Anatomical and chemical characteristics associated with lodging resistance in wheat

Anatomical and chemical characteristics of stems affect lodging in wheat (Triticum aestivum L.) cultivars. Traits associated with lodging resistance, such as plant height, stem strength, culm wall thickness, pith diameter, and stem diameter, were extensively investigated in earlier studies. However, the solid stem trait was rarely considered. In this study, we measured a range of anatomical and chemical characteristics on solid and hollow stemmed wheat cultivars. Significant correlations were detected between resistance to lodging and several anatomical features, including width of mechanical tissue, weight of low internodes, and width of stem walls. Morphological features that gave the best indication of improved lodging resistance were increased stem width, width of mechanical tissue layer, and stem density. Multiple linear regression analysis showed that 99% of the variation in lodging resistance could be explained by the width of the mechanical tissue layer, suggesting that solid stemmed wheat has several anatomical features for increasing resistance to lodging. In addition, microsatellite markers GWM247 and GWM340 were linked to a single solid stem QTL on chromosome 3BL in a population derived from the cross Xinongshixin (solid stem)/Line 3159 (hollow stem). These markers should be valuable in breeding wheat for solid stem

Spatial population distribution dynamics of big cats and ungulates with seasonal and disturbance changes in temperate natural forest

Wildlife conservation and management in human-dominated landscapes are major concerns for wildlife ecologists and managers. The dynamics of human disturbance, combined with seasonal limitations in the availability of nutritious foods, may restrict wildlife population growth and recovery. However, understanding how large mammal species adjust their population distribution in forest habitats with seasonal changes in food and disturbances requires a deeper and more extensive analysis. In this study, we found that three ungulate species, roe deer (Capreolus pygargus), sika deer (Cervus nippon), and wild boar (Sus scrofa), employ robust, conservative, and flexible distribution strategies, respectively, to adapt to the effects of seasonal changes and human disturbances. Moreover, croplands, villages, and grazing have some negative effects on the distribution of roe deer and sika deer, while wild boar can be highly abundant near human land use. Additionally, roe deer, sika deer, and wild boar are also affected by the abundance of shrub species they consume. During the cold season, the populations of the Amur tiger (Panthera tigris altaica) and Amur leopard (P. pardus orientalis) were primarily located near roads and dense forests, respectively. In the warm season, the distribution of both big cats was influenced by prey abundance, and Amur tigers also avoided grazing livestock. Nevertheless, the negative effects of human land use on Amur tigers and wild boars increased during the warm season, which was attributed to more frequent human activities during that time. Consequently, it is crucial to implement season-specific habitat management, particularly by regulating human disturbances during the warm season, in order to promote the recovery and expansion of populations of big cats and ungulates

Zdhhc2 Is Essential for Plasmacytoid Dendritic Cells Mediated Inflammatory Response in Psoriasis

International audienceZdhhc family genes are composed of 24 members that regulate palmitoylation, a post-translational modification process for proteins. Mutations in genes that alter palmitoylation orde-palmitoylation could result in neurodegenerative diseases and inflammatory disorders. Inthis study, we found that Zdhhc2 was robustly induced in psoriatic skin and loss of Zdhhc2in mice by CRISPR/Cas9 dramatically inhibited pathology of the ear skin followingimiquimod treatment. As psoriasis is an inflammatory disorder, we analyzed tissueinfiltrating immune cells and cytokine production. Strikingly we found that a masterpsoriatic cytokine interferon-a(IFN-a) in the lesioned skin of wildtype (WT) mice was 23-fold higher than that in Zdhhc2 deficient counterparts. In addition, we found that CD45+white blood cells (WBC) infiltrating in the skin of Zdhhc2 deficient mice were also significantlyreduced. Amelioration in psoriasis and dramatically reduced inflammation of Zdhhc2deficient mice led us to analyze the cellular components that were affected by loss ofZdhhc2. We found that imiquimod induced plasmacytoid dendritic cell (pDC) accumulationin psoriatic skin, spleen, and draining lymph nodes (DLN) were drastically decreased inZdhhc2 deficient mice, and the expression of pDC activation marker CD80 also exhibitedsignificantly inhibited in psoriatic skin. In further experiments, we confirmed the cell intrinsiceffect of Zdhhc2 on pDCs as we found that loss of zDHHC2 in human CAL-1 pDCdampened both interferon regulatory factor 7 (IRF7) phosphorylation and IFN-aproduction.Therefore, we identified novel function of Zdhhc2 in controlling inflammatory response inpsoriasis in mice and we also confirmed that crucial role of Zdhhc2 in pDCs by regulatingIRF7 activity and production of the critical cytokine. Our resultsfinding the dependence ofIFN-aproduction on Zdhhc2 in inflamed murine skin and in human pDCs provide rationalefor targeting this new molecule in treatment of inflammation

