scholarly journals Interactive Regulations of Dynamic Methylation and Transcriptional Responses to Recurring Environmental Stresses During Biological Invasions

2021 ◽  
Vol 8 ◽  
Author(s):  
Ruiying Fu ◽  
Xuena Huang ◽  
Yiyong Chen ◽  
Zaohuang Chen ◽  
Aibin Zhan
Keyword(s):  
Dna Methylation ◽  
Biological Invasions ◽  
Gene Transcription ◽  
Methylation Level ◽  
Environmental Stresses ◽  
Invasion Success ◽  
Transcriptional Level ◽  
Transcriptional Responses ◽  
Environmental Challenges ◽  
Stress Memory

Deoxyribonucleic acid methylation and gene transcription have been proved as two underlying mechanisms involved in rapid plastic response to environmental stresses. However, it remains elusive on how DNA methylation regulates gene transcription under acute and recurring environmental challenges to form the stress memory, further contributing to invasion success during range expansions. Using a model invasive species Ciona robusta, we investigated the regulatory roles of DNA methylation on gene transcription and their contribution to the formation of stress memory at 30 genes under acute and recurring osmotic challenges simulated during the invasion process. We found the bimodal distribution of methylation level for the 68 mCpGs identified across all the genes after challenges, but only five sites were significantly correlated with the expression of their corresponding genes. These genes participated in the biological processes of Ca2+ transport and metabolism of lipid and proline. At the DNA methylation level, we found two early-responding and four tardy-responding sites of stress memory and these sites were functionally related to genes involved in the biosynthesis of proline, metabolism of lipid, and transport of taurine and Ca2+. At the transcriptional level, three tardy-responding and five early-responding memory genes were involved in the transport of ions, regulation of water channels, biosynthesis of taurine, and metabolism of lipid. Altogether, the findings here suggest that DNA methylation and gene transcription should work in concert to facilitate the formation of stress memory, thus further improving the performance of invaders under recurring environmental challenges during biological invasions.

Transcriptional responses to low temperature and their regulation in Arabidopsis

2003 ◽  
Vol 81 (12) ◽  
pp. 1168-1174 ◽  
Author(s):  
Tong Zhu ◽  
Nicholas J Provart
Keyword(s):  
Low Temperature ◽  
Signaling Pathways ◽  
Low Temperatures ◽  
Quantitative Difference ◽  
Transcriptional Response ◽  
Environmental Stresses ◽  
Transcriptional Level ◽  
Mrna Levels ◽  
Transcriptional Responses ◽  
Cold Response

Recent studies have used a transcriptional profiling approach to identify genes in Arabidopsis that respond at the level of transcript abundance to cold (4 °C) or chilling (13 °C) temperatures. Results have shown that plants respond to low temperatures by altering mRNA levels of a large number of genes belonging to different independent pathways. Early transcriptional response to low temperatures frequently involves signaling pathways used to respond to other environmental stresses, indicating the existence and involvement of a complex genetic network. Genes with functions specific to low-temperature signaling pathways, and those with functions in multiple signaling pathways, especially those encoding transcription factors and other signaling molecules, have been identified based on their transcriptional responses to different environmental stresses. The qualitative and quantitative difference in transcriptional response to chilling and cold suggests that plants might have different molecular mechanisms to acclimate to different types of low-temperature stresses. The regulation and interactions of genes involved in low-temperature response at the transcriptional level has been further explored by computational methods, and preliminary results have identified motifs that are known to be important for cold response, raising the possibility of a better understanding of the processes involved.Key words: Arabidopsis, low-temperature stress, gene expression, transcriptional regulation, microarray.

scholarly journals Association between the extent of DNA methylation at the CpG sites of HIF3A and parameters of obesity in the general Japanese population

2020 ◽  
Author(s):  
Genki Mizuno ◽  
Hiroya Yamada ◽  
Eiji Munetsuna ◽  
Mirai Yamazaki ◽  
Yoshitaka Ando ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Dna Methylation ◽  
Body Mass ◽  
Methylation Level ◽  
Japanese Population ◽  
Public Health Problem ◽  
Major Public Health Problem ◽  
Transcriptional Responses ◽  
General Japanese Population ◽  
Cpg Sites

AbstractObesity is a major public health problem worldwide owing to the substantial increase in risk of metabolic diseases. Hypoxia-inducible factors (HIFs) regulate transcriptional responses to hypoxic stress. DNA methylation in the CpG sites of intron 1 of HIF3A is associated with body mass index in the whole blood and adipose tissue. This study investigates the correlation between DNA methylation of HIF3A and parameters of obesity, including thickness of visceral (VAT) and subcutaneous adipose tissues, in the general Japanese population. Participants (220 men and 253 women) who underwent medical examination were enrolled in this cross-sectional study. We used pyrosequencing to quantify DNA methylation (CpG sites of cg16672562, cg22891070, and cg27146050) in HIF3A. DNA methylation of HIF3A was only different in women. Multiple regression analysis showed that DNA methylation level at cg27146050 was associated with thickness of VAT in women. DNA methylation level at cg27146050 also correlated with body mass index and percentage of body fat in women after excluding smokers and non-smokers who quit smoking with the last 5 years. DNA methylation in the CpG site (cg27146050) of HIF3A correlated with parameters of obesity in Japanese women.

