Questions related to Epigenomics
If you can change your lifestyle/behaviour, how soon can these changes be detected in the epigenome? How long (estimate) would this change be detected in the majority of cells? Can this change also be detected in gametes? Will these changes be passed onto offspring?
By behaviour I mean things like having a good diet, working in less stressful environment, stopping smoking or even more taking more exercize.
As it's well known, breast cancer can be caused through genetics factor. How did it happen? Does it have corelation with epigenetics? And what are the chances that it can be lowered?
Democracy links to a genetic or epigenetic regulation? Can we create democratic mice or humans? The switch on/off of Democratic values depend on the social; memories; spatial properties of the individual or the society?
Are we democratic individuals or just members of social groups who follow?
I am trying to look at the epigenetic modification statuses of a set of genes, does anyone knows whether there is a epigenetic modification database for individual genes?
What is the best bioinformatics approach to study epigenetic effects transferred from parent to offspring in trauma cases. Are there data repositories available in this domain?
Epigenetics is one of the key areas of research in the coming decades. Because it has the potential to fundamentally alter a human being's life by altering the expressions of beneficial or bad genes. I would like to read the work of the best scientists in the area of epigenetics, especially as it applies to the functioning of the brain. Also, I shall be grateful if you could suggest the best ten papers in this domain, by reading which I can get a reasonable update of the current status in this exciting research area.
I'm very new at epigenetics and I came across some processed files from GEO database specially this one:
More specific to the file called:
If I look at cg02162324, I can see that all the columns related to Sample[n]detectionPValue have 0 as value.
It doesn't happen to all cpgs.
I'm wondering if p-value = 0 would mean that this value is not valid.
Centers in India that offer hands-on training in bisulfite conversion, DNA methylation, expression, and epigenetics are preferred.
Dear Ladies and Gentlemen,
I would like to find a database with Neisseria sp genomes with methylated adenines.
Could you advise my something?
good day! I am a currently researching about epigenetic variations (Mainly on DNA methylation) of a fish that can change habitats (from saltwater to freshwater), my main goal/topic is about osmoregulation and my target tissue is gills. my original plan was to get samples from both habitats regardless of what sex of the fish is. however, most of the literatures that I have been reading collected male only fish. I would be very grateful for your insights.
I want to publish an article on "Behavioral Epigenetics" in a Journal without APC. If anyone can give me any suggestion, that would be very helpful.
Thank you in advance.
My work is with highly plastic eukaryote taxa, with real time visible structural variation on individuals. I suspect they have high epigenetic fluidity while growing, and would like to understand the underlying mechanism(s) that alters epigenetic expression in this group. Methylation studies are what are most easy to study now for epigenetics, and may be of some use. However, methylation studies require existence of a gene map or maps, that this taxon does not have yet, and methylation is only one of many ways that epigenetic expression is impacted. Are there other methods that researchers are using now to get at how cells alter and/or manage epigenetic expression? Please tell me about other approaches, include equipment, supplies and approximate costs if you can. Anything useful on methylation would also be of use. Thank you.
I need epigenetic data file run through the hovarth clock. DNA Methylation Age Calulator, but did not find any description how it should be done?
Please can you help me to find link to describe the process of running the data?
perhaps the most useful aspect of epigenetic processes is that they are readily reversible. Unlike genetic effects that also play a role in cancer and aging, epigenetic aberrations can be relatively easily corrected. One of the most widespread approaches to epigenetic alterations in cancer and ageing is dietary control. now, I would like to know more about the types and mechanisms of that nutrition that have a positive impact on epigenetic alteration during cancer???
we are going to carry out some epigenetic experimentations. definitely we need to count the cells. however some samples are dried-freeze cell pellet and had reserved in -80 freezer. the question is can we use them for cell counting after that long-term freezing? are they intact? is it authenticated??
We integrated a gene in a cell line genome, when we culture them, the gene turn to silencing. We collected non-silencing cells and culture them, some of them turn to silencing again. We already check the gene, it is fine and still there.
We want to figure out what factors cause the silencing, but we are not familiar to epigenetic.
Any one and any suggestions will appreciate.
