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Ewen, A.

Publications and source records attributed to Ewen, A..

3 recordsLinked to original sources

Quantifying Crop Disease Trait Dynamics through Longitudinal Imaging and Temporal Analytics

Reliable and objective phenotyping is essential for plant breeding programs to characterize genetic variation and accelerate crop improvement. Conventional disease assessment relies on expert visual scoring, which is labor-intensive, subjective, and prone to inter- and intra-rater variability. Although image-based phenotyping methods have been proposed, many require manual intervention, specialized imaging setups, or single time-point measurements, limiting their ability to capture disease progression over time. Here, we present a pipeline for longitudinal plant disease phenotyping that quantifies wheat stripe rust and leaf rust progression from time-series images. The pipeline performs semi-automated leaf and automated pustule segmentation from images acquired in situ, enabling objective disease severity estimation with minimal user intervention and without requiring solid backgrounds or manual leaf manipulation or detachment. By extracting temporal traits, including disease severity trajectories and standardized area under the disease progress curve, the method provides a comprehensive characterization of disease development throughout infection. Association between automated and expert assessments was moderate for stripe rust (R2 = 0.58) and strong for leaf rust (R2 = 0.85), while expert inter-rater reliability was moderate for both diseases (ICC = 0.675 and 0.800, respectively). The proposed approach establishes a scalable and reproducible framework for longitudinal disease phenotyping in controlled environments, with broad applications in disease resistance screening and crop breeding.

bioinformatics↗

DJ-1 mediates regulation of metabolism and immune response in Parkinsons disease astrocytes and Glioblastoma cells

An inverse correlation for the expression of Parkinsons disease (PD)- and cancer-associated genes has been previously reported. Genes that are upregulated in cancer are frequently downregulated in PD and vice versa. PARK7, encoding DJ-1, was initially identified as an oncogene, but loss of DJ-1 causes early-onset PD. However, it remains elusive how differential DJ-1 levels contribute to opposite cell fates in cancer and PD. Here, we demonstrate specific effects of differential DJ-1 protein levels on the energy metabolism and cell growth in patient-derived cellular models of PD and glioblastoma (GBM) cell lines. Impaired energy metabolism was associated with an increased immune response upon IL-1{beta} stimulation and increased apoptosis and decreased cell growth in models of PD, whereas in GBM cells increased metabolic activity translated into a reduced immune response and increased cell growth. Furthermore, we found decreased glutathione (GSH) synthesis and therefore increased levels of reactive oxygen species (ROS) and oxidized glutathione (GSSG) in models of DJ-1 deficiency and decreased ROS levels in GBM cell lines. Thus, the mechanism by which DJ-1 modulates these phenotypes is the same in both diseases. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=84 SRC="FIGDIR/small/621212v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@4eccb4org.highwire.dtl.DTLVardef@161669corg.highwire.dtl.DTLVardef@197bfc3org.highwire.dtl.DTLVardef@1aecb36_HPS_FORMAT_FIGEXP M_FIG C_FIG DJ-1 levels modulate GSSG/GSH ratio and ROS levels, which results in divergent effects on cell growth and immune response in DJ-1-dependent glial pathologies in glioblastoma and PD. In models of PD, DJ-1 level dependent phenotypes can be rescued by antioxidant treatment that reduces the GSSG/GSH ratio and ROS levels.

neuroscience↗

A Th17 cell-intrinsic glutathione/mitochondrial-IL-22 axis protects against intestinal inflammation

Although the intestinal tract is a major site of reactive oxygen species (ROS) generation, the mechanisms by which antioxidant defense in gut T cells contribute to intestinal homeostasis are currently unknown. Here we show, using T cell-specific ablation of the catalytic subunit of glutamate cysteine ligase (Gclc), that the ensuing loss of glutathione (GSH) impairs the production of gut-protective IL-22 by Th17 cells within the lamina propria. Although Gclc ablation does not affect T cell cytokine secretion in the gut of mice at steady-state, infection with C. rodentium increases ROS, inhibits mitochondrial gene expression and mitochondrial function in Gclc-deficient Th17 cells. These mitochondrial deficits affect the PI3K/AKT/mTOR pathway, leading to reduced phosphorylation of the translation repressor 4E-BP1. As a consequence, the initiation of translation is restricted, resulting in decreased protein synthesis of IL-22. Loss of IL-22 results in poor bacterial clearance, enhanced intestinal damage, and high mortality. ROS-scavenging, reconstitution of IL-22 expression or IL-22 supplementation in vivo prevent the appearance of these pathologies. Our results demonstrate the existence of a previously unappreciated role for Th17 cell-intrinsic GSH coupling to promote mitochondrial function, IL-22 translation and signaling. These data reveal an axis that is essential for maintaining the integrity of the intestinal barrier and protecting it from damage caused by gastrointestinal infection. Executive summary- GSH-regulated Th17 cell-derived IL-22, but not IL-17 is required to maintain intestinal barrier integrity and to revent lethality following C. rodentium infection. - GCLC expression in IBD patients correlates positively with expression of genes related to gut integrity. - Gclc-deficient Th17 cells accumulate mitochondrial ROS, which is linked to impaired mitochondrial function, ysregulated PI3K/AKT/mTOR signaling and impaired translation of IL-22. - ROS-scavenging, IL-22 reconstitution or T cell-specific expression of IL-22 in Gclc-deficient T cells rescues utant mice from the lethal infection outcome in vivo.

immunology↗