Fragmentation Increases Impact of Wind Disturbance on Forest Structure and Carbon Stocks in a Western Amazonian Landscape

Tropical second-growth forests could help mitigate climate change, but the degree to which their carbon potential is achieved will depend on exposure to disturbance. Wind disturbance is common in tropical forests, shaping structure, composition, and function, and influencing successional trajectories. However, little is known about the impacts of extreme winds in fragmented landscapes, though second-growth forests are often located in mosaics of forest, pasture, cropland, and other land cover types. Though indirect evidence suggests that fragmentation increases risk of wind damage, few studies have found such impacts following severe storms. In this study, we ask whether fragmentation and forest type (old vs. second growth) were associated with variation in wind damage after a severe convective storm in a fragmented production landscape in western Amazonia. We applied linear spectral unmixing to Landsat 8 imagery from before and after the storm, and combined it with field observations of damage to map wind effects on forest structure and biomass (Figure 4, 5). We also used Landsat 8 imagery to map land cover with the goals of identifying old- and second-growth forest and characterizing fragmentation. We used these data to assess variation in wind disturbance across 95,596 hectares of forest, distributed over 6,110 patches. We find that fragmentation is significantly associated with wind damage, with damage severity higher at forest edges and in edgier, more isolated patches (Figure 7). Damage was more severe in old-growth than in second-growth forests, but this effect was weaker than that of fragmentation (Figure 8). These results illustrate the importance of considering spatial configuration and landscape context in planning tropical forest restoration and predicting carbon sequestration in second-growth forests. Future research should address the mechanisms behind these results, to minimize wind damage risk in second-growth forests so their carbon potential can be maximally achieved

Reversals of Reforestation Across Latin America Limit Climate Mitigation Potential of Tropical Forests

Carbon sequestration through tropical reforestation and natural regeneration could make an important contribution to climate change mitigation, given that forest cover in many tropical regions increased during the early part of the 21st century. The size of this carbon sink will depend on the degree to which second-growth forests are permanent and protected from re-clearing. Yet few studies have assessed permanence of reforestation, especially not at a large spatial scale. Here, we analyzed a 14-year time series (2001–2014) of remotely sensed land-cover data, covering all tropical Latin America and the Caribbean, to quantify the extent of second-growth forest permanence. Our results show that in many cases, reforestation in Latin America and the Caribbean during the early 21st century reversed by 2014, limiting carbon sequestration. In fact, reversals of reforestation, in which some or all gains in forest cover in the early 2000s were subsequently lost, were ten times more common than sustained increases in forest cover. Had reversals of reforestation been avoided, forests could have sequestered 0.58 Pg C, over four times more carbon than we estimate was sequestered after accounting for impermanence (0.14 Pg), representing a loss of 75% of carbon sequestration potential. Differences in the prevalence of reforestation reversals across countries suggest an important role for socio-economic, political, and ecological context, with political transitions and instability increasing the likelihood of reversals. These findings suggest that national commitments to reforestation may fall short of their carbon sequestration goals without provisions to ensure long-term permanence of new forests.Fil: Schwartz, Naomi B.. University of British Columbia; CanadáFil: Aide, T. Mitchell. Universidad de Puerto Rico; Puerto RicoFil: Graesser, Jordan. University of Queensland; AustraliaFil: Grau, Hector Ricardo. Universidad Nacional de Tucumán. Instituto de Ecología Regional. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Instituto de Ecología Regional; ArgentinaFil: Uriarte, María. Columbia University; Estados Unido