Can anyone suggest to me what will be the best way to learn how to use the Perl or R bioconductor? Can anyone suggest a good link so I am able to learn on my own? Though my PhD was focussed on immunology, I want to learn how to use these two tools in the field of epigenetics?
I am working on cancer genomics. I downloaded TCGA BRCA FPKM data for my analysis. after some preliminary analysis, I categorised 250 samples in total 2 distinct categories. Now I want to analyse and compare their epigenetic and mutation patterns.
After downloading all mutation and epigenetic data from TCGA BRCA, none of the samples from my previous analysis is matching.
Suppose, TCGA-AN-A0AK-01A-21R-A00Z-07 sample is present in my previously downloaded FPKM data.
But TCGA-AN-A0AK-01A-21W-A019-09 is available in the mutation data. Are these ids the same? For FPKM data and mutation data, do the same sample (individual) be represented by different Ids?
Please help me, Thank you in advance.
I am searching information about increasing yield of secondary metabolites that are heterogeneously produce in S. cerevisiae.
First I transfer several genes into yeast, then I wanna to optimized the yield of these metabolites. I wonder that whether epigenetic modifications play any roles in enhancing the production of these metabolites in the yeast transformants?
Thank you very much!
We know that epigenetic factors are denoted by alterations in DNA methylation, histone modification abd transcription of regulatory non coding RNA such as microRNAd but are there additional epigenetic changes that take place that do NOT involve these mechanisms?
Conventional Darwinian evolution is based on random mutations causing adaptive change. In contrast to that, evolution due to epigenetic inheritance offers the opportunity to trace the causal relationships, particularly when seen from the cellular-molecular level. Using this approach, the exaptive changes in adaptation to gas exchange from the lung alveolus to the unicellular have been traced (Torday JS, Rehan VK. The evolutionary continuum from lung development to homeostasis and repair. Am J Physiol Lung Cell Mol Physiol. 2007 Mar;292(3):L608-11; Torday and Rehan. Evolution, the Logic of Biology. Wiley, Hoboken, 2017) with gaps along the way due to the novelty of this approach. However, such gaps could be filled, and other physiologic traits could similarly be elucidated, leading to a new way of understanding physiologic evolution independent of function, particularly as it relates to dysfunction in disease.
I need to know if cells are arresting in S or G2/M phase , some cells are still trying to replicate themselves by mutations or other epigenetic factors because we are giving stress by any drug to stop their growth. Those cells can have the properties to carryout re-replication. If one can look at them through flow cytometry, then how to analyze them. I welcome suggestion from anybody expertise on this field. Please suggest.
We have conducted an experiment on epigenetic allele identification and quantification for some quantitative trait. we are trying to map epigenes using epigenome association mapping (EWAS). Please share related information for better mapping and also share r codes for the same.
How epigenetic mechanism affects an organism response to environment? If the DNA structure is not changed through epigenetic mechanism, how it could epigenetic said to be heritable?
Hi everyone. I need to read about protocols for preparing tissues before using them to measure epigenetic histone marks. I've been told these may be based on the 'Marburg protocol', however, I have not been able to find much info about this. Would really appreciate any help.
Hi, I have a question if anyone can answer. I have identified two co-factors for my transcription factor. But the mass spec data seems insignificant. Now I want to find if some other co-factors are involved in regulating my transcription factor? So, how can I do this? Should I cut my gel band at different molecular weight or should I go for ChIP-seq to determine their binding complex?
Hello all. I am trying to isolate buffy coat from whole blood (sodium citrate), and planning on cyropreserving it for later analysis (~3-5 years). As to what analysis would include, we are leaving it as open ended as we can, but mostly am thinking of extracting DNA (Qiagen or home extraction) and looking at epigenetics.
What freezing media is typically used for this type of storage? Would a standard 90% PBS and 10% DMSO work, and what are the drawbacks.
Additionally, I read about the potentiality of platelets clumping and potentially interfering with the sample. Does anyone have any advice on purifying platelets from the buffy coat on that end? Thank you all very much.
I am trying to repress expression of GFP which is expressed from a plasmid using dCas9-KRAB. I know KRAB represses genes through epigenetic modifications, and so I was wondering, will it still work if the gene that dCas9-KRAB targets is not integrated into the genome, but rather, expressed from a plasmid? Thank you.
