15 research outputs found
Overlapping Signatures of Chronic Pain in the DNA Methylation Landscape of Prefrontal Cortex and Peripheral T Cells
We tested the hypothesis that epigenetic mechanisms in the brain and the immune system are associated with chronic pain. Genome-wide DNA methylation assessed in 9 months post nerve-injury (SNI) and Sham rats, in the prefrontal cortex (PFC) as well as in T cells revealed a vast difference in the DNA methylation landscape in the brain between the groups and a remarkable overlap (72%) between differentially methylated probes in T cells and prefrontal cortex. DNA methylation states in the PFC showed robust correlation with pain score of animals in several genes involved in pain. Finally, only 11 differentially methylated probes in T cells were sufficient to distinguish SNI or Sham individual rats. This study supports the plausibility of DNA methylation involvement in chronic pain and demonstrates the potential feasibility of DNA methylation markers in T cells as noninvasive biomarkers of chronic pain susceptibility
Isolation and characterization of malate dehydrogenase mutant of Sinorhizobium meliloti
A Sinorhizobium meliloti (S. meliloti ) mutant, Rm30O49, deficient in malate dehydrogenase (MDH) activity was isolated via random Tn5tac1 mutagenesis. DNA sequence analyses revealed 60 the inaction is within the mdh gene. Rm30049 lacks MDH activity under all growth conditions, but shows increased or decreased activities of the TCA cycle enzymes 2-oxoglutarate dehydrogenase and succinate dehydrogenase in the presence or absence, respectively, of IPTG (isopropyl beta-D-thiogalactoside). The symbiotic phenotype of the mutant is an inability to fix nitrogen. Alfalfa seedlings inoculated with Rm30049 produced small white root nodules, but were chlorotic and failed to reach a wild-type shoot dry weight. Cosmid clone pDS15 was isolated by heterologous complementation of a Rhizobium leguminosarum sucD mutant by the S. meliloti pLAFR1 clone bank. This cosmid also restored MDH activity to Rm30049, and complemented the mutant growth and symbiotic phenotypes. Three Tn5 insertions isolated in pDS15 within sucA failed to complement Rm30049. DNA sequence analyses indicate that the mdh gene is part of the TCA cycle operon with sucCD, and that downstream and upstream of this, are operons encoding sucAB and sdhCDAB, respectively
Additional file 6: Table S6. of The signature of liver cancer in immune cells DNA methylation
Annotated non-redundant list of 350CGs and 369 CGs that are differentially methylated between stages of HCC and healthy controls. (CSV 41 kb
Additional file 10: Table S9. of The signature of liver cancer in immune cells DNA methylation
Multifactorial ANOVA analysis of 350 CGs. No interaction detected between group (HCC) and sex and age as independent variables with CG methylation as a dependent variable. (CSV 31 kb
Additional file 3: Table S3. of The signature of liver cancer in immune cells DNA methylation
Differentially methylated sites between Stage 2 HCC and healthy controls. (CSV 1433 kb
Additional file 16: Table S15. of The signature of liver cancer in immune cells DNA methylation
Descriptive statistics for (Fig. 6a). (XLS 87 kb
Additional file 11: Table S10. of The signature of liver cancer in immune cells DNA methylation
Differentially methylated CG sites in T cell DNA between healthy controls and HCC. (CSV 1586 kb