Differential gene expression signatures for cell wall integrity found in chitin synthase II (chs2Δ) and myosin II (myo1Δ) deficient cytokinesis mutants of Saccharomyces cerevisiae

<p>Abstract</p> <p>Background</p> <p>Myosin II-dependent contraction of the cytokinetic ring and primary septum formation by chitin synthase II are interdependent processes during cytokinesis in <it>Saccharomyces cerevisiae</it>. Hence, null mutants of myosin II <it>(myo1</it>Δ<it>) </it>and chitin synthase II <it>(chs2</it>Δ<it>) </it>share multiple morphological and molecular phenotypes. To understand the nature of their interdependent functions, we will seek to identify genes undergoing transcriptional regulation in <it>chs2</it>Δ strains and to establish a transcription signature profile for comparison with <it>myo1</it>Δ strains.</p> <p>Results</p> <p>A total of 467 genes were commonly regulated between <it>myo1Δ </it>and <it>chs2Δ </it>mutant strains (p ≤ 0.01). Common regulated biological process categories identified by Gene Set Enrichment Analysis (GSEA) in both gene expression profiles were: protein biosynthesis, RNA processing, and stress response. Expression of 17/20 genes in the main transcriptional fingerprint for cell wall stress was confirmed in the <it>chs2Δ </it>strain versus 5/20 for the <it>myo1Δ </it>strain. One of these genes, <it>SLT2/MPK1</it>, was up-regulated in both strains and both strains accumulated the hyperphosphorylated form of Slt2p thereby confirming that the <it>PKC1 </it>cell wall integrity pathway (CWIP) was activated by both mutations. The <it>SLT2/MPK1 </it>gene, essential for <it>myo1Δ </it>strains, was not required in the <it>chs2Δ </it>strain.</p> <p>Conclusion</p> <p>Comparison of the <it>chs2Δ </it>and <it>myo1</it>Δ gene expression profiles revealed similarities in the biological process categories that respond to the <it>chs2Δ </it>and <it>myo1</it>Δ gene mutations. This supports the view that these mutations affect a common function in cytokinesis. Despite their similarities, these mutants exhibited significant differences in expression of the main transcriptional fingerprint for cell wall stress and their requirement of the CWIP for survival.</p

Autoimmune neurological conditions associated with Zika virus infection

Zika virus (ZIKV) is an emerging flavivirus rapidly spreading throughout the tropical Americas. mosquitoes is the principal way of transmission of the virus to humans. ZIKV can be spread by transplacental, perinatal, and body fluids. ZIKV infection is often asymptomatic and those with symptoms present minor illness after 3 to 12 days of incubation, characterized by a mild and self-limiting disease with low-grade fever, conjunctivitis, widespread pruritic maculopapular rash, arthralgia and myalgia. ZIKV has been linked to a number of central and peripheral nervous system injuries such as Guillain-Barré syndrome (GBS), transverse myelitis (TM), meningoencephalitis, ophthalmological manifestations, and other neurological complications. Nevertheless, mechanisms of host-pathogen neuro-immune interactions remain incompletely elucidated. This review provides a critical discussion about the possible mechanisms underlying the development of autoimmune neurological conditions associated with Zika virus infection

Model biopsychicalsocial in the syndromes of vertebral pain: implications for the protocolize

[Resumen] De forma tradicional el modelo biomédico ha predominado en la práctica asistencial. A diferencia de éste, el modelo biopsicosocial considera a la persona como un todo y hace énfasis sobre la función en lugar de centrarse exclusivamente en el alivio del dolor. En este sentido, la Fisioterapia para el tratamiento de los problemas de espalda, y en concreto para la cervicalgia, tiene que considerar, además del alivio del dolor, la cronicidad y la recurrencia como elementos a considerar en el diseño de actividades protocolizadas.[Abstract] In a traditional way the biomedical model has prevailed in the health care. Against it the biopsychicalsocial pattern considers to the person as a whole and it makes emphasis on the function instead of being centered exclusively in the relief of the pain. In this sense, Physiotheraphy for the treatment of the back problems and in this case for the neck pain, it has to consider besides the relief of the pain, the chronic and the new episodies like elements to consider in the design of protocolized activities

Systematic identification of phenotypically enriched loci using a patient network of genomic disorders

Background Network medicine is a promising new discipline that combines systems biology approaches and network science to understand the complexity of pathological phenotypes. Given the growing availability of personalized genomic and phenotypic profiles, network models offer a robust integrative framework for the analysis of "omics" data, allowing the characterization of the molecular aetiology of pathological processes underpinning genetic diseases. Methods Here we make use of patient genomic data to exploit different network-based analyses to study genetic and phenotypic relationships between individuals. For this method, we analyzed a dataset of structural variants and phenotypes for 6,564 patients from the DECIPHER database, which encompasses one of the most comprehensive collections of pathogenic Copy Number Variations (CNVs) and their associated ontology-controlled phenotypes. We developed a computational strategy that identifies clusters of patients in a synthetic patient network according to their genetic overlap and phenotype enrichments. Results Many of these clusters of patients represent new genotype-phenotype associations, suggesting the identification of newly discovered phenotypically enriched loci (indicative of potential novel syndromes) that are currently absent from reference genomic disorder databases such as ClinVar, OMIM or DECIPHER itself. Conclusions We provide a high-resolution map of pathogenic phenotypes associated with their respective significant genomic regions and a new powerful tool for diagnosis of currently uncharacterized mutations leading to deleterious phenotypes and syndromes