Project description:Rhododendron is well known woody plant, as having high ornamental and economic values. Heat stress is one of the important environmental stresses that effects Rhododendron growth. Recently, melatonin was reported to alleviate abiotic stress in plants. However, the role of melatonin in Rhododendron is still unknown. In the present study, the effect of melatonin on Rhododendron under heat stress and the potential mechanism was investigated. Through morphological characterization and chlorophyll a fluorescence analysis, 200µM was selected for the best melatonin concentration to mitigate heat stress in Rhododendron. To reveal the mechanism of melatonin priming alleviating the heat stress, the photosynthesis indexes, Rubisco activity and ATP content were detected in 25 ℃, 35 ℃ and 40 ℃. The results showed that melatonin improves electron transport rate (ETR), PSII and PSI activity, Rubisco activity and ATP content under high temperature stress. Furthermore, transcriptome analysis showed that a significant enrichment of differentially expressed genes in the photosynthesis pathway, and most of genes in photosynthesis pathway displayed a more significantly slight down-regulation under high temperature stress in melatonin-treatment plants, compared with melatonin-free plants. We identified PGR5……Together, these results demonstrate that melatonin could promote the photosynthetic electron transport, improve the enzymes activities in Calvin cycle and the production of ATP, and thereby increase photosynthetic efficiency and CO2 assimilation capacity under heat stress, through regulating the expression of some key genes, such as PGR5…Therefore, melatonin application displayed great potential to cope with the heat stress in Rhododendron.
Project description:In the present study, genomic binding sites of glucocorticoid receptors (GR) were identified in vivo in the rat hippocampus applying chromatin immunoprecipitation followed by next-generation sequencing. We identified 2470 significant GR-binding sites (GBS) and were able to confirm GR binding to a random selection of these GBS covering a wide range of P values. Analysis of the genomic distribution of the significant GBS revealed a high prevalence of intragenic GBS. Gene ontology clusters involved in neuronal plasticity and other essential neuronal processes were overrepresented among the genes harboring a GBS or located in the vicinity of a GBS. Male adrenalectomized rats were challenged with increasing doses of the GR agonist corticosterone (CORT) ranging from 3 to 3000 μg/kg, resulting in clear differences in the GR-binding profile to individual GBS. Two groups of GBS could be distinguished: a low-CORT group that displayed GR binding across the full range of CORT concentrations, and a second high-CORT group that displayed significant GR binding only after administering the highest concentration of CORT. All validated GBS, in both the low-CORT and high-CORT groups, displayed mineralocorticoid receptor binding, which remained relatively constant from 30 μg/kg CORT upward. Motif analysis revealed that almost all GBS contained a glucocorticoid response element resembling the consensus motif in literature. In addition, motifs corresponding with new potential GR-interacting proteins were identified, such as zinc finger and BTB domain containing 3 (Zbtb3) and CUP (CG11181 gene product from transcript CG11181-RB), which may be involved in GR-dependent transactivation and transrepression, respectively. In conclusion, our results highlight the existence of 2 populations of GBS in the rat hippocampal genome. - See more at: http://press.endocrine.org/doi/10.1210/en.2012-2187?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed#sthash.LqK088DP.dpuf
Project description:The CiaRH and LiaFSR two-component regulatory systems in Streptococcus agalactiae (Group B Streptococcus, GBS) are essential mediators of the organism s response to biologically important sources of environmental stress, and positive regulators of GBS virulence. Transcriptional profiling of CiaR mutant GBS and LiaR mutant GBS reveals that LiaR is positively-regulated by CiaR, and the individual mutant transcriptomes share a number of commonly-regulated genes. To determine the GBS response to loss of both of these key regulatory systems, we constructed a GBS mutant strain with non-polar deletions in both ciaR and liaR, and performed transcriptional profiling using DNA microarray analysis, comparing wild-type GBS to CiaR/LiaR double mutant GBS under non-stressed conditions.
Project description:Genome wide expression profiling was used to identify signifnificantly changed genes in fetal membranes after GBS treatment Genome-wide expression profiles in GBS-inoculated human extraplacental membranes in vitro were used to identify transcriptomic pathways altered by GBS . Using bioinformatics analysis of these expression profiles we aimed to test our hypothesis that GBS activates pathways related to inflammation and premature birth in human extraplacental membranes.
Project description:In the transition from recto-vaginal colonizing organism to invasive pathogen, Streptococcus agalactiae (Group B Streptococcus, GBS) must adapt to changes in host temperature, including elevated temperatures due to host fever. To identify genes important to the survival of GBS in response to heat stress, transcriptional profiling was performed using DNA microarray analysis, comparing GBS grown at normal temperature (37˚C) to GBS exposed to elevated temperature (42˚C).
Project description:We have conducted RNA-seq analysis on Group B Streptococcus (GBS) when interacting with human stem-cell (hSC) derived BECs. The study contains a control group for GBS and a control group for BECs each with three biological replicates. The last group contains GBS infection BECs and also has three replicates.
Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) is a leading cause of early-onset neonatal bacterial infection. Evasion of innate immune defenses is critical to neonatal GBS disease pathogenesis. Effectors of the innate immune system such as antimicrobial peptides, as well as numerous antibiotics, target the peptidoglycan layer of the gram positive bacterial cell wall. The intramembrane-sensing histidine kinase class of two-component regulatory systems has recently been identified as important to the gram-positive response to cell wall stress. We identified and characterized the GBS homolog of LiaR, the response regulator component of the LiaFSR system and constructed site-directed, non-polar deletion mutations in the regulator gene liaR. GBS LiaR deletion mutant strains are more susceptible to cell wall active antibiotics (vancomycin and bacitracin) as well as antimicrobial peptides (colistin, nisin and the human cathelicidin LL-37) compared to isogenic wild-type GBS. LiaR mutant GBS are significantly attenuated in mouse models of both GBS sepsis and GBS pneumonia. To determine the genes regulated by LiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to LiaR mutant GBS under non-stressed conditions.
Project description:We asked whether Campylobacter jejuni isolated from patients with Guillain-Barri syndrome (GBS) differ from isolates isolated from patients with uncomplicated gastrointestinal infection using DNA microarray analysis. We found that specific GBS genes or regions were not identified, and microarray analysis confirmed significant genomic heterogeneity among the isolates. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs
Project description:Regulation of gene expression in response to variable and often adverse environmental conditions is an essential component of microbial pathogenesis. We identified the two-component regulatory system CiaRH in a screen for genes essential for the survival of Streptococcus agalactiae (Group B Streptococcus, GBS) on exposure to in vitro models of environmental stress. We constructed site-directed, non-polar deletion mutations in the regulator gene ciaR and compared the growth of CiaR mutant GBS to wild-type GBS under stressed conditions. CiaR mutant GBS are more sensitive than wild-type GBS to elevated temperature, low pH, chemical mutagens and ultraviolet light; the mutants are also more sensitive to cell-wall active antibiotics and antimicrobial peptides. CiaR mutant strains are markedly attenuated in a mouse model of GBS sepsis. To determine the genes regulated by CiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to CiaR mutant GBS under non-stressed conditions.