scholarly journals Profile of copper-associated DNA methylation and its association with incident acute coronary syndrome

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Pinpin Long ◽  
Qiuhong Wang ◽  
Yizhi Zhang ◽  
Xiaoyan Zhu ◽  
Kuai Yu ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Acute Coronary Syndrome ◽  
Methylation Level ◽  
Meta Analysis ◽  
Regulation Of Gene Expression ◽  
Density Lipoprotein ◽  
Blood Leukocytes ◽  
Coronary Syndrome ◽  
A Genome ◽  
Increased Risk

Abstract Background Acute coronary syndrome (ACS) is a cardiac emergency with high mortality. Exposure to high copper (Cu) concentration has been linked to ACS. However, whether DNA methylation contributes to the association between Cu and ACS is unclear. Methods We measured methylation level at > 485,000 cytosine-phosphoguanine sites (CpGs) of blood leukocytes using Human Methylation 450 Bead Chip and conducted a genome-wide meta-analysis of plasma Cu in a total of 1243 Chinese individuals. For plasma Cu-related CpGs, we evaluated their associations with the expression of nearby genes as well as major cardiovascular risk factors. Furthermore, we examined their longitudinal associations with incident ACS in the nested case-control study. Results We identified four novel Cu-associated CpGs (cg20995564, cg18608055, cg26470501 and cg05825244) within a 5% false discovery rate (FDR). DNA methylation level of cg18608055, cg26470501, and cg05825244 also showed significant correlations with expressions of SBNO2, BCL3, and EBF4 gene, respectively. Higher DNA methylation level at cg05825244 locus was associated with lower high-density lipoprotein cholesterol level and higher C-reactive protein level. Furthermore, we demonstrated that higher cg05825244 methylation level was associated with increased risk of ACS (odds ratio [OR], 1.23; 95% CI 1.02–1.48; P = 0.03). Conclusions We identified novel DNA methylation alterations associated with plasma Cu in Chinese populations and linked these loci to risk of ACS, providing new insights into the regulation of gene expression by Cu-related DNA methylation and suggesting a role for DNA methylation in the association between copper and ACS.

scholarly journals Epigenetic Contribution and Genomic Imprinting Dlk1-Dio3 miRNAs in Systemic Lupus Erythematosus

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 680
Author(s):  
Rujuan Dai ◽  
Zhuang Wang ◽  
S. Ansar Ahmed
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Dna Methylation ◽  
Lupus Erythematosus ◽  
Critical Role ◽  
Methylation Status ◽  
Transcriptional Level ◽  
Dna Hypomethylation ◽  
Systemic Lupus ◽  
Multiple Organs ◽  
Genetic Imprinting

Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease that afflicts multiple organs, especially kidneys and joints. In addition to genetic predisposition, it is now evident that DNA methylation and microRNAs (miRNAs), the two major epigenetic modifications, are critically involved in the pathogenesis of SLE. DNA methylation regulates promoter accessibility and gene expression at the transcriptional level by adding a methyl group to 5′ cytosine within a CpG dinucleotide. Extensive evidence now supports the importance of DNA hypomethylation in SLE etiology. miRNAs are small, non-protein coding RNAs that play a critical role in the regulation of genome expression. Various studies have identified the signature lupus-related miRNAs and their functional contribution to lupus incidence and progression. In this review, the mutual interaction between DNA methylation and miRNAs regulation in SLE is discussed. Some lupus-associated miRNAs regulate DNA methylation status by targeting the DNA methylation enzymes or methylation pathway-related proteins. On the other hand, DNA hyper- and hypo-methylation are linked with dysregulated miRNAs expression in lupus. Further, we specifically discuss the genetic imprinting Dlk1-Dio3 miRNAs that are subjected to DNA methylation regulation and are dysregulated in several autoimmune diseases, including SLE.

scholarly journals Associations among phthalate exposure, DNA methylation of TSLP, and childhood allergy

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Wan-Ru Wang ◽  
Nai-Tzu Chen ◽  
Nai-Yun Hsu ◽  
I-Ying Kuo ◽  
Hsin-Wen Chang ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Methylation Level ◽  
Respiratory Symptoms ◽  
Smoking Status ◽  
Phthalate Esters ◽  
Allergic Diseases ◽  
Percentage Increase ◽  
Phthalate Exposure ◽  
Settled Dust ◽  
Butyl Phthalate