Soil biogeochemistry across Central and South American tropical dry forests

The availability of nitrogen (N) and phosphorus (P) controls the flow of carbon (C) among plants, soils, and the atmosphere, thereby shaping terrestrial ecosystem responses to global change. Soil C, N, and P cycles are linked by drivers operating at multiple spatial and temporal scales: landscape-level variation in macroclimate and soil geochemistry, stand-scale heterogeneity in forest composition, and microbial community dynamics at the soil pore scale. Yet in many biomes, we do not know at which scales most of the biogeochemical variation emerges, nor which processes drive cross-scale feedbacks. Here, we examined the drivers and spatial/temporal scales of variation in soil biogeochemistry across four tropical dry forests spanning steep environmental gradients. To do so, we quantified soil C, N, and P pools, extracellular enzyme activities, and microbial community structure across wet and dry seasons in 16 plots located in Colombia, Costa Rica, Mexico, and Puerto Rico. Soil biogeochemistry exhibited marked heterogeneity across the 16 plots, with total organic C, N, and P pools varying fourfold, and inorganic nutrient pools by an order of magnitude. Most soil characteristics changed more across space (i.e., among sites and plots) than over time (between dry and wet season samplings). We observed stoichiometric decoupling among C, N, and P cycles, which may reflect their divergent biogeochemical drivers. Organic C and N pool sizes were positively correlated with the relative abundance of ectomycorrhizal trees and legumes. By contrast, the distribution of soil P pools was driven by soil geochemistry, with larger inorganic P pools in soils with P-rich parent material. Most earth system models assume that soils within a texture class operate similarly, and ignore subgrid cell variation in soil properties. Here we reveal that soil nutrient pools and fluxes exhibit as much variation among four Neotropical dry forests as is observed across terrestrial ecosystems at the global scale. Soil biogeochemical patterns are driven not only by regional differences in soil parent material and climate, but also by local-scale variation in plant and microbial communities. Thus, the biogeochemical patterns we observed across the Neotropical dry forest biome challenge representation of soil processes in ecosystem models

14-3-3 Mediates Histone Cross-Talk during Transcription Elongation in Drosophila

Post-translational modifications of histone proteins modulate the binding of transcription regulators to chromatin. Studies in Drosophila have shown that the phosphorylation of histone H3 at Ser10 (H3S10ph) by JIL-1 is required specifically during early transcription elongation. 14-3-3 proteins bind H3 only when phosphorylated, providing mechanistic insights into the role of H3S10ph in transcription. Findings presented here show that 14-3-3 functions downstream of H3S10ph during transcription elongation. 14-3-3 proteins localize to active genes in a JIL-1–dependent manner. In the absence of 14-3-3, levels of actively elongating RNA polymerase II are severely diminished. 14-3-3 proteins interact with Elongator protein 3 (Elp3), an acetyltransferase that functions during transcription elongation. JIL-1 and 14-3-3 are required for Elp3 binding to chromatin, and in the absence of either protein, levels of H3K9 acetylation are significantly reduced. These results suggest that 14-3-3 proteins mediate cross-talk between histone phosphorylation and acetylation at a critical step in transcription elongation

Multiple Independent Loci at Chromosome 15q25.1 Affect Smoking Quantity: a Meta-Analysis and Comparison with Lung Cancer and COPD

Recently, genetic association findings for nicotine dependence, smoking behavior, and smoking-related diseases converged to implicate the chromosome 15q25.1 region, which includes the CHRNA5-CHRNA3-CHRNB4 cholinergic nicotinic receptor subunit genes. In particular, association with the nonsynonymous CHRNA5 SNP rs16969968 and correlates has been replicated in several independent studies. Extensive genotyping of this region has suggested additional statistically distinct signals for nicotine dependence, tagged by rs578776 and rs588765. One goal of the Consortium for the Genetic Analysis of Smoking Phenotypes (CGASP) is to elucidate the associations among these markers and dichotomous smoking quantity (heavy versus light smoking), lung cancer, and chronic obstructive pulmonary disease (COPD). We performed a meta-analysis across 34 datasets of European-ancestry subjects, including 38,617 smokers who were assessed for cigarettes-per-day, 7,700 lung cancer cases and 5,914 lung-cancer-free controls (all smokers), and 2,614 COPD cases and 3,568 COPD-free controls (all smokers). We demonstrate statistically independent associations of rs16969968 and rs588765 with smoking (mutually adjusted p-values<10$^{−35}$ and <10$^{−8}$ respectively). Because the risk alleles at these loci are negatively correlated, their association with smoking is stronger in the joint model than when each SNP is analyzed alone. Rs578776 also demonstrates association with smoking after adjustment for rs16969968 (p<10$^{−6}$). In models adjusting for cigarettes-per-day, we confirm the association between rs16969968 and lung cancer (p<10$^{−20}$) and observe a nominally significant association with COPD (p = 0.01); the other loci are not significantly associated with either lung cancer or COPD after adjusting for rs16969968. This study provides strong evidence that multiple statistically distinct loci in this region affect smoking behavior. This study is also the first report of association between rs588765 (and correlates) and smoking that achieves genome-wide significance; these SNPs have previously been associated with mRNA levels of CHRNA5 in brain and lung tissue

