The Phosphorus Economy of Mediterranean Oak Saplings Under Global Change

While a severe decrease in phosphorus (P) availability is already taking place in a large number of ecosystems, drought and nitrogen (N) deposition will likely further decrease the availability of P under global change. Plants have developed physiological strategies to cope with decreasing P resources, but it is unclear how these strategies respond to elevated N deposition and summer droughts. We investigated the influence of N and P availability and soil drought on P uptake (H333PO4 feeding experiment) and use efficiencies in young Quercus calliprinos Webb. trees. We hypothesized that (H1) the expected increases in soil N:P ratios will increase the efficiencies of P uptake and use of oak saplings but will decrease the efficiencies of N uptake and use, whereas (H2) drought will affect P uptake efficiency more than N uptake efficiency. In confirmation of (H1) we found that a sharp increase of the soil N:P ratio from 4 to 42 g g-1 significantly increased the instantaneous 33P uptake efficiency (33PUptakeE) by five-fold and long-term P uptake efficiency (PUptakeE) by six-fold, while it decreased N uptake efficiency (NUptakeE) and N use efficiency (NUE). In contradiction to (H1), P use efficiency (PUE) did not respond to the simulated extended gradient of soil N:P ratios but remained relatively constant. (H2) was only partially confirmed as soil drought reduced PUptakeE by up to a fourth at high soil N:P ratios but had no significant effect on NUptakeE. As a consequence, increasing summer droughts may decrease the response of PUptakeE to increasing P limitation, which – in the absence of adjustments of the efficiency of P use – can aggravate growth reductions in this eastern Mediterranean tree species under global change

Surplus Carbon Drives Allocation and Plant-Soil Interactions

Plant growth is usually constrained by the availability of nutrients, water, or temperature, rather than photosynthetic carbon (C) fixation. Under these conditions leaf growth is curtailed more than C fixation, and the surplus photosynthates are exported from the leaf. In plants limited by nitrogen (N) or phosphorus (P), photosynthates are converted into sugars and secondary metabolites. Some surplus C is translocated to roots and released as root exudates or transferred to root-associated microorganisms. Surplus C is also produced under low moisture availability, low temperature, and high atmospheric CO2 concentrations, with similar below-ground effects. Many interactions among above- and below-ground ecosystem components can be parsimoniously explained by the production, distribution, and release of surplus C under conditions that limit plant growth.Non peer reviewe

Root Exudates Induce Soil Macroaggregation Facilitated by Fungi in Subsoil

Subsoils are known to harbor large amounts of soil organic carbon (SOC) and may represent key global carbon (C) sinks given appropriate management. Although rhizodeposition is a major input pathway of organic matter to subsoils, little knowledge exists on C dynamics, particularly stabilization mechanisms, such as soil aggregation, in the rhizosphere of different soil depths. The aim of this study was to investigate the influence of natural and elevated root exudation on C allocation and aggregation in the topsoil and subsoil of a mature European beech (Fagus sylvatica L.) forest. We experimentally added model root exudates to soil at two different concentrations using artificial roots and analyzed how these affect SOC, nitrogen, microbial community composition, and size distribution of water-stable aggregates. Based on the experimental data, a mathematical model was developed to describe the spatial distribution of the formation of soil aggregates and their binding strength. Our results demonstrate that greater exudate additions affect the microbial community composition in favor of fungi which promote the formation of macroaggregates. This effect was most pronounced in the C-poor subsoil, where macroaggregation increased by 86% and SOC content by 10%. Our modeling exercise reproduced the observed increase in subsoil SOC at high exudate additions. We conclude that elevated root exudation has the potential to increase biotic macroaggregation and thus the C sink strength in the rhizosphere of forest subsoils

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment

The renal cortical interstitium: morphological and functional aspects

The renal interstitial compartment, situated between basement membranes of epithelia and vessels, contains two contiguous cellular networks. One network is formed by interstitial fibroblasts, the second one by dendritic cells. Both are in intimate contact with each other. Fibroblasts are interconnected by junctions and connected to basement membranes of vessels and tubules by focal adhesions. Fibroblasts constitute the “skeleton” of the kidney. In the renal cortex, fibroblasts produce erythropoietin and are distinguished from other interstitial cells by their prominent F-actin cytoskeleton, abundance of rough endoplasmic reticulum, and by ecto-5′-nucleotidase expression in their plasma membrane. The resident dendritic cells belong to the mononuclear phagocyte system and fulfil a sentinel function. They are characterized by their expression of MHC class II and CD11c. The central situation of fibroblasts suggests that signals from tubules, vessels, and inflammatory cells converge in fibroblasts and elicit an integrated response. Following tubular damage and inflammatory signals fibroblasts proliferate, change to the myofibroblast phenotype and increase their collagen production, potentially resulting in renal fibrosis. The acquisition of a profibrotic phenotype by fibroblasts in renal diseases is generally considered a main causal event in the progression of chronic renal failure. However, it might also be seen as a repair process

Integrative Genomic Analysis of Cholangiocarcinoma Identifies Distinct IDH -Mutant Molecular Profiles

Cholangiocarcinoma (CCA) is an aggressive malignancy of the bile ducts, with poor prognosis and limited treatment options. Here, we describe the integrated analysis of somatic mutations, RNA expression, copy number, and DNA methylation by The Cancer Genome Atlas of a set of predominantly intrahepatic CCA cases and propose a molecular classification scheme. We identified an IDH mutant-enriched subtype with distinct molecular features including low expression of chromatin modifiers, elevated expression of mitochondrial genes, and increased mitochondrial DNA copy number. Leveraging the multi-platform data, we observed that ARID1A exhibited DNA hypermethylation and decreased expression in the IDH mutant subtype. More broadly, we found that IDH mutations are associated with an expanded histological spectrum of liver tumors with molecular features that stratify with CCA. Our studies reveal insights into the molecular pathogenesis and heterogeneity of cholangiocarcinoma and provide classification information of potential therapeutic significance