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Sesuvium portulacastrum (L.) is a halophyte, adapted to grow naturally under saline environments. The ability to use Na and K interchangeably indicated its facultative halophyte nature. No significant growth reduction occurs in seedlings up to 250 mM NaCl, except for curling of the youngest leaf. Within 8 h of salt treatment, seedlings accumulate proline, glycine betaine and other amino acids in both root and shoot. Despite a continued increase of tissue Na content, the number of differentially expressed genes (DEGs) decreases between 8 and 24 h of salt exposure, indicating transcriptional restoration after the initial osmotic challenge. At 8 h, upregulated genes mainly encode transporters and transcription factors, while genes in growth‐related pathways such as photosynthesis and ribosome‐associated biogenesis are suppressed. Overexpression of SpRAB18 (an ABA‐responsive dehydrin), one of the most strongly induced DEGs, in soybean was found to increase biomass in control conditions and the growth benefit was maintained when plants were grown in 100 mM NaCl, indicating conservation of function in halophyte and glycophyte. An open‐access transcriptome database "SesuviumKB" (https://cb.imsc.res.in/sesuviumkb/) was developed to involve the scientific community in wide‐scale functional studies of S. portulacastrum genes, that could pave the way to engineer salt tolerance in crops. Summary Statement: We provide data on the physiology, transcriptome and metabolome of the halophyte Sesuvium portulacastrum (L.). An open acccess database "SesuviumKB" was constructed to facilitate data access and enable future wide‐scale functional testing of the genes through the community. [ABSTRACT FROM AUTHOR]

Summary: Early responses of plants to environmental stress factors prevent damage but can delay growth and development in fluctuating conditions. Optimising these trade‐offs requires tunability of plant responsiveness to environmental signals.We have previously reported that Histone Deacetylase Complex 1 (HDC1), which interacts with multiple proteins in histone deacetylation complexes, regulates the stress responsiveness of Arabidopsis seedlings, but the underlying mechanism remained elusive.Here, we show that HDC1 attenuates transcriptome re‐programming in salt‐treated seedlings, and we identify two genes (LEA and MAF5) that inhibit seedling establishment under salt stress downstream of HDC1. HDC1 attenuates their transcriptional induction by salt via a dual mechanism involving H3K9/14 deacetylation and H3K27 trimethylation. The latter, but not the former, was also abolished in a triple knockout mutant of the linker histone H1, which partially mimics the hypersensitivity of the hdc1‐1 mutant to salt stress. Although stress‐induced H3K27me3 accumulation required both H1 and HDC1, it was not fully recovered by complementing hdc1‐1 with a truncated, H1‐binding competent HDC1 suggesting other players or independent inputs.The combined findings reveal a dual brake function of HDC1 via regulating both active and repressive epigenetic marks on stress‐inducible genes. This natural 'anti‐panic' device offers a molecular leaver to tune stress responsiveness in plants. See also the Commentary on this article by Archacki, 241: 7–9. [ABSTRACT FROM AUTHOR]

Many dementias are propagated through the spread of "prion-like" misfolded proteins. This includes prion diseases themselves (such as Creutzfeldt-Jakob disease) and Alzheimer's disease (AD), for which no treatments are available to slow or stop progression. The M1 acetylcholine muscarinic receptor (M1 receptor) is abundant in the brain, and its activity promotes cognitive function in preclinical models and in patients with AD. Here, we investigated whether activation of the M1 receptor might slow the progression of neurodegeneration associated with prion-like misfolded protein in a mouse model of prion disease. Proteomic and transcriptomic analysis of the hippocampus revealed that this model had a molecular profile that was similar to that of human neurodegenerative diseases, including AD. Chronic enhancement of the activity of the M1 receptor with the positive allosteric modulator (PAM) VU0486846 reduced the abundance of prion-induced molecular markers of neuroinflammation and mitochondrial dysregulation in the hippocampus and normalized the abundance of those associated with neurotransmission, including synaptic and postsynaptic signaling components. PAM treatment of prion-infected mice prolonged survival and maintained cognitive function. Thus, allosteric activation of M1 receptors may reduce the severity of neurodegenerative diseases caused by the prion-like propagation of misfolded protein. Protecting against prions: Various neurodegenerative diseases are caused by misfolded proteins that aggregate and propagate through the brain and lack effective treatments. Because loss of acetylcholine signaling is associated with cognitive deficits in patients, Dwomoh et al. investigated the effect of enhancing acetylcholine signaling with positive allosteric modulators (PAMs) targeting the M1 acetylcholine receptor in a mouse model of prion disease. Systemic administration of PAMs reduced the abundance of prion-induced molecular markers in the hippocampus, restored various cognitive functions, and slowed disease progression in the mice. The proteomic and transcriptomic data from the prion mouse model substantially overlapped with those associated with Alzheimer's disease, suggesting that M1 receptor PAMs may be therapeutic in patients with prion and prion-like neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