I'm just learning how to perform an analysis of methylation patterns using bisulfite sequencing data, but I have some questions:
1. What database I can use for obtain bisulfite sequencing data?
2. I should start performing an analysis focused on one chromosome or on one whole genome?
3. Because I want to perform this type of analysis in the context of cancer epigenomics (specifically methylation patterns of promoters and genes), is it good idea to use RRBS data instead of WGBS data?
As we all know mutations drive cell carcinogenesis. However, does DNA change(not epigenetic modification) play a role in the occurrence of benign diseases? Such as drug complications.
I am working on epigenetic modifications with aging, especially DNA methylation. I have .bed, .sam and .bedgraph files obtained in bisulfite DNA sequencing.
1) Is there any software other than methylkit for DNA methylation analysis? I am looking for global and chromatin level DNA methylation analysis.
2) Any tool that can analyse CpG methylation level in specif regions e.g promoter region, 5 and 3 UTRs or a specific genes.
I am writing a paper with the title (above) and am wondering whether anybody could recommend a journal, or book, that may be interested in such an article.
Thanks in advance,
I'm working on bio-informatics. And my current project is to analyze public data from TCGA and GEO to find novel genes' relation to diagnosis or prognosis of cancer. The special feature of TCGA data is the enclosing clinical data, which we can use for further analysis.
I'm just want to know that is there any platform or source of public data like TCGA or GEO? Because sometimes I need to validate the data. But I can find another source for validation, and I have no available clinical data of the interest problem in my hospital.
Thank you very much for reading and sharing experience!!!
I will start a study using peripheral cells in blood samples of new coronavirus infected individuals in São Paulo, Brazil. The aim of the project is to perform epigenetic and transcriptomic analyzes in these patients. However, is necessary to inactivate the virus first. For this, we intent to use Biomerieux lysis buffer. Can this inactivation process affects the analysis?
Thank you for attention.
I want to perform DNA methylation profiling in leukocytes for an epigenetic analysis. However, I want to preserve the leukocytes for DNA methylation profiling for later. What is the best way to preserve the leukocytes for the epigenetic analysis?
When we want to study epigenetic effects of bush/wild fires, using an ongoing cohort, we need to focus on a limited list of CpGs. Although necessary, the funding agency does not allow exploratory research. We are considering to include CpGs that are differentially methylation after exposure to smoking (568 CpGs), to PM10 and PM2.5 exposure (~70CpGs), and to stress (?? CpGs).
However, we need a smaller list.
Any preliminary data is welcome.
I want to study the relationship between different epigenetic factors and the different types of cancer using existing records in epigenetic and / or oncological databases, but, as a bioinformatician, I have never worked with epigenetics data, so I do not know they are available in what format, they require what type of preprocessing, nor what tools I can use to analyze them.
I would really appreciate if someone gave me some basic indications of how I should start, or if someone recommended me a paper or tutorial about how to work with epigenetic data in cancer bioinformatics.
I'm just a freshman in the field of epigenetics. I have questions about methylation data analysis:
The data from Infinium HumanMethylation450 BeadChip will tell us which CpG sites are methylated or not, but I do not know the corresponding genes. so how do we tell which genes are methylated or not? which tools are appropriate to interpret this data? is QDMR useful for this purpose?
Thank you very much
I an currently working on a project that will involve the Horvath epigenetic clock as a quantitative measure of ageing. The clock is based on assessing the methylation of 353 CpG sites. I'm new to this area, but it appears that the standard approach is to use the methylation array chips from illumina. I'v found that the current Illumina chip (850k) is fairly expensive and lacks coverage of 17 CpG sites required for the clock.
Does anyone know of an alternative for assessing these specific 353 CpG sites?
A method to help narrow down which sample are worth analyzing with the chip?
Happy new year! I have a very rudimental question to bother you with. I'm interested in the principles of epigenetics. All the cells I'm familiar with are in cell cycle, such as HEK293 cells and a variety of tumor cell lines. I became very interested in post-mitotic cells that are not cycling anymore but I couldn't figure out a good (and easy) model to work on. I thought about using BMDM, but then I realized that they need around 7 days to fully mature, after which they will stay healthy only for a couple of days. Essentially, I'm looking for a primary post-mitotic cell that is:
1. easy to culture for a long time
2. easy to acquire from companies or mice.