Abstract Background Dysregulation of thymic stromal lymphopoietin (TSLP) expressions is linked to asthma and allergic disease. Exposure to phthalate esters, a widely used plasticizer, is associated with respiratory and allergic morbidity. Dibutyl phthalate (DBP) causes TSLP upregulation in the skin. In addition, phthalate exposure is associated with changes in environmentally induced DNA methylation, which might cause phenotypic heterogeneity. This study examined the DNA methylation of the TSLP gene to determine the potential mechanism between phthalate exposure and allergic diseases. Results Among all evaluated, only benzyl butyl phthalate (BBzP) in the settled dusts were negatively correlated with the methylation levels of TSLP and positively associated with children’s respiratory symptoms. The results revealed that every unit increase in BBzP concentration in the settled dust was associated with a 1.75% decrease in the methylation level on upstream 775 bp from the transcription start site (TSS) of TSLP (β =  − 1.75, p = 0.015) after adjustment for child’s sex, age, BMI, parents’ smoking status, allergic history, and education levels, PM2.5, formaldehyde, temperature; and relative humidity. Moreover, every percentage increase in the methylation level was associated with a 20% decrease in the risk of morning respiratory symptoms in the children (OR 0.80, 95% CI 0.65–0.99). Conclusions Exposure to BBzP in settled dust might increase children’s respiratory symptoms in the morning through decreasing TSLP methylation. Therefore, the exposure to BBzP should be reduced especially for the children already having allergic diseases.

scholarly journals MBD2 acts as a repressor to maintain the homeostasis of the Th1 program in type 1 diabetes by regulating the STAT1-IFN-γ axis

2021 ◽  
Author(s):  
Tiantian Yue ◽  
Fei Sun ◽  
Faxi Wang ◽  
Chunliang Yang ◽  
Jiahui Luo ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Type 1 Diabetes ◽  
Adoptive Transfer ◽  
Nod Mice ◽  
Transcriptional Level ◽  
Clinical Settings ◽  
Cpg Dna ◽  
Ifn Γ

AbstractThe methyl-CpG-binding domain 2 (MBD2) interprets DNA methylome-encoded information through binding to the methylated CpG DNA, by which it regulates target gene expression at the transcriptional level. Although derailed DNA methylation has long been recognized to trigger or promote autoimmune responses in type 1 diabetes (T1D), the exact role of MBD2 in T1D pathogenesis, however, remains poorly defined. Herein, we generated an Mbd2 knockout model in the NOD background and found that Mbd2 deficiency exacerbated the development of spontaneous T1D in NOD mice. Adoptive transfer of Mbd2−/− CD4 T cells into NOD.scid mice further confirmed the observation. Mechanistically, Th1 stimulation rendered the Stat1 promoter to undergo a DNA methylation turnover featured by the changes of DNA methylation levels or patterns along with the induction of MBD2 expression, which then bound to the methylated CpG DNA within the Stat1 promoter, by which MBD2 maintains the homeostasis of Th1 program to prevent autoimmunity. As a result, ectopic MBD2 expression alleviated CD4 T cell diabetogenicity following their adoptive transfer into NOD.scid mice. Collectively, our data suggest that MBD2 could be a viable target to develop epigenetic-based therapeutics against T1D in clinical settings.

scholarly journals The mediating effect of lifestyles on the association between social factors and DNA methylation

2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
A Maugeri ◽  
M Barchitta ◽  
G Favara ◽  
C La Mastra ◽  
MC La Rosa ◽  
...  
Keyword(s):  
Physical Activity ◽  
Dna Methylation ◽  
Socioeconomic Status ◽  
Mediterranean Diet ◽  
Educational Level ◽  
Methylation Level ◽  
Mediating Effect ◽  
High Educational Level ◽  
Age Related ◽  
High Educational

