Science topic
Epigenetics - Science topic