3. a good transfection host.
At this stage I don't have a lot of plans regarding epigenome editing yet, and above are the only criteria I have. May I ask for some recommendations?
Thank you so much and best regards,
Hi, I'm a psychology student and want to know that intergenerational and parent's jobs affect mental activities or not?
For example, if your grandfather was an engineer does it affect your spatial intelligence?
I think it's related to evolution, epigenetic and Lamarckism subjects.
I hope you can help me.
Cancer tumor change bucause it´s an independent animal using the normal mechanism and resources in his own benefit and all the time the tumor found ways to scape from therapies and from the normal mechanism of conttrol, in other way epigenetic has a very important influence in the couse of disesase and in therapies results.
Usually when we discuss about epigenetic modifications specifically DNA methylation, we observe hypermethylation of promotor or CpG usually results in gene silensing/ low regulation.
In my case promotor region of this specific gene is hypermethylated but mRNA levels and protein levels are upregulated which results in increased in metastasis in breast cancer.
Could you please suggest me some papers, textbooks and basic tools for learning in silico methods? Primarily, I want to research about cancer metabolism, drug resistance, and epigenetics. For example, how can I work on and understand "possible" protein-protein interactions, non-coding RNA targets and cell to cell communication?
Thank you in advance
As we see that the speed breeding is mainly based on considerable modifications in the plant growth environments to gain rapid generation advancements, does such pre-disposal of plants to changing environments have epigenetic influences over generations?
I would like to construct truncated TFs to performed protein interaction and luciferase coactivation assay. I am not sure where tag should be inserted. TFs have different domains. Should the tag be away from the most critical domains. Are there any general principles for determination of tag inserted positions?
Hi everyone, I'm working on seagrass samples and I was thinking of preserving the tissues for methylation analysis in silica gel. Do you think it could have any influence on epigenetic mechanisms and therefore it is better to use liquid nitrogen directly?
Here is a question:
Suppose you have T cell "A" that gets activated by cognate antigen and differentiates into an effector cell.
Part of the differentiation is epigenetic programming into an effector cell fate. Activation results in its engaging the cell cycle and proliferating into Cells "B" and "C" Do cells "B" and "C" inherit the effector epigenome? Or do they start as naive T cells until they see antigen?
In other words, suppose that only cell "A" sees antigen and becomes an effector, do cells "B" and "C" become effectors by default? Thank you...
I'm trying to understand epigenetic variability but the study I'm performing involves measuring the gene expression in a given region according to the SNP's alleles associated with the increase of that gene's expression. But epigenetic is related to heritable variations that affect the phenotype without affecting the DNA sequence, so can SNPs be used in this study?
I'm new in the genetics field and really confused in this matter, any help would be appreciated! Thank you
I am currently working on the epigenetic (methylation) aspect of coronary artery disease. After short-listing a list of CpG sites with the help of microarray data I am currently working on HRM to semi-quantitate the extent of methylation of few sites.
The standards procured are mixed in equimolar concentration and 0% ,25%, 50%, 75% and 100%. All the input DNA are maintained at 20ng/ul.
However, in the process of standardization, I am facing a concurrent issue where a few samples are consistently coming as beyond 100%. How can I interpret this data?
Mack et al studied subtypes of three ependymoma(same histopathology) brain tumors and found that one subtype carries an intrachromosomal translocation that creates a new tumor-driving gene, another lacks tumor-driving mutations but has aberrant epigenetic modifications, and a third shows neither gene mutations nor epigenetic aberrations. There were three genotype but one cancer phenotype. Similarly Martincorena and colleagues found thousands of mutations in cancer-relevant genes, including cancer-driver genes, in normal eyelid epidermis .(multiple cancer genotypes but no cancer phenotype).
In disparate classes of biological systems, there are more genotypes than phenotypes. Where sufficient information exists to enumerate these phenotypes, there are exponentially more genotypes than phenotypes, as a function of the number of system parts. This means that any one phenotype typically has many genotypes that form it.
In a brief, cancer is the decision of the cell to choose the innovative/adaptive phenotype and understanding the genotype does not mean understanding cancer.
