Effects of 24-Epibrassinolide on DNA Methylation Variation in Soybean (Glycine max) Leaf and Root Under Saline-Alkali Stress

2021 ◽  
Vol 15 (2) ◽  
pp. 194-202
Author(s):  
Ya-Nan Peng ◽  
Jing Li ◽  
Dan-Dan Sun ◽  
Nan Chen ◽  
Quan-Wei Wang
Keyword(s):  
Dna Methylation ◽  
Glycine Max ◽  
Genomic Dna ◽  
Alkali Resistance ◽  
Alkali Stress ◽  
Global Methylation ◽  
Methylation Rate ◽  
Stressed Leaf ◽  
Different Tissues ◽  
Methylation Variation

Saline-alkali stress is major stress that severely reduces plant growth and productivity, it is necessary to make clear whether exogenous 24-epibrassinolide (EBR) can improve the salt-alkali resistance of soybean (Glycine max) by affecting its DNA methylation. In this study, the effects of EBR on soybean adaptation to saline-alkali stress, genomic DNA methylation level and pattern changes in saline-alkali-stressed leaf and root with or without EBR treatment were compared using methylation-sensitive amplified polymorphism (MSAP). In the results, saline-alkali stress increased DNA methylation levels in leaf and root, with higher respective hemi-methylation and global methylation rates observed in leaf (6.22, 22.24%) than root (5.72, 21.76%). EBR application reduced leaf and root DNA methylation levels, with leaf hemi-methylation rate (6.15%) exceeding that of root (4.25%) and leaf global methylation rate (21.79%) below that of root (22.51%). There were distinct DNA remethylation and demethylation variations across different tissues and treatments, demethylation in leaves was dominant. Meanwhile, untreated saline-alkali-stressed roots exhibited major demethylation-based variations, while remethylation variations predominated post-treatment. Under saline-alkali stress, root remethylation and demethylation rates (6.17, 7.55%, respectively) both exceeded respective leaf rates (5.18 and 7.46%); however, post-EBR treatment, root methylation rate (6.45%) exceeded leaf rate (5.38%), while root demethylation rate (6.13%) fell below leaf rate (6.94%). In conclusion, exogenous EBR application to saline-alkali-stressed soybean can influence leaf and root genomic DNA methylation levels and patterns via distinct tissue-specific methylation mechanisms.

scholarly journals S8. GRIN1 PROMOTER METHYLATION CHANGES IN BLOOD OF EARLY-ONSET PSYCHOTIC PATIENTS AND UNAFFECTED SIBLINGS WITH CHILDHOOD TRAUMA

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S32-S33
Author(s):  
Camila Loureiro ◽  
Corsi-Zuelli Fabiana ◽  
Fachim Helene Aparecida ◽  
Shuhama Rosana ◽  
Menezes Paulo Rossi ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Childhood Trauma ◽  
Genomic Dna ◽  
Plasma Concentrations ◽  
First Episode ◽  
Emotional Neglect ◽  
Community Based ◽  
Global Methylation ◽  
Physical Neglect

Abstract Background Childhood trauma may lead to impairments in brain development and increases risk at psychiatric disorders. Evidence also suggests that childhood trauma may affect DNA methylation patterns consequently influencing gene expression (Tomassi et al., 2017). Some of this linking may be correlated with N-methyl-d-aspartate receptor (NMDAR) hypofunction, which plays a major role of central aspects of cognitive and negative features of schizophrenia (Lakhan et al., 2013). Specifically, the GRIN1 gene codes the biologically relevant NMDAR subunit involved in the synaptic plasticity which is expressed in a broad of non-neuronal cells (Hogan-Cann et al., 2016). Aims: We investigated DNA methylation in the promoter region of GRIN1 and LINE-1 methylation in first-episode psychosis patients (FEP), their unaffected siblings and community-based controls with and without childhood trauma. We also tested for correlations between GRIN1 methylation and NR1 concentrations in peripheral blood. Methods This study is a part of the epidemiological investigation that estimated the incidence of psychosis and the role of environmental and biological factors in psychosis aetiology in the catchment area of Ribeirão Preto, Brazil, from 1st April 2012 to 31st March 2015. The genomic DNA was extracted from blood of 60 FEP patients, 30 of their unaffected siblings and 60 age- and sex-matched community-based controls. Diagnosis and clinical characteristics were assessed using the DSM-IV (First et al., 1997; Del-Ben et al., 2001) and history of childhood trauma was assessed using the Childhood Trauma Questionnaire (Grassi-Oliverira et al., 2006). The genomic DNA was bisulfite converted and pyrosequencing was used to determine methylation levels in three CpGs sites of the GRIN1 gene and of LINE-1, as a measure of global methylation. NR1 plasma concentrations were measured using ELISA (MyBioSource, San Diego, USA). Data were analyzed using General Linear Model with post-hoc Bonferroni correction and Pearson’s correlations. Results Individuals, independent of groups, who had experienced childhood trauma presented higher levels of GRIN1 methylation than those without trauma (CpG1: p=0.004; CpG3: p=0.009). Moreover, individuals with physical neglect demonstrated GRIN1 hypermethylation in comparison to individuals without trauma (CpG1: p=0.027; CpG3: p=0.006). Specifically, siblings with emotional neglect presented increased GRIN1 methylation levels at CpG1 when compared with FEP patients and controls with emotional neglect (p=0.028; p=0.001, respectively) and in relation to siblings without trauma (p=0.004). Siblings with physical neglect also showed increased GRIN1 methylation levels at CpG1 when compared to FEP patients and controls with physical neglect (p=0.010; p=0.003, respectively) and in relation to siblings without physical neglect (p=0.001). Furthermore, FEP patients with emotional neglect showed increased GRIN1 methylation at CpG3 when compared to FEP patients without emotional neglect (p=0.010). No differences were observed in the LINE-1 methylation between individuals with or without childhood trauma. Discussion This is the first study demonstrating the association between DNA methylation in GRIN1 and childhood trauma in FEP patients, their unaffected siblings and community-based controls. In addition, the interaction between DNA methylation changes in GRIN1 and childhood trauma may be a predict factor of susceptibility for siblings. All these findings suggest evidence for NMDAR dysfunction in response to trauma, contributing the understanding of some of the epigenetics mechanisms by which early life stress affects the glutamatergic system.