Abstract Background Social disadvantage and unhealthy lifestyles may induce molecular changes associated with aging and age-related diseases. For instance, previous studies reported socioeconomic difference in DNA methylation, which in turn led to aberrant gene expression and genome instability. Socioeconomic status (SES) alone, however, does not completely explain this difference, and further studies are needed to unveil what factors contribute to it. Methods We conducted a cross-sectional study on 349 Italian women, aged 25-64 years, to assess SES differences in LINE-1 methylation level - a surrogate marker of global DNA methylation - and to examine the mediating effect of lifestyles (i.e. diet, smoking habits, physical activity, and weight status). Educational level was used as SES indicator. The adherence to Mediterranean diet (MD) was assessed by the Mediterranean Diet Score (MDS). Leukocyte LINE-1 methylation was assessed by pyrosequencing. Mediation analysis was conducted using the PROCESS macro for the SPSS software. Results We first observed that women with high educational level were more likely to be normal weight (p < 0.001) and to adhere to MD (p = 0.018), and less likely to perform physical activity (p = 0.012) than their less educated counterpart. Moreover, age-adjusted linear regression demonstrated that LINE-1 methylation level increased with increasing educational level (β = 0.016; SE = 0.003; p < 0.001). In line, mediation analysis demonstrated an indirect effect of high educational level on LINE-1 methylation through the adherence to MD (β = 0.003; 95%CI=0.001-0.006). Specifically, the mediator could account for 9.5% of the total effect. None of the other lifestyles, instead, exhibited a significant mediating effect. Conclusions To our knowledge, this is the first study demonstrating the mediation of diet in the relationship between SES and DNA methylation. Thus, our findings add even more value to the promotion of healthy dietary habits among social disadvantaged people. Key messages Social disadvantage is associated with epigenetic changes related to aging and age-related diseases. Adherence to the Mediterranean diet might mediate the association between socioeconomic status and DNA methylation.

scholarly journals CSN5A Subunit of COP9 Signalosome Is Required for Resetting Transcriptional Stress Memory after Recurrent Heat Stress in Arabidopsis

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 668
Author(s):  
Amit Kumar Singh ◽  
Shanmuhapreya Dhanapal ◽  
Alin Finkelshtein ◽  
Daniel A. Chamovitz
Keyword(s):  
Transcription Factors ◽  
Heat Stress ◽  
Histone Methylation ◽  
Environmental Stresses ◽  
Cop9 Signalosome ◽  
Stress Memory ◽  
Transcriptional Stress ◽  
Transcriptional Memory

In nature, plants are exposed to several environmental stresses that can be continuous or recurring. Continuous stress can be lethal, but stress after priming can increase the tolerance of a plant to better prepare for future stresses. Reports have suggested that transcription factors are involved in stress memory after recurrent stress; however, less is known about the factors that regulate the resetting of stress memory. Here, we uncovered a role for Constitutive Photomorphogenesis 5A (CSN5A) in the regulation of stress memory for resetting transcriptional memory genes (APX2 and HSP22) and H3K4me3 following recurrent heat stress. Furthermore, CSN5A is also required for the deposition of H3K4me3 following recurrent heat stress. Thus, CSN5A plays an important role in the regulation of histone methylation and transcriptional stress memory after recurrent heat stress.

scholarly journals DNA methylation mediated RSPO2 to promote follicular development in mammals

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Xiaofeng Zhou ◽  
Yingting He ◽  
Nian Li ◽  
Guofeng Bai ◽  
Xiangchun Pan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Methylation Level ◽  
Molecular Mechanisms ◽  
Cpg Island ◽  
Wnt Signaling Pathway ◽  
Follicular Development ◽  
Expression Level

AbstractIn female mammals, the proliferation, apoptosis, and estradiol-17β (E2) secretion of granulosa cells (GCs) have come to decide the fate of follicles. DNA methylation and RSPO2 gene of Wnt signaling pathway have been reported to involve in the survival of GCs and follicular development. However, the molecular mechanisms for how DNA methylation regulates the expression of RSPO2 and participates in the follicular development are not clear. In this study, we found that the mRNA and protein levels of RSPO2 significantly increased during follicular development, but the DNA methylation level of RSPO2 promoter decreased gradually. Inhibition of DNA methylation or DNMT1 knockdown could decrease the methylation level of CpG island (CGI) in RSPO2 promoter and upregulate the expression level of RSPO2 in porcine GCs. The hypomethylation of −758/−749 and −563/−553 regions in RSPO2 promoter facilitated the occupancy of transcription factor E2F1 and promoted the transcriptional activity of RSPO2. Moreover, RSPO2 promoted the proliferation of GCs with increasing the expression level of PCNA, CDK1, and CCND1 and promoted the E2 secretion of GCs with increasing the expression level of CYP19A1 and HSD17B1 and inhibited the apoptosis of GCs with decreasing the expression level of Caspase3, cleaved Caspase3, cleaved Caspase8, cleaved Caspase9, cleaved PARP, and BAX. In addition, RSPO2 knockdown promoted the apoptosis of GCs, blocked the development of follicles, and delayed the onset of puberty with decreasing the expression level of Wnt signaling pathway-related genes (LGR4 and CTNNB1) in vivo. Taken together, the hypomethylation of −758/−749 and −563/−553 regions in RSPO2 promoter facilitated the occupancy of E2F1 and enhanced the transcription of RSPO2, which further promoted the proliferation and E2 secretion of GCs, inhibited the apoptosis of GCs, and ultimately ameliorated the development of follicles through Wnt signaling pathway. This study will provide useful information for further exploration on DNA-methylation-mediated RSPO2 pathway during follicular development.

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