ahrb1 C57BL6/J mice compared with wild‐type mice (Ahrb1 = high AHR affinity). Here we exposed gravid Cyp1a2?/?::Ahrb1 mice to a PCB mixture on embryonic day 10.5 by gavage and examined the F1 and F3 offspring (not F2). PCB‐exposed F1 mice exhibited increased open‐field central time, reduced acoustic startle, greater conditioned contextual freezing and reduced CA1 hippocampal long‐term potentiation with no change in spatial learning or memory. F1 mice also had inhibited growth, decreased heart rate and cardiac output, and impaired fertility. F3 mice showed few effects. Gene expression changes were primarily in F1 PCB males compared with wild‐type males. There were minimal RNA and DNA methylation changes in the hippocampus from F1 to F3 with no clear relevance to the functional effects. F0 PCB exposure during a period of rapid DNA de‐/remethylation in a susceptible genotype produced clear F1 effects with little evidence of transgenerational effects in the F3 generation. While PCBs show clear developmental neurotoxicity, their effects do not persist across generations for effects assessed herein. 相似文献
998.
Pei-Chung Lee Stephanie Elizabeth Zmina Charles Morgan Stopford Jonida Toska Arne Rietsch 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(19):E2027-E2036
Pathogenic Gram-negative bacteria use syringe-like type III secretion systems (T3SS) to inject effector proteins directly into targeted host cells. Effector secretion is triggered by host cell contact, and before contact is prevented by a set of conserved regulators. How these regulators interface with the T3SS apparatus to control secretion is unclear. We present evidence that the proton motive force (pmf) drives T3SS secretion in Pseudomonas aeruginosa, and that the cytoplasmic regulator PcrG interacts with distinct components of the T3SS apparatus to control two important aspects of effector secretion: (i) It coassembles with a second regulator (Pcr1) on the inner membrane T3SS component PcrD to prevent effectors from accessing the T3SS, and (ii) In conjunction with PscO, it controls protein secretion activity by modulating the ability of T3SS to convert pmf.Many Gram-negative bacterial pathogens rely on a type III secretion system (T3SS) to promote disease by directly injecting effector proteins into the cytoplasm of host cells. This apparatus consists of a base that spans the bacterial envelope and a needle that projects from the base and ends in a specialized tip structure. The bacterium secretes two translocator proteins via the T3SS, which insert into the host cell membrane to form a pore, through which effector proteins are then transferred (1, 2).One of the hallmarks of type III secretion is that export of effector proteins is triggered by host cell contact (3–5). The secretion apparatus is fully assembled before cell contact, but effector secretion is prevented through the concerted action of needle tip-associated proteins and regulators that control secretion from the bacterial cytoplasm.In most systems, the needle tip protein prevents premature effector secretion, most likely by allosterically constraining the T3SS in an effector secretion “off” conformation (6–10). PcrG, the needle tip protein chaperone, as well as PopN, a member of the YopN/MxiC family of proteins, control effector secretion from the bacterial cytoplasm in Pseudomonas aeruginosa. PcrG’s regulatory function is independent of its function in promoting the export of needle tip protein PcrV. Deletion of pcrG or pcrV results in partial deregulation of effector secretion, whereas removal of both genes results in high-level secretion of effectors (8). In some bacteria, the needle tip protein promotes its own export with the aid of a self-chaperoning domain, rather than with a separate export chaperone (11). Recent evidence suggests that in these systems, the needle tip protein itself also regulates effector secretion from the cytoplasm, in addition to its regulatory role at the T3SS needle tip (12). The mechanism of this regulation is unclear.YopN/MxiC family proteins, PopN in P. aeruginosa, are T3SS regulators that are exported once effector secretion is triggered (13–17). These proteins control effector secretion from the bacterial cytoplasm (18–20). P. aeruginosa PopN and the closely related YopN associate with three other proteins that are required to prevent premature effector secretion (21–23). For PopN, these three proteins are Pcr1, Pcr2, and PscB. Pcr2 and PscB form a heterodimeric export chaperone, and Pcr1 is thought to tether the PopN complex to the apparatus (23). The prevailing model for explaining how PopN and related regulators control effector secretion is that they partially insert and plug the secretion channel while being tethered to the T3SS, either directly via a C-terminal interaction or indirectly via a C-terminal–associated protein, i.e., Pcr1 in P. aeruginosa (19, 20). The apparatus component with which these regulators interact is unknown, however.Triggering of effector secretion results in the rapid injection of effector proteins into the host cell (4, 5). How this rapid burst of secretion is energized is a matter of some controversy. The flagellum, which also uses a type III secretion mechanism, uses the proton motive force (pmf) to catalyze the rapid export of flagellar subunits. In fact, secretion is possible in mutants lacking the flagellum-associated ATPase, FliI, if the associated regulatory protein, FliH, is eliminated as well (24–26). The pmf’s contribution to the rate of secretion relative to the ATPase has been questioned in the case of virulence-associated T3SS (27), where removal of the ATPase results in a complete block of secretion (28, 29) that is not alleviated by deletion of the associated FliH homolog (30).Here we present evidence that export via the P. aeruginosa T3SS is energized primarily by the pmf, thereby offering a unified model for how protein secretion is energized in all T3SSs. The cytoplasmic T3SS regulator PcrG controls both the access of effectors to the T3SS and, surprisingly, the secretion activity of the apparatus. These two functions are controlled by separate regions of PcrG. Control of secretion activity involves the central portion of PcrG as well as PscO, which regulate the pmf-dependent export of secretion substrates. Mutants that up-regulate translocator secretion without turning on effector export confirm that effector secretion is not blocked by physical obstruction of the secretion channel. Instead, access of effectors to the T3SS is controlled by the C terminus of PcrG in conjunction with the PopN complex through an interaction with the inner membrane T3SS component PcrD. This protein complex likely blocks an acceptor site for effectors. Thus, PcrG is a multifaceted protein that, along with its export chaperone function, serves as a brake and a switch to control effector secretion. 相似文献
999.
Ricardo Ribeiro Dias Fábio Fernandes Félix José Alvarez Ramires Charles Mady Cícero Piva Albuquerque Fábio Biscegli Jatene 《Arquivos brasileiros de cardiologia》2014,103(1):13-18