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A hypothesis for progressive nitrogen limitation (PNL) proposes that net primary production (NPP) will decline through time in ecosystems subjected to a step-function increase in atmospheric CO₂. The primary mechanism driving this response is a rapid rate of N immobilization by plants and microbes under elevated CO₂ that depletes soils of N, causing slower rates of N mineralization. Under this hypothesis, there is little long-term stimulation of NPP by elevated CO₂ in the absence of exogenous inputs of N. We tested this hypothesis using data on the pools and fluxes of C and N in tree biomass, microbes, and soils from 1997 through 2002 collected at the Duke Forest free-air CO₂ enrichment (FACE) experiment. Elevated CO₂ stimulated NPP by 18-24% during the first six years of this experiment. Consistent with the hypothesis for PNL, significantly more N was immobilized in tree biomass and in the O horizon under elevated CO₂. In contrast to the PNL hypothesis, microbial-N immobilization did not increase under elevated CO₂, and although the rate of net N mineralization declined through time, the decline was not significantly more rapid under elevated CO₂. Ecosystem C-to-N ratios widened more rapidly under elevated CO₂ than ambient CO₂ indicating a more rapid rate of C fixation per unit of N, a processes that could delay PNL in this ecosystem. Mass balance calculations demonstrated a large accrual of ecosystem N capital. Is PNL occurring in this ecosystem and will NPP decline to levels under ambient CO₂? The answer depends on the relative strength of tree biomass and O-horizon N immobilization vs. widening C-to-N ratios and ecosystem-N accrual as processes that drive and delay PNL, respectively. Only direct observations through time will definitively answer this question.

Net primary productivity (NPP) is enhanced under future atmospheric [CO₂] in temperate forests representing a broad range of productivity. Yet questions remain in regard to how elevated [CO₂]-induced NPP enhancement may be affected by climatic variations and limiting nutrient resources, as well as how this additional production is distributed among carbon (C) pools of different longevities. Using 10 years of data from the Duke free-air CO₂ enrichment (Duke FACE) site, we show that spatially, the major control of NPP was nitrogen (N) availability, through its control on canopy leaf area index (L). Elevated CO₂ levels resulted in greater L, and thus greater NPP. After canopy closure had occurred, elevated [CO₂] did not enhance NPP at a given L, regardless of soil water availability. Additionally, using published data from three other forest FACE sites and replacing L with leaf area duration (L(D)) to account for differences in growing season length, we show that aboveground NPP responded to [CO₂] only through the enhancement of L(D). For broadleaf forests, the fraction of aboveground NPP partitioned to wood biomass saturated with increasing LD and was not enhanced by [CO₂], whereas it linearly decreased for the conifer forest but was enhanced by [CO₂]. These results underscore the importance of resolving [CO₂] effects on L to assess the response of NPP and C allocation. Further study is necessary to elucidate the mechanisms that control the differential allocation of C among aboveground pools in different forest types.

The partitioning among carbon (C) pools of the extra C captured under elevated atmospheric CO₂ concentration ([CO₂]) determines the enhancement in C sequestration, yet no clear partitioning rules exist. Here, we used first principles and published data from four free-air CO₂ enrichment (FACE) experiments on forest tree species to conceptualize the total allocation of C to below ground (TBCA) under current [CO₂] and to predict the likely effect of elevated [CO₂]. We show that at a FACE site where leaf area index (L) of Pinus taeda L. was altered through nitrogen fertilization, ice-storm damage, and droughts, changes in L, reflecting the aboveground sink for net primary productivity, were accompanied by opposite changes in TBCA. A similar pattern emerged when data were combined from the four FACE experiments, using leaf area duration (L(D)) to account for differences in growing-season length. Moreover, elevated [CO₂]-induced enhancement of TBCA in the combined data decreased from approximately equal to 50% (700 g C m⁻² y⁻¹) at the lowest L(D) to approximately equal to 30% (200 g C m⁻² y⁻¹) at the highest L(D). The consistency of the trend in TBCA with L and its response to [CO₂] across the sites provides a norm for predictions of ecosystem C cycling, and is particularly useful for models that use L to estimate components of the terrestrial C balance.

Ongoing climate change will negatively impact tree populations unless they are able to acclimate to the changes in their local environment. Effective planning for climate adaptation management requires an understanding of the current state of local adaptation and physiological performance to assess whether populations are at risk of local extinction, determine if assisted migration is appropriate, and to select appropriate seed sources if intervention is needed. We established a new reciprocal transplant experiment (ACE, Adaptation to Climate and Environment) across a latitudinal gradient in North America to examine the impacts of warming on three bur oak (Quercus macrocarpa) populations across much of the species range. We established common gardens in Minnesota, Illinois, and Oklahoma with seedlings grown from seeds collected within 50 km of each of those locations from a total of sixty maternal families. We aimed to 1) assess local adaptation in each of the populations using survival and size as fitness metrics, and 2) evaluate physiological responses to different environments along the latitudinal gradient. We found that northern populations are maladapted to hotter climates as evidenced by their low survival, growth, and photosynthetic rates in the warmest common garden. The southernmost population had the highest survival rate, growth rate, and fitness of the three populations in the southernmost garden, providing evidence for local adaptation to the warmest site. However, conditions in the middle garden resulted in the highest fitness and best physiological performance for all populations. Growth and survival were correlated in the middle garden but were decoupled in the northern and southern gardens. This decoupling is likely due to stress associated with the relatively extreme climates in the gardens at the ends of the gradient that led to greater resource allocation to survival than growth. Our results suggest that southern seed sources may perform well in warmer conditions in the north brought on by climate change, which has important implications for managers assisting broadly ranged tree species in adapting to climate change.

