Individual variability in tree allometry determines light resource allocation in forest ecosystems: a hierarchical Bayesian approach

Tree species differences in crown size and shape are often highlighted as key characteristics determining light interception strategies and successional dynamics. The phenotypic plasticity of species in response to light and space availability suggests that intraspecific variability can have potential consequences on light interception and community dynamics. Species crown size varies depending on site characteristics and other factors at the individual level which differ from competition for light and space. These factors, such as individual genetic characteristics, past disturbances or environmental micro-site effects, combine with competition-related phenotypic plasticity to determine the individual variability in crown size. Site and individual variability are typically ignored when considering crown size and light interception by trees, and residual variability is relegated to a residual error term, which is then ignored when studying ecological processes. In the present study, we structured and quantified variability at the species, site, and individual levels for three frequently used tree allometric relations using fixed and random effects in a hierarchical Bayesian framework. We focused on two species: Abies alba (silver fir) and Picea abies (Norway spruce) in nine forest stands of the western Alps. We demonstrated that species had different allometric relations from site to site and that individual variability accounted for a large part of the variation in allometric relations. Using a spatially explicit radiation transmission model on real stands, we showed that individual variability in tree allometry had a substantial impact on light resource allocation in the forest. Individual variability in tree allometry modulates species’ light-intercepting ability. It generates heterogeneous light conditions under the canopy, with high light micro-habitats that may promote the regeneration of light-demanding species and slow down successional dynamics.     

Shifts in the height‐related competitiveness of tree species following recent climate warming and implications for tree community composition: the case of common beech and sessile oak as predominant broadleaved species in Europe

Height growth is a trait that contributes to tree species fitness. How height growth responds to environmental changes may therefore provide indications on species ability to compete and maintain, and on changes in tree community composition. Common beech Fagus sylvatica and sessile oak Quercus petraea are the predominant late‐successional broadleaved species in Europe, and they differ in their shade‐tolerance. On common beech (a shade tolerant species), recent observations across Europe have shown a growth decline during recent climate warming. Because sessile oak is a warmth‐ and light‐demanding species, we therefore hypothesised that it may gain in competitiveness relative to common beech. We conducted analyses of historical height growth in several regions spanning the distributional range of the two species across a temperate‐continental gradient in France. Common beech and sessile oak were sampled in two and four regions, respectively, and were compared in two neighbouring regions. We documented the climatic and nutritional conditions of regional samples. Height growth of 408 trees of various ages was reconstituted from stem analyses. We estimated 20th‐century regional chronologies of height growth using a statistical modelling approach that filtered out the effects of ontogeny and site fertility. In regions where both species were sampled, modelled height trajectories were compared at different periods over the 20th century. Growth chronologies revealed 1) long‐term growth rate increases of a magnitude of 50–100% over 100 years in both species, more acute in the continental domain, 2) recurrent historical inversions in growth fluctuations between species, 3) a recent divergence, with growth decline in common beech versus a dramatic growth increase in sessile oak, more acute in colder regions. The analysis of height trajectories indicated a recent reduction in common beech competitiveness relative to sessile oak. In the face of future climate warming, we conclude that increased prevalence of beech–oak mixtures may arise.     

Nitrogen footprint in a long-term observation of forest growth over the twentieth century

Environmental drivers of forest productivity increases have been much debated. Evidence for the suggested role of increasing nitrogen supply is lacking over long-term time scales. Tracking the footprint of environmental factors by using long-term growth records may thus prove decisive. We analysed growth chronologies of common beech in two areas of contrasting nutritional status in France. Dominant height growth was used as a proxy for productivity. Growth was compared between old and young paired stands sampled at the same sites to factor out effects of ageing and site. Growth chronologies were estimated with a statistical modelling procedure. The environmental causality of growth changes was addressed by combining (1) a comparison of growth changes between regions, (2) a regional comparison of growth chronologies with chronologies of environmental factors and (3) growth–environment relationships established from climate/soil data. Historical growth increases followed very similar courses in the two areas. Remarkably, the magnitude of change was 50% lower in the area that had reduced nutritional status and nitrogen deposition. Historical variations in environmental factors and growth were congruent with the roles of nitrogen availability and deposition, and of atmospheric CO₂ increase. Low-frequency variations in climate and growth were not coincident. However, our analysis demonstrated the role of climatic anomalies in short-term growth variations. Growth–environment relationships further indicated a nitrogen constraint. These observations corroborate the enhancing role of increased nitrogen availability on forest biomass accumulation previously reported in ecosystem experiments and process-based modelling explorations.     

Il1-β Involvement in Cognitive Impairment after Sepsis

Sepsis is defined as the host's reaction to infection and characterised by a systemic inflammatory response with important clinical implications. Central nervous system dysfunction secondary to sepsis is associated with local generation of pro- and anti-inflammatory cytokines, impaired cerebral microcirculation, an imbalance of neurotransmitters, apoptosis and cognitive impairment. It's known that the IL-1β is one of the first cytokines to be altered. Thus, the objective of this study was to evaluate the role of IL-1β in cognitive parameters in brain tissue through the use of an IL-1β (IL-1ra) receptor antagonist up to 10 days and to assess blood–brain barrier permeability, cytokine levels, oxidative parameters and energetic metabolism up to 24 h, after sepsis induction. To this aim, we used sham-operated Wistar rats or submitted to the cecal ligation and perforation (CLP) procedure. Immediately after, the animals received one dose of 10 μg of IL-1ra. After 24 h, the rats were killed and were evaluated for biochemical parameters in the pre-frontal cortex, hippocampus and striatum. After 10 days, the animals were submitted to the habituation to the open field and step-down inhibitory avoidance task. We observed that the use of IL-1ra reverted the increase of blood–brain barrier permeability in the pre-frontal cortex, hippocampus and striatum; the increase of IL-1β, IL1-6 and TNF-α levels in the pre-frontal cortex and striatum; the decrease of complex I activity in the pre-frontal, hippocampus and striatum; the increase of oxidative parameters in pre-frontal cortex, hippocampus and striatum; and cognitive impairment. In conclusion, the results observed in this study reinforce the role of acute brain inflammatory response, in particular, the IL1β response, in the cognitive impairment associated with sepsis.     

Coadministration of Branched-Chain Amino Acids and Lipopolysaccharide Causes Matrix Metalloproteinase Activation and Blood–Brain Barrier Breakdown

Maple syrup urine disease (MSUD) is an inborn error of metabolism caused by a severe deficiency in the activity of the branched-chain α-keto acid dehydrogenase complex, leading to accumulation of the branched-chain amino acids (BCAA) leucine, isoleucine, and valine. Infections have a significant role in precipitating acute metabolic decompensation in patients with MSUD; however, the mechanisms underlying the neurotoxicity in this disorder are poorly understood. In this study, we subjected rats to the coadministration of lipopolysaccharide (LPS), which is a major component of gram-negative bacteria cell walls, and high concentrations of BCAA (H-BCAA) to determine their effects on the permeability of the blood–brain barrier (BBB) and on the levels of matrix metalloproteinases (MMP-2 and MMP-9). Our results demonstrated that the coadministration of H-BCAA and LPS causes breakdown of the BBB and increases the levels of MMP-2 and MMP-9 in the hippocampus of these rats. On the other hand, examination of the cerebral cortex of the 10- and 30-day-old rats revealed a significant difference in Evan’s Blue content after coadministration of H-BCAA and LPS, as MMP-9 levels only increased in the cerebral cortex of the 10-day-old rats. In conclusion, these results suggest that the inflammatory process associated with high levels of BCAA causes BBB breakdown. Thus, we suggest that BBB breakdown is relevant to the perpetuation of brain inflammation and may be related to the brain dysfunction observed in MSUD patients.     

Excision of 8-methylguanine site-specifically incorporated into oligonucleotide substrates by the AlkA protein of Escherichia coli

8-Methyl-2'-deoxyguanosine (8-medGuo) has been shown to be a major stable alkylation product of 2'-deoxyguanosine induced by methyl radical attack on DNA. Moreover, by using primer extension assays, the latter DNA modification has recently been reported to be a miscoding lesion by generating G to C and G to T transversions and deletions in vitro. However, no data have been reported up to now, concerning the processing of this C8-alkylated nucleoside by the DNA repair machinery. Therefore, we have investigated the capability of excision of 8-methylguanine (8-meGua) site specifically incorporated into oligonucleotide substrates by several bacterial, yeast and mammalian DNA N-glycosylases. The results show that the 3-methyladenine (3-meAde) DNA glycosylase II (AlkA protein) from Escherichia coli is the only DNA N-glycosylase tested able to remove 8-meGua from double-stranded DNA fragments. Moreover, the activity of AlkA for 8-meGua varied markedly depending on the opposite base in DNA, being the highest with Adenine and Thymine and the lowest with Cytosine and Guanine. The removal of 8-meGua by AlkA protein was compared to that of 7-methylguanine (7-meGua) and hypoxanthine (Hx). The rank of damage as a substrate for AlkA being 7-meGua>8-meGua>Hx. In contrast, the human 3-meAde DNA N-glycosylase (Mpg) is not able to release 8-meGua paired with any of the four DNA bases. We also show that, DNA N-glycosylases involved in the removal of oxidative damage, such as Fpg or Nth proteins from E. coli, Ntg1, Ntg2 or Ogg1 proteins of Saccharomyces cerevisiae, or human Ogg1 do not release 8-meGua placed opposite any of the four DNA bases. Furthermore, HeLa and Chinese hamster ovary (CHO) cell free protein extracts do not show any cleavage activity at 8-meGua paired with adenine or cytosine, which suggests the absence of base excision repair (BER) of this lesion in mammalian cells.     

Excision repair of 8-hydroxyguanine in mammalian cells: the mouse Ogg1 protein as a model

8-Hydroxyguanine (8-OH-Gua) is a major mutagenic lesion produced on DNA by the oxidative stress induced by either the endogen metabolism or the exposure to external agents. In bacteria and yeast this modified base can be removed by specific DNA glycosylases. Recently a human gene coding for an 8-OH-Gua DNA glycosylase/AP lyase has been identified by its homology to the yeast OGG1. This gene is located in human chromosome 3p25, a region commonly rearranged in various cancers, specially in lung tumor cells. We report here the cloning, by sequence homology to the yeast OGG1, of a mouse cDNA coding for a 8-OH-Gua DNA glycosylase with 84% and 38% identity to the human and yeast relevant proteins, respectively. The Ogg1 gene is localized to the mouse chromosome 6E. The mouse Ogg1 cDNA, when expressed in Escherichia coli, is capable of suppressing the spontaneous mutator phenotype of a DNA repair deficient fpg mutY strain. The mouse Ogg1 protein acts efficiently on duplexes in which the 8-OH-Gua is paired with a cytosine but is inactive on 8-OH-Gua:Ade pair, consistently with its proposed biological role in the avoidance of mutations. A comparison of the mouse enzyme with other eukaryotic Ogg1 enzymes is also presented. The isolation of this gene will allow the development of an animal model to study the effects of oxidative stress on carcinogenesis and degenerative diseases.     

N-acetylcysteine effects on a murine model of chronic critical limb ischemia

During chronic limb ischemia, oxidative damage and inflammation are described. Besides oxidative damage, the decrease of tissue oxygen levels is followed by several adaptive responses. The purpose of this study was to determine whether supplementation with N-acetylcysteine (NAC) is effective in an animal model of chronic limb ischemia. Chronic limb ischemia was induced and animals were treated once a day for 30 consecutive days with NAC (30 mg/kg). After this time clinical scores were recorded and soleus muscle was isolated and lactate levels, oxidative damage and inflammatory parameters were determined. In addition, several mechanisms associated with hypoxia adaptation were measured (vascular endothelial growth factor - VEGF and hypoxia inducible factor - HIF levels, ex vivo oxygen consumption, markers of autophagy/mitophagy, and mitochondrial biogenesis). The adaptation to chronic ischemia in this model included an increase in muscle VEGF and HIF levels, and NAC was able to decrease VEGF, but not HIF levels. In addition, ex vivo oxygen consumption under hypoxia was increased in muscle from ischemic animals, and NAC was able to decrease this parameter. This effect was not mediated by a direct effect of NAC on oxygen consumption. Ischemia was followed by a significant increase in muscle myeloperoxidase activity, as well as interleukin-6 and thiobarbituric acid reactive substances species levels. Supplementation with NAC was able to attenuate inflammatory and oxidative damage parameters, and improve clinical scores. In conclusion, NAC treatment decreases oxidative damage and inflammation, and modulates oxygen consumption under hypoxic conditions in a model of chronic limb ischemia.