UV-B radiation in sunlight has diverse effects on humans, animals, plants, and microorganisms. UV-B can cause damage to molecules and cells, and consequently organisms need to protect against and repair UV damage to survive in sunlight. In plants, low non damaging levels of UV-B stimulate transcription of genes involved in UV-protective responses. However, remarkably little is known about the underlying mechanisms of UV-B perception and signal transduction. Here we report that Arabist's UV RESISTANCE LOCUS 8 (UVR8) is a UV-B-specific signaling component that orchestrates expression of a range of genes with vital UV-protective functions. Moreover, we show that UVR8 regulates expression of the transcription factor HY5 specifically when the plant is exposed to UV-B. We demonstrate that HY5 is a key effector of the UVR8 pathway, and that it is required for survival under UV-B radiation. UVR8 has sequence similarity to the neurotically guanine nucleotide exchange factor RCC1, but we found that it has little exchange activity. However, UVR8, like RCC1, is located principally in the nucleus and associates with chromatin via hi stones. Chromatin precipitation's showed that UVR8 associates with chromatin in the HY5 promoter region, providing a mechanistic basis for its involvement in regulating transcription. We conclude that UVR8 defines a UV-B-specific signaling pathway in plants that orchestrates the protective gene expression responses to UV-B required for plant survival in sunlight. pathogenesis's | ultraviolet-B radiation | UV RESISTANCE LOCUS 8

Abstract Background Outer membrane proteins (OMPs) of Pasteurella multocida have various functions related to virulence and pathogenesis and represent important targets for vaccine development. Various bioinformatic algorithms can predict outer membrane localization and discriminate OMPs by structure or function. The designation of a confident prediction framework by integrating different predictors followed by consensus prediction, results integration and manual confirmation will improve the prediction of the outer membrane proteome. Results In the present study, we used 10 different predictors classified into three groups (subcellular localization, transmembrane β-barrel protein and lipoprotein predictors) to identify putative OMPs from two available P. multocida genomes: those of avian strain Pm70 and porcine non-toxigenic strain 3480. Predicted proteins in each group were filtered by optimized criteria for consensus prediction: at least two positive predictions for the subcellular localization predictors, three for the transmembrane β-barrel protein predictors and one for the lipoprotein predictors. The consensus predicted proteins were integrated from each group into a single list of proteins. We further incorporated a manual confirmation step including a public database search against PubMed and sequence analyses, e.g. sequence and structural homology, conserved motifs/domains, functional prediction, and protein-protein interactions to enhance the confidence of prediction. As a result, we were able to confidently predict 98 putative OMPs from the avian strain genome and 107 OMPs from the porcine strain genome with 83% overlap between the two genomes. Conclusions The bioinformatic framework developed in this study has increased the number of putative OMPs identified in P. multocida and allowed these OMPs to be identified with a higher degree of confidence. Our approach can be applied to investigate the outer membrane proteomes of other Gram-negative bacteria.

Abstract Background At present, there are no clinically reliable disease markers for chronic fatigue syndrome. DNA chip microarray technology provides a method for examining the differential expression of mRNA from a large number of genes. Our hypothesis was that a gene expression signature, generated by microarray assays, could help identify genes which are dysregulated in patients with post-infectious CFS and so help identify biomarkers for the condition. Methods Human genome-wide Affymetrix GeneChip arrays (39,000 transcripts derived from 33,000 gene sequences) were used to compare the levels of gene expression in the peripheral blood mononuclear cells of male patients with post-infectious chronic fatigue (n = 8) and male healthy control subjects (n = 7). Results Patients and healthy subjects differed significantly in the level of expression of 366 genes. Analysis of the differentially expressed genes indicated functional implications in immune modulation, oxidative stress and apoptosis. Prototype biomarkers were identified on the basis of differential levels of gene expression and possible biological significance Conclusion Differential expression of key genes identified in this study offer an insight into the possible mechanism of chronic fatigue following infection. The representative biomarkers identified in this research appear promising as potential biomarkers for diagnosis and treatment.