scholarly journals Global DNA methylation pattern and correlation with complement system proteins in Brazilian patients with systemic lupus erythematosus

2015 ◽  
Vol 13 (4) ◽  
pp. 516-523
Author(s):  
Paolo Ruggero Errante ◽  
Sandro Félix Perazzio ◽  
Francisco Sandro Menezes Rodrigues ◽  
Renato Ribeiro Nogueira Ferraz ◽  
Afonso Caricati-Neto
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Dna Methylation ◽  
Lupus Erythematosus ◽  
Genomic Dna ◽  
Expression Patterns ◽  
Global Dna Methylation ◽  
Healthy Individuals ◽  
Systemic Lupus ◽  
Global Methylation ◽  
Laboratory Parameters

Introduction: Nucleic acid methylation may have major effects on gene expression patterns and, by consequence, on the development of autoimmunity, like Systemic Lupus Erythematosus (SLE). Objective: To investigate the pattern of global DNA methylation in SLE patients and compare this pattern with laboratory parameters. Methods: Genomic DNA was isolated from SLE patients with non-active disease (SLEDAI6), and healthy individuals. Global DNA methylation was evaluated by digestion of genomic DNA with HpaII and MspI and compared with laboratory parameters. Results and conclusion: A statistical difference in DNA global methylation was observed when SLE patients were compared to healthy individuals. A positive correlation was observed between the frequency of global methylation and C3 and C4 serum levels for SLE patients with SLEDAI

Examination of the dynamics of global DNA methylation pattern establishment during spermatogenesiss

2007 ◽  
Vol 30 (4) ◽  
pp. 90
Author(s):  
Kirsten Niles ◽  
Sophie La Salle ◽  
Christopher Oakes ◽  
Jacquetta Trasler
Keyword(s):  
Dna Methylation ◽  
Germ Cell ◽  
Germ Cells ◽  
Epigenetic Modification ◽  
Methylation Pattern ◽  
Chromosome 9 ◽  
Specific Gene ◽  
Global Methylation ◽  
Dna Methylation Pattern ◽  
Methylation Patterns

Background: DNA methylation is an epigenetic modification involved in gene expression, genome stability, and genomic imprinting. In the male, methylation patterns are initially erased in primordial germ cells (PGCs) as they enter the gonadal ridge; methylation patterns are then acquired on CpG dinucleotides during gametogenesis. Correct pattern establishment is essential for normal spermatogenesis. To date, the characterization and timing of methylation pattern acquisition in PGCs has been described using a limited number of specific gene loci. This study aimed to describe DNA methylation pattern establishment dynamics during male gametogenesis through global methylation profiling techniques in a mouse model. Methods: Using a chromosome based approach, primers were designed for 24 regions spanning chromosome 9; intergenic, non-repeat, non-CpG island sequences were chosen for study based on previous evidence that these types of sequences are targets for testis-specific methylation events. The percent methylation was determined in each region by quantitative analysis of DNA methylation using real-time PCR (qAMP). The germ cell-specific pattern was determined by comparing methylation between spermatozoa and liver. To examine methylation in developing germ cells, spermatogonia from 2 day- and 6 day-old Oct4-GFP (green fluorescent protein) mice were isolated using fluorescence activated cell sorting. Results: As compared to liver, four loci were hypomethylated and five loci were hypermethylated in spermatozoa, supporting previous results indicating a unique methylation pattern in male germ cells. Only one region was hypomethylated and no regions were hypermethylated in day 6 spermatogonia as compared to mature spermatozoa, signifying that the bulk of DNA methylation is established prior to type A spermatogonia. The methylation in day 2 spermatogonia, germ cells that are just commencing mitosis, revealed differences of 15-20% compared to day 6 spermatogonia at five regions indicating that the most crucial phase of DNA methylation acquisition occurs prenatally. Conclusion: Together, these studies provide further evidence that germ cell methylation patterns differ from those in somatic tissues and suggest that much of methylation at intergenic sites is acquired during prenatal germ cell development. (Supported by CIHR)