Excessive immunosuppression by regulatory T cells antagonizes T cell response to schistosome infection in PD-1-deficient mice

Schistosomiasis is caused by parasitic flatworms known as schistosomes and affects over 200 million people worldwide. Prevention of T cell exhaustion by blockade of PD-1 results in clinical benefits to cancer patients and clearance of viral infections, however it remains largely unknown whether loss of PD-1 could prevent or cure schistosomiasis in susceptible mice. In this study, we found that S. japonicum infection dramatically induced PD-1 expression in T cells of the liver where the parasites chronically inhabit and elicit deadly inflammation. Even in mice infected by non-egg-producing unisex parasites, we still observed potent induction of PD-1 in liver T cells of C57BL/6 mice following S. japonicum infection. To determine the function of PD-1 in schistosomiasis, we generated PD-1-deficient mice by CRISPR/Cas9 and found that loss of PD-1 markedly increased T cell count in the liver and spleen of infected mice. IL-4 secreting Th2 cells were significantly decreased in the infected PD-1-deficient mice whereas IFN-γ secreting CD4 + and CD8 + T cells were markedly increased. Surprisingly, such beneficial changes of T cell response did not result in eradication of parasites or in lowering the pathogen burden. In further experiments, we found that loss of PD-1 resulted in both beneficial T cell responses and amplification of regulatory T cells that prevented PD-1-deficient T cells from unleashing anti-parasite activity. Moreover, such PD-1-deficient Tregs exert excessive immunosuppression and express larger amounts of adenosine receptors CD39 and CD73 that are crucial for Treg-mediated immunosuppression. Our experimental results have elucidated the function of PD-1 in schistosomiasis and provide novel insights into prevention and treatment of schistosomiasis on the basis of modulating host adaptive immunity

Excessive immunosuppression by regulatory T cells antagonizes T cell response to schistosome infection in PD-1-deficient mice

Schistosomiasis is caused by parasitic flatworms known as schistosomes and affects over 200 million people worldwide. Prevention of T cell exhaustion by blockade of PD-1 results in clinical benefits to cancer patients and clearance of viral infections, however it remains largely unknown whether loss of PD-1 could prevent or cure schistosomiasis in susceptible mice. In this study, we found that S . japonicum infection dramatically induced PD-1 expression in T cells of the liver where the parasites chronically inhabit and elicit deadly inflammation. Even in mice infected by non-egg-producing unisex parasites, we still observed potent induction of PD-1 in liver T cells of C57BL/6 mice following S . japonicum infection. To determine the function of PD-1 in schistosomiasis, we generated PD-1-deficient mice by CRISPR/Cas9 and found that loss of PD-1 markedly increased T cell count in the liver and spleen of infected mice. IL-4 secreting Th2 cells were significantly decreased in the infected PD-1-deficient mice whereas IFN-γ secreting CD4 + and CD8 + T cells were markedly increased. Surprisingly, such beneficial changes of T cell response did not result in eradication of parasites or in lowering the pathogen burden. In further experiments, we found that loss of PD-1 resulted in both beneficial T cell responses and amplification of regulatory T cells that prevented PD-1-deficient T cells from unleashing anti-parasite activity. Moreover, such PD-1-deficient Tregs exert excessive immunosuppression and express larger amounts of adenosine receptors CD39 and CD73 that are crucial for Treg-mediated immunosuppression. Our experimental results have elucidated the function of PD-1 in schistosomiasis and provide novel insights into prevention and treatment of schistosomiasis on the basis of modulating host adaptive immunity