Abdominal aortic aneurysm is associated with a variant in low-density lipoprotein receptor-related protein 1

Abdominal aortic aneurysm (AAA) is a common cause of morbidity and mortality and has a significant heritability. We carried out a genome-wide association discovery study of 1866 patients with AAA and 5435 controls and replication of promising signals (lead SNP with a p value &lt; 1 × 10-5) in 2871 additional cases and 32,687 controls and performed further follow-up in 1491 AAA and 11,060 controls. In the discovery study, nine loci demonstrated association with AAA (p &lt; 1 × 10-5). In the replication sample, the lead SNP at one of these loci, rs1466535, located within intron 1 of low-density-lipoprotein receptor-related protein 1 (LRP1) demonstrated significant association (p = 0.0042). We confirmed the association of rs1466535 and AAA in our follow-up study (p = 0.035). In a combined analysis (6228 AAA and 49182 controls), rs1466535 had a consistent effect size and direction in all sample sets (combined p = 4.52 × 10-10, odds ratio 1.15 [1.10-1.21]). No associations were seen for either rs1466535 or the 12q13.3 locus in independent association studies of coronary artery disease, blood pressure, diabetes, or hyperlipidaemia, suggesting that this locus is specific to AAA. Gene-expression studies demonstrated a trend toward increased LRP1 expression for the rs1466535 CC genotype in arterial tissues; there was a significant (p = 0.029) 1.19-fold (1.04-1.36) increase in LRP1 expression in CC homozygotes compared to TT homozygotes in aortic adventitia. Functional studies demonstrated that rs1466535 might alter a SREBP-1 binding site and influence enhancer activity at the locus. In conclusion, this study has identified a biologically plausible genetic variant associated specifically with AAA, and we suggest that this variant has a possible functional role in LRP1 expression

Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes.

OBJECTIVE: Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired β-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS: We have conducted a meta-analysis of genome-wide association tests of ∼2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS: Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10(-8)). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 × 10(-4)), improved β-cell function (P = 1.1 × 10(-5)), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10(-6)). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS: We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis

Global maps of soil temperature

Research in global change ecology relies heavily on global climatic grids derived from estimates of air temperature in open areas at around 2 m above the ground. These climatic grids do not reflect conditions below vegetation canopies and near the ground surface, where critical ecosystem functions occur and most terrestrial species reside. Here, we provide global maps of soil temperature and bioclimatic variables at a 1-km2 resolution for 0–5 and 5–15 cm soil depth. These maps were created by calculating the difference (i.e. offset) between in situ soil temperature measurements, based on time series from over 1200 1-km2 pixels (summarized from 8519 unique temperature sensors) across all the world\u27s major terrestrial biomes, and coarse-grained air temperature estimates from ERA5-Land (an atmospheric reanalysis by the European Centre for Medium-Range Weather Forecasts). We show that mean annual soil temperature differs markedly from the corresponding gridded air temperature, by up to 10°C (mean = 3.0 ± 2.1°C), with substantial variation across biomes and seasons. Over the year, soils in cold and/or dry biomes are substantially warmer (+3.6 ± 2.3°C) than gridded air temperature, whereas soils in warm and humid environments are on average slightly cooler (−0.7 ± 2.3°C). The observed substantial and biome-specific offsets emphasize that the projected impacts of climate and climate change on near-surface biodiversity and ecosystem functioning are inaccurately assessed when air rather than soil temperature is used, especially in cold environments. The global soil-related bioclimatic variables provided here are an important step forward for any application in ecology and related disciplines. Nevertheless, we highlight the need to fill remaining geographic gaps by collecting more in situ measurements of microclimate conditions to further enhance the spatiotemporal resolution of global soil temperature products for ecological applications