Effect of low temperature on genomic DNA methylation in Nile tilapia (Oreochromis niloticus)

2013 ◽  
Vol 37 (10) ◽  
pp. 1460 ◽  
Author(s):  
Huaping ZHU ◽  
Maixin LU ◽  
Zhanghan HUANG ◽  
Fengying GAO ◽  
Xiaoli KE ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Low Temperature ◽  
Oreochromis Niloticus ◽  
Genomic Dna ◽  
Nile Tilapia ◽  
Nile Tilapia Oreochromis Niloticus

scholarly journals Altered DNA methylation pattern reveals epigenetic regulation of Hox genes in thoracic aortic dissection and serves as a biomarker in disease diagnosis

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Peiru Liu ◽  
Jing Zhang ◽  
Duo Du ◽  
Dandan Zhang ◽  
Zelin Jin ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Aortic Dissection ◽  
Epigenetic Regulation ◽  
Heart Development ◽  
Type A ◽  
Methylation Pattern ◽  
Healthy Controls ◽  
Global Methylation ◽  
Thoracic Aortic Dissection

Abstract Background Thoracic aortic dissection (TAD) is a severe disease with limited understandings in its pathogenesis. Altered DNA methylation has been revealed to be involved in many diseases etiology. Few studies have examined the role of DNA methylation in the development of TAD. This study explored alterations of the DNA methylation landscape in TAD and examined the potential role of cell-free DNA (cfDNA) methylation as a biomarker in TAD diagnosis. Results Ascending aortic tissues from TAD patients (Stanford type A; n = 6) and healthy controls (n = 6) were first examined via whole-genome bisulfite sequencing (WGBS). While no obvious global methylation shift was observed, numerous differentially methylated regions (DMRs) were identified, with associated genes enriched in the areas of vasculature and heart development. We further confirmed the methylation and expression changes in homeobox (Hox) clusters with 10 independent samples using bisulfite pyrosequencing and quantitative real-time PCR (qPCR). Among these, HOXA5, HOXB6 and HOXC6 were significantly down-regulated in TAD samples relative to controls. To evaluate cfDNA methylation pattern as a biomarker in TAD diagnosis, cfDNA from TAD patients (Stanford type A; n = 7) and healthy controls (n = 4) were examined by WGBS. A prediction model was built using DMRs identified previously from aortic tissues on methylation data from cfDNA. Both high sensitivity (86%) and specificity (75%) were achieved in patient classification (AUC = 0.96). Conclusions These findings showed an altered epigenetic regulation in TAD patients. This altered epigenetic regulation and subsequent altered expression of genes associated with vasculature and heart development, such as Hox family genes, may contribute to the loss of aortic integrity and TAD pathogenesis. Additionally, the cfDNA methylation in TAD was highly disease specific, which can be used as a non-invasive biomarker for disease prediction.

scholarly journals Oxidative damage, inflammation, genotoxic effect, and global DNA methylation caused by inhalation of formaldehyde and the purpose of melatonin

2020 ◽  
Vol 9 (6) ◽  
pp. 778-789
Author(s):  
Letícia Bernardini ◽  
Eduardo Barbosa ◽  
Mariele Feiffer Charão ◽  
Gabriela Goethel ◽  
Diana Muller ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Bronchoalveolar Lavage ◽  
Bone Marrow Cells ◽  
Histological Study ◽  
Global Dna Methylation ◽  
Protective Effects ◽  
Global Methylation ◽  
Protein Thiols

