Project description:Acute Oak Decline (AOD) is a decline-disease currently spreading in Britain, threatening oak trees. Here, we analyze and compare the proteomes of inner bark tissue sampled from oak stems of trees symptomatic with AOD and non-symptomatic trees.
Project description:The liver can fully regenerate after partial resection and its underlying mechanisms have been extensively studied. The liver can also rapidly regenerate after injury with most studies focusing on hepatocyte proliferation; however, how hepatic necrotic lesions during acute or chronic liver diseases are eliminated and repaired remains obscure. Here we demonstrate that monocyte-derived macrophages (MoMFs) are rapidly recruited to and encapsulate necrotic areas during immune-mediated liver injury, and this feature is essential in repairing necrotic lesions. At the early stage of injury, infiltrating MoMFs activate the JAG1-NOTCH2 axis to induce cell death-resistant SOX9+ hepatocytes near the necrotic lesions, which acts as a barrier from further injury. Subsequently, necrotic environment (hypoxia and dead cells) induces a cluster of C1q+MoMFs that promote necrotic removal and liver repair, while Pdgfb+MoMFs activate hepatic stellate cells (HSCs) to express a-smooth muscle actin and induce a strong contraction signal (YAP, pMLC) to squeeze and finally eliminate the necrotic lesions. In conclusion, MoMFs play a key role in repairing the necrotic lesions not only by removing necrotic tissues but also by inducing cell death resistant hepatocytes to form a perinecrotic capsule and by activating a-smooth actin expressing HSCs to facilitate necrotic lesion resolution.
Project description:Atherosclerosis is a leading cause of death due to the rupture of arterial lesions characterized by a necrotic core and inflammatory activity. Although lesion vulnerability follows a diurnal pattern with a higher incidence of rupture in the morning, the role of circadian rhythms in atherosclerotic lesions is unclear. Here we show that apoptosis in lesions follows a diurnal pattern that is controlled through the circadian regulation of the pro-apoptotic XIAP associated factor 1 (Xaf1) by the Mir21 strands. The increased apoptosis during the transition from the inactive to the active phase is not matched with the efferocytic removal of dead cells resulting in increased necrotic core formation. Lack of Mir21 expression in macrophages decreases atherosclerosis and necrotic core formation in mice, suggesting that Mir21-mediated diurnal apoptosis promotes lesion growth. In human atherosclerotic lesions, apoptosis also follows a diurnal pattern with a peak in the morning and oscillates in-phase with XAF1 expression and anti-phase with miR-21 expression. Thus, diurnal apoptosis regulated by a Mir21-controlled macrophage death clock may contribute to circadian regulation of lesion vulnerability.
Project description:The aim of this experiment was to determine if the development of resistance to antibiotics can be driven by the concentration and speciation of Cu. Experimental setup was designed to investigate two hypotheses for which two strains of Gram- bacteria have been selected: - Do TE enhance AR in resistant bacteria? Resistant strain: Bioluminescent Pseudomonas aeruginosa PAO1 (Xen41, Tetracycline resistant) - Do TE induce AR in sensitive bacteria? Sensitive strain: Pseudomonas aeruginosa PAO1 (Wild Type)
Project description:The pathological interaction between oak trees and Phytophthora cinnamomi has implications in the cork oak decline observed over the last decades in the Iberian Peninsula. During host colonization, the phytopathogen secretes effector molecules like elicitins to increase disease effectiveness. The objective of this study was to unravel the proteome changes associated to with the cork oak immune response triggered by P. cinnamomi inoculation in a long-term assay, through SWATH-MS quantitative proteomics performed in the oak leaves. Using the Arabidopis thaliana proteome database as a reference, 424 proteins have been confidently quantified in cork oak leaves, of which 80 proteins showed a p-value below 0.05 or a fold-change greater than 2 or less than 0.5 in their levels between control and inoculated samples being considered as altered. The inoculation of cork oak roots with P. cinnamomi increased the levels of proteins associated with protein-DNA complex assembly, lipid oxidation, response to endoplasmic reticulum stress, and pyridine-containing compound metabolic process in the leaves. In opposition, several proteins associated with cellular metabolic compound salvage and monosaccharide catabolic process had significantly decreased abundances. The most significant abundance variations were observed for the Ribulose 1,5-Bisphosphate Carboxylase small subunit (RBCS1A), Heat Shock protein 90-1 (Hsp90-1), Lipoxygenase 2 (LOX2) and Histone superfamily protein H3.3 (A8MRLO/At4G40030) revealing a pertinent role for these proteins in the host-pathogen interaction mechanism. This work represents the first SWATH-MS analysis performed in cork oak plants inoculated with P. cinnamomi and highlights host proteins that have a relevant action in the homeostatic states that emerge from the interaction between the oomycete and the host in the long term and in a distal organ.