1. Mack, S. C., Witt, H., Piro, R. M., Gu, L., Zuyderduyn, S., Stütz, A. M., et al. (2014). Epigenomic alterations define lethal CIMP-positive ependymomas of infancy. Nature 506, 445–450.
2. Martincorena, I., Roshan, A., Gerstung, M., Ellis, P., Van Loo, P., McLaren, S., et al. (2015). High burden and pervasive positive selection of somatic mutations in normal human skin. Science 348, 880–886.
How to give NGS-Seq data as input to AI tools?
Tell me about some Autoencoders and decoders with examples, or any detail tutorial ..?
I would like to analyse epigenetic changes in response to dietary phytochemical supplementation in humans.
Can anyone explain if this is feasible and how would such analysis be conducted?
Hello everybody, I am working in a conifer tree species, initially i need to propagate the plant through callus, i have established the callus induction but i struggle to regenerate the plant through callus, so i have planned to regenerate the plant through epigenetic remodeling. can we regenerate the plant through DNA methylation process..? i looked at the protocol for this. i would appreciate if anyone have experience in the plant regeneration via epigenetics. Thank you.
Epigenetics is the study of heritable phenotype changes that do not involve alterations in the DNA sequence. Genetics involve with change of DNA sequence. Then what is more effecting.....
People are born into the world for a purpose is a popular promise backed by epigenetics and other new paradigms. It is believed we choose the situations we come into to reinforce our creative skills needed to do what we are here for. The physical environment and the people in it are still in the survival dimensions of life which today is demanding that we grow into spiritual beings we truly are. The emotional and mental faculties are the tools to accomplish the transformation into higher consciousness, where we can live fully, love and be divine beings. If this is not the path our children are on the journey becomes on of perpetual seeking and PAIN. The sins of the parents are inherited by their children, says the good book and it is so. Children are not OUR future They are their own future that we might enjoy if we let them define it for themselves with our love and support.
I performed a large scale methylation analysis by RRBS-Seq on Infinium Human Methylation 450K BeadChip platform with generated raw data in FASTQ format. What are the main steps to do the bioinformatic analysis?
I have found in preliminary tests that many (6 tested so far) of the commercially available H4K20me3 antibodies can be blocked in ChIP assays by K20me2 peptides as well as K20me3.
Has anybody had similar experiences with other histone modifications like H3K4me2/3 or H3K9me2/3 etc? Come to think of it - most ChIP-seq studies show quite similar profiles for KXme2 and KXme3 histone modifications while KXme1 tends to be less overlapping.
Hi, I'm going to research on mechanisms by which cells differentiate in different directions at the epigenetic level. And I choose WGBS to study DNA methylation. Do you have any suggestions on what does the WGBS data sue for, or any research ideas on my project, or any related articles？Thanks!!!
By certain type of cancer, mutations are well known. Genome/epigenome editing could possibly "repair" such genes or silence them by methylation of their promoter.
It is widely accepted that E-cadherin expression is suppressed in metastatic cancer cell. However, there are two possibilities in vivo underlying the down-regulation of E-cadherin;
1) Tumor cells undergo epithelial-mesenchymal transition, thereby decreasing E-cadherin expression level.
2) The promoter region of gene encoding E-cadherin is methylated and this epigenetic alteration is responsible for down-regulation of E-cadherin
Which theory is more likely in vivo (not in vitro)?
Mostly, CRC carcinogenesis or other neoplasms mainly occurs due to epigenetics such as change in food habits. Though, western life style foods is an main cause of CRC.
Can we consider quorum-sensing regulation in bacteria as epigenetic regulation in eukaryotic cells ?
I am trying to observe epigenetic markers that may identify early stages of COPD or predict disease prognosis in patients with COPD, I'm not quite sure how to calculate the sample size I need as there will be no intervention, only observation. I already calculated based on COPD prevailence of 2% against general population and got a sample size of 385, is this correct? it does seem too large.
Dr. Magnus Nordborg recently pointed out in a presentation that is no evidence that methylation is involved in either development or adaptation and there is still little evidence of the involvement with gene regulation.
Also, the paper "Epigenomic Diversity in a Global Collection of Arabidopsis thaliana Accessions" (Kawakatsu et al. 2016) showed methylation in Arabidopsis strongly correlated with geography and climate of origin.