Abstract Formaldehyde (FA) exposure has been proven to increase the risk of asthma and cancer. This study aimed to evaluate for 28 days the FA inhalation effects on oxidative stress, inflammation process, genotoxicity, and global DNA methylation in mice as well as to investigate the potential protective effects of melatonin. For that, analyses were performed on lung, liver and kidney tissues, blood, and bone marrow. Bronchoalveolar lavage was used to measure inflammatory parameters. Lipid peroxidation (TBARS), protein carbonyl (PCO), non-protein thiols (NPSH), catalase activity (CAT), comet assay, micronuclei (MN), and global methylation were determined. The exposure to 5-ppm FA resulted in oxidative damage to the lung, presenting a significant increase in TBARS and NO levels and a decrease in NPSH levels, besides an increase in inflammatory cells recruited for bronchoalveolar lavage. Likewise, in the liver tissue, the exposure to 5-ppm FA increased TBARS and PCO levels and decreased NPSH levels. In addition, FA significantly induced DNA damage, evidenced by the increase of % tail moment and MN frequency. The pretreatment of mice exposed to FA applying melatonin improved inflammatory and oxidative damage in lung and liver tissues and attenuated MN formation in bone marrow cells. The pulmonary histological study reinforced the results observed in biochemical parameters, demonstrating the potential beneficial role of melatonin. Therefore, our results demonstrated that FA exposure with repeated doses might induce oxidative damage, inflammatory, and genotoxic effects, and melatonin minimized the toxic effects caused by FA inhalation in mice.

scholarly journals DNA methylation is associated with airflow obstruction in patients living with HIV

Thorax ◽  
2020 ◽  
pp. thoraxjnl-2020-215866
Author(s):  
Ana I Hernandez Cordero ◽  
Chen Xi Yang ◽  
Maen Obeidat ◽  
Julia Yang ◽  
Julie MacIsaac ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Lung Function ◽  
Viral Infections ◽  
Airflow Obstruction ◽  
Normal Lung ◽  
People Living With Hiv ◽  
Global Methylation ◽  
Age Related ◽  
Impaired Lung Function ◽  
Living With Hiv

IntroductionPeople living with HIV (PLWH) suffer from age-related comorbidities such as COPD. The processes responsible for reduced lung function in PLWH are largely unknown. We performed an epigenome-wide association study to investigate whether blood DNA methylation is associated with impaired lung function in PLWH.MethodsUsing blood DNA methylation profiles from 161 PLWH, we tested the effect of methylation on FEV1, FEV1/FVC ratio and FEV1 decline over a median of 5 years. We evaluated the global methylation of PLWH with airflow obstruction by testing the differential methylation of transposable elements Alu and LINE-1, a well-described marker of epigenetic ageing.ResultsAirflow obstruction as defined by a FEV1/FVC<0.70 was associated with 1393 differentially methylated positions (DMPs), while 4676 were associated with airflow obstruction based on the FEV1/FVC<lower limit of normal. These DMPs were enriched for biological pathways associated with chronic viral infections. The airflow obstruction group was globally hypomethylated compared with those without airflow obstruction. 103 and 7112 DMPs were associated with FEV1 and FEV1/FVC, respectively. No positions were associated with FEV1 decline.ConclusionA large number of DMPs were associated with airflow obstruction and lung function in a unique cohort of PLWH. Airflow obstruction in even relatively young PLWH is associated with global hypomethylation, suggesting advanced epigenetic ageing compared with those with normal lung function. The disturbance of the epigenetic regulation of key genes not previously identified in non-HIV COPD cohorts could explain the unique risk of COPD in PLWH.

scholarly journals DNA Methylation in T-Cell Acute Lymphoblastic Leukemia: In Search for Clinical and Biological Meaning

2021 ◽  
Vol 22 (3) ◽  
pp. 1388
Author(s):  
Natalia Maćkowska ◽  
Monika Drobna-Śledzińska ◽  
Michał Witt ◽  
Małgorzata Dawidowska
Keyword(s):  
Dna Methylation ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Epigenetic Modification ◽  
Lymphoblastic Leukemia ◽  
Leukemic Cells ◽  
Global Methylation ◽  
Current State ◽  
History Of ◽  
Cell Acute Lymphoblastic Leukemia

Distinct DNA methylation signatures, related to different prognosis, have been observed across many cancers, including T-cell acute lymphoblastic leukemia (T-ALL), an aggressive hematological neoplasm. By global methylation analysis, two major phenotypes might be observed in T-ALL: hypermethylation related to better outcome and hypomethylation, which is a candidate marker of poor prognosis. Moreover, DNA methylation holds more than a clinical meaning. It reflects the replicative history of leukemic cells and most likely different mechanisms underlying leukemia development in these T-ALL subtypes. The elucidation of the mechanisms and aberrations specific to (epi-)genomic subtypes might pave the way towards predictive diagnostics and precision medicine in T-ALL. We present the current state of knowledge on the role of DNA methylation in T-ALL. We describe the involvement of DNA methylation in normal hematopoiesis and T-cell development, focusing on epigenetic aberrations contributing to this leukemia. We further review the research investigating distinct methylation phenotypes in T-ALL, related to different outcomes, pointing to the most recent research aimed to unravel the biological mechanisms behind differential methylation. We highlight how technological advancements facilitated broadening the perspective of the investigation into DNA methylation and how this has changed our understanding of the roles of this epigenetic modification in T-ALL.

Sign in / Sign up

Export Citation Format

Share Document