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In the post-genome-wide association study era, multi-omics techniques have shown great power and potential for candidate gene mining and functional genomics research. However, due to the lack of effective data integration and multi-omics analysis platforms, such techniques have not still been applied widely in rapeseed, an important oil crop worldwide. Here, we report a rapeseed multi-omics database (BnIR; http://yanglab.hzau.edu.cn/BnIR), which provides datasets of six omics including genomics, transcriptomics, variomics, epigenetics, phenomics, and metabolomics, as well as numerous "variation–gene expression–phenotype" associations by using multiple statistical methods. In addition, a series of multi-omics search and analysis tools are integrated to facilitate the browsing and application of these datasets. BnIR is the most comprehensive multi-omics database for rapeseed so far, and two case studies demonstrated its power to mine candidate genes associated with specific traits and analyze their potential regulatory mechanisms. BnIR (http://yanglab.hzau.edu.cn/BnIR), a multi-omics database for rapeseed, is constructed in this work, which integrates six omics datasets and "variation–gene expression–phenotype" associations. The database is equipped with a range of multi-omics tools for streamlined browsing and analysis. Through several case studies, BnIR's potential in identifying candidate genes associated with specific traits are demonstrated. [ABSTRACT FROM AUTHOR]

Summary Among the myriad cues that constantly inform plant growth and development, mechanical forces are unique in that they are an intrinsic result of cellular turgor pressure and also imposed by the environment [ 1 ]. Although the key role of mechanical forces in shaping plant architecture from the cellular level to the level of organ formation is well established [ 1–4 ], the components of the early mechanical signal transduction machinery remain to be defined at the molecular level. Here, we show that an Arabidopsis mutant lacking the receptor-like kinase FERONIA (FER) shows severely altered Ca 2+ signaling and growth responses to different forms of mechanical perturbation. Ca 2+ signals are either abolished or exhibit qualitatively different signatures in feronia ( fer ) mutants exposed to local touch or bending stimulation. Furthermore, mechanically induced upregulation of known touch-responsive genes is significantly decreased in fer mutants. In addition to these defects in mechanical signaling, fer mutants also exhibit growth phenotypes consistent with impaired mechanical development, including biased root skewing, an inability to penetrate hard agar layers, and abnormal growth responses to impenetrable obstacles. Finally, high-resolution kinematic analysis of root growth revealed that fer mutants show pronounced spatiotemporal fluctuations in root cell expansion profiles with a timescale of minutes. Based on these results, we propose that FER is a key regulator of mechanical Ca 2+ signaling and that FER-dependent mechanical signaling functions to regulate growth in response to external or intrinsic mechanical forces. [ABSTRACT FROM AUTHOR]

Viral infections induce a conserved host response distinct from bacterial infections. We hypothesized that the conserved response is associated with disease severity and is distinct between patients with different outcomes. To test this, we integrated 4,780 blood transcriptome profiles from patients aged 0 to 90 years infected with one of 16 viruses, including SARS-CoV-2, Ebola, chikungunya, and influenza, across 34 cohorts from 18 countries, and single-cell RNA sequencing profiles of 702,970 immune cells from 289 samples across three cohorts. Severe viral infection was associated with increased hematopoiesis, myelopoiesis, and myeloid-derived suppressor cells. We identified protective and detrimental gene modules that defined distinct trajectories associated with mild versus severe outcomes. The interferon response was decoupled from the protective host response in patients with severe outcomes. These findings were consistent, irrespective of age and virus, and provide insights to accelerate the development of diagnostics and host-directed therapies to improve global pandemic preparedness. [Display omitted] • Conserved host response distinguishes non-severe and severe viral infections • Increased hematopoiesis, myelopoiesis, and myeloid-derived suppression with severity • Protective and detrimental modules define trajectories for mild and severe outcomes • Interferon response is decoupled from the protective response in severe outcomes Viral infections induce a conserved host response distinct from bacterial infections, but whether this conserved response distinguishes severity is unclear. Zheng et al. analyzed >5000 bulk and single-cell transcriptome profiles from patients infected with one of 16 viruses, including SARS-CoV-2, Ebola, and chikungunya. They identified protective and detrimental host response modules that distinguish patients with mild or severe outcomes. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS) are inevitable by-products of aerobic metabolic processes, causing non-specific oxidative damage and also acting as second messengers. Superoxide is a short-lived ROS that functions in various cellular responses, including aging and cell death. However, it is unclear as to how superoxide brings about age-dependent cell death and senescence. Here, we show that the accumulation and signaling of superoxide are mediated by three Arabidopsis proteins-RPK1, CaM4, and RbohF-which trigger subsequent cellular events leading to age-dependent cell death. We demonstrate that the NADPH oxidase RbohF is responsible for RPK1-mediated transient accumulation of superoxide, SIRK kinase induction, and cell death, all of which are positively regulated by CaM4. RPK1 physically interacts with and phosphorylates CaM4, which, in turn, interacts with RbohF. Overall, we demonstrate how the protein trio governs the superoxide accumulation and signaling at the cell surface to control senescence and cell death., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)