The Coordination of Leaf Photosynthesis Links C and N Fluxes in C3 Plant Species

Photosynthetic capacity is one of the most sensitive parameters in vegetation models and its relationship to leaf nitrogen content links the carbon and nitrogen cycles. Process understanding for reliably predicting photosynthetic capacity is still missing. To advance this understanding we have tested across C3 plant species the coordination hypothesis, which assumes nitrogen allocation to photosynthetic processes such that photosynthesis tends to be co-limited by ribulose-1,5-bisphosphate (RuBP) carboxylation and regeneration. The coordination hypothesis yields an analytical solution to predict photosynthetic capacity and calculate area-based leaf nitrogen content (Na). The resulting model linking leaf photosynthesis, stomata conductance and nitrogen investment provides testable hypotheses about the physiological regulation of these processes. Based on a dataset of 293 observations for 31 species grown under a range of environmental conditions, we confirm the coordination hypothesis: under mean environmental conditions experienced by leaves during the preceding month, RuBP carboxylation equals RuBP regeneration. We identify three key parameters for photosynthetic coordination: specific leaf area and two photosynthetic traits (k3, which modulates N investment and is the ratio of RuBP carboxylation/oxygenation capacity () to leaf photosynthetic N content (Npa); and Jfac, which modulates photosynthesis for a given k3 and is the ratio of RuBP regeneration capacity (Jmax) to). With species-specific parameter values of SLA, k3 and Jfac, our leaf photosynthesis coordination model accounts for 93% of the total variance in Na across species and environmental conditions. A calibration by plant functional type of k3 and Jfac still leads to accurate model prediction of Na, while SLA calibration is essentially required at species level. Observed variations in k3 and Jfac are partly explained by environmental and phylogenetic constraints, while SLA variation is partly explained by phylogeny. These results open a new avenue for predicting photosynthetic capacity and leaf nitrogen content in vegetation models

The interstitium in cardiac repair: role of the immune-stromal cell interplay

Cardiac regeneration, that is, restoration of the original structure and function in a damaged heart, differs from tissue repair, in which collagen deposition and scar formation often lead to functional impairment. In both scenarios, the early-onset inflammatory response is essential to clear damaged cardiac cells and initiate organ repair, but the quality and extent of the immune response vary. Immune cells embedded in the damaged heart tissue sense and modulate inflammation through a dynamic interplay with stromal cells in the cardiac interstitium, which either leads to recapitulation of cardiac morphology by rebuilding functional scaffolds to support muscle regrowth in regenerative organisms or fails to resolve the inflammatory response and produces fibrotic scar tissue in adult mammals. Current investigation into the mechanistic basis of homeostasis and restoration of cardiac function has increasingly shifted focus away from stem cell-mediated cardiac repair towards a dynamic interplay of cells composing the less-studied interstitial compartment of the heart, offering unexpected insights into the immunoregulatory functions of cardiac interstitial components and the complex network of cell interactions that must be considered for clinical intervention in heart diseases

Régulation du débourrement des bourgeons axillaires par l'intensité lumineuse: modélisation des interactions hormones et sucre.

International audienc

Régulation du débourrement des bourgeons axillaires par l'intensité lumineuse: modélisation des interactions hormones et sucre.

International audienc

The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport

Unc-93 homolog B1 (UNC93B1) is a key regulator of nucleic acid (NA)-sensing Toll-like receptors (TLRs). Loss of NA-sensing TLR responses in UNC93B1-deficient patients facilitates Herpes simplex virus type 1 (HSV-1) encephalitis. UNC93B1 is thought to guide NA-sensing TLRs from the endoplasmic reticulum (ER) to their respective endosomal signaling compartments and to guide the flagellin receptor TLR5 to the cell surface, raising the question of how UNC93B1 mediates differential TLR trafficking. Here, we report that UNC93B1 regulates a step upstream of the differential TLR trafficking process. We discovered that UNC93B1 deficiency resulted in near-complete loss of TLR3 and TLR7 proteins in primary splenic mouse dendritic cells and macrophages, showing that UNC93B1 is critical for maintaining TLR expression. Notably, expression of an ER-retained UNC93B1 version was sufficient to stabilize TLRs and largely restore endosomal TLR trafficking and activity. These data are critical for an understanding of how UNC93B1 can regulate the function of a broad subset of TLRs

Trypanosoma cruzi High Mobility Group B (TcHMGB) can act as an inflammatory mediator on mammalian cells

When an infection occurs, the innate immune cells recognize Pathogen Associated Molec ular Patterns (PAMPs) through their Pattern Recognition Receptors. This triggers an inflammatory response intended to kill the foreign microbe. But inflammation can also be triggered by the recognition of endogenous molecules called “Danger (or Damage) Asso ciated Molecular Patterns” (DAMPs) that are released by damaged or necrotic cells to “ring the alarm” of the immune system that repair is needed, so some of them are also known as “alarmins”. High Mobility group box 1 protein (HMGB1) is a prototypical alar min molecule released by injured cells and it is also actively secreted by cells of the innate immune system in response to invasion as well as to sterile damage. Trypanosoma cruzi, the causal agent of Chagas Disease, has its own HMGB protein that we called TcHMGB. Using in vitro and in vivo experimental systems, we demonstrated for the first time that TcHMGB is able to mediate inflammation on mammalian cells, inducing the expression of both pro-inflammatory and anti-inflammatory cytokines. Our results suggest that the parasite´s protein could have a role in the immune response and the pathogenesis of Cha gas disease, probably overlapping to some extent with the host cell DAMP molecules´ functions.Para citar este articulo: Cribb P, Perdomo V, Alonso VL, Manarin R, Barrios-Paya´n J, Marquina-Castillo B, et al. (2017) Trypanosoma cruzi High Mobility Group B (TcHMGB) can act as an inflammatory mediator on mammalian cells. PLoS Negl Trop Dis 11(2): e0005350. doi:10.1371/journal.pntd.0005350Fil: Cribb, Pamela. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR -CONICET); Argentina.Fil: Cribb, Pamela. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas; Argentina.Fil: Perdomo, Virginia Gabriela. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR -CONICET); Argentina.Fil: Perdomo, Virginia Gabriela. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas; Argentina.Fil: Alonso, Victoria Lucía. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas; Argentina.Fil: Manarin, Romina. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas; Argentina.Fil: Barrios-Payán, Jorge. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán. Sección de Patología Experimental; México.Fil: Marquina-Castillo, Brenda. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán. Sección de Patología Experimental; México.Fil: Tavernelli, Luis. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR -CONICET); Argentina.Fil: Hernández-Pando, Rogelio. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán. Sección de Patología Experimental; México