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Biology subjects

Gill, J. S.

Publications and source records attributed to Gill, J. S..

2 recordsLinked to original sources

Harnessing within-cultivar variation to identify hidden genetic resistance using single plant-omics

Fusarium graminearum is a fungal pathogen that causes scab or head blight in small grain cereals and threatens global cereal production. Disease progression varies widely among individual plants of the same cultivar, reflecting both genetic and environmental heterogeneity. This complicates the identification of early host responses, because each individual plant in a population is at a slightly different phase of disease progression. Here we apply single plant-transcriptomics to a population of 121 malt-barley exposed to F. graminearum, enabling us to reconstruct a temporal sequence of regulatory processes during early infection. We identified several disease-resistance associated genetic variants that are already endemic in this high-yielding cultivar, suggesting potential as breeding targets. These variants were within proteins involved in ROS-burst production, a lectin-kinase PRR, and enzymes with DON-detoxification activity. Single plant-transcriptomics offers a novel strategy for characterising early plant-pathogen interactions, turning intra-population heterogeneity from an experimental barrier into an asset.

plant biology↗

Human and mouse cerebellar inhibitory circuits in dystonic crisis and their modulation with therapeutic stimulation

Dystonia is a neurological movement disorder characterized by abnormal muscle contractions that, at their most severe, lead to a life-threatening condition - dystonic crisis. Yet, therapeutic options remain limited by our incomplete understanding of what neural circuits underly the condition. Although cerebellar nuclei neurons are implicated in the origin of baseline dystonic symptoms, it is unclear whether their activity drives dystonic crisis. To explore this role, we found that cerebellar abnormalities and neural inhibition were recurring targets in patients with dystonic crisis, implicating cerebellar inhibitory neurons in its development. We devised a mouse genetics approach to test whether inhibitory cerebellar nuclei neurons (iCNNs) induce dystonic crisis. Directional optogenetic modulation of iCNNs induced dystonic crises on-demand and alleviated spontaneous crises in mice that mimic spontaneous dystonic crises. To investigate whether iCNNs interact with other motor areas during dystonic crisis, we identified monosynaptic iCNN projections to the centrolateral nucleus of the thalamus (CL). Deep brain stimulation of the CL alleviated dystonic crises induced by iCNN photoactivation. Our data uncover a cell type-specific cerebellar origin of dystonic crisis and highlight its therapeutic potential.

neuroscience↗