Psychiatric disorders are a group of genetically related diseases with highly polygenic architectures. Genome-wide association analyses have made substantial progress towards understanding the genetic architecture of these disorders. More recently, exome- and whole-genome sequencing of cases and families have identified rare, high penetrant variants that provide direct functional insight. There remains, however, a gap in the heritability explained by these complementary approaches. To understand how multiple genetic variants combine to modify both severity and penetrance of a highly penetrant variant, we sequenced 48 whole genomes from a family with a high loading of psychiatric disorder linked to a balanced chromosomal translocation. The (1;11)(q42;q14.3) translocation directly disrupts three genes: DISC1, DISC2, DISC1FP and has been linked to multiple brain imaging and neurocognitive outcomes in the family. Using DNA sequence-level linkage analysis, functional annotation and population-based association, we identified common and rare variants in GRM5 (minor allele frequency (MAF) > 0.05), PDE4D (MAF > 0.2) and CNTN5 (MAF < 0.01) that may help explain the individual differences in phenotypic expression in the family. We suggest that whole-genome sequencing in large families will improve the understanding of the combined effects of the rare and common sequence variation underlying psychiatric phenotypes.

Introduction Longitudinal studies to investigate effects of disease, aging, and clinical interventions on brain volumetry and morphometry rely on the assessment of variance between data sets obtained over time. Conclusions We assumed that subjects did not have structural brain changes between scans and established that the segmentation programs gave reproducible results. [...]we attributed all changes in the experimental variable (ROI voxel counts) to changes in scanner parameters such as head placement and noise.

Recent genome-wide association (GWA) studies described 95 loci controlling serum lipid levels. These common variants explain ∼25% of the heritability of the phenotypes. To date, no unbiased screen for gene-environment interactions for circulating lipids has been reported. We screened for variants that modify the relationship between known epidemiological risk factors and circulating lipid levels in a meta-analysis of genome-wide association (GWA) data from 18 population-based cohorts with European ancestry (maximum N = 32,225). We collected 8 further cohorts (N = 17,102) for replication, and rs6448771 on 4p15 demonstrated genome-wide significant interaction with waist-to-hip-ratio (WHR) on total cholesterol (TC) with a combined P-value of 4.79×10(-9). There were two potential candidate genes in the region, PCDH7 and CCKAR, with differential expression levels for rs6448771 genotypes in adipose tissue. The effect of WHR on TC was strongest for individuals carrying two copies of G allele, for whom a one standard deviation (sd) difference in WHR corresponds to 0.19 sd difference in TC concentration, while for A allele homozygous the difference was 0.12 sd. Our findings may open up possibilities for targeted intervention strategies for people characterized by specific genomic profiles. However, more refined measures of both body-fat distribution and metabolic measures are needed to understand how their joint dynamics are modified by the newly found locus.

Recent work has highlighted a possible role for altered epigenetic modifications, including differential DNA methylation, in susceptibility to psychiatric illness. Here, we investigate blood-based DNA methylation in a large family where a balanced translocation between chromosomes 1 and 11 shows genome-wide significant linkage to psychiatric illness. Genome-wide DNA methylation was profiled in whole-blood-derived DNA from 41 individuals using the Infinium HumanMethylation450 BeadChip (Illumina Inc., San Diego, CA). We found significant differences in DNA methylation when translocation carriers (n = 17) were compared to related non-carriers (n = 24) at 13 loci. All but one of the 13 significant differentially methylated positions (DMPs) mapped to the regions surrounding the translocation breakpoints. Methylation levels of five DMPs were associated with genotype at SNPs in linkage disequilibrium with the translocation. Two of the five genes harbouring significant DMPs, DISC1 and DUSP10, have been previously shown to be differentially methylated in schizophrenia. Gene Ontology analysis revealed enrichment for terms relating to neuronal function and neurodevelopment among the genes harbouring the most significant DMPs. Differentially methylated region (DMR) analysis highlighted a number of genes from the MHC region, which has been implicated in psychiatric illness previously through genetic studies. We show that inheritance of a translocation linked to major mental illness is associated with differential DNA methylation at loci implicated in neuronal development/function and in psychiatric illness. As genomic rearrangements are over-represented in individuals with psychiatric illness, such analyses may be valuable more widely in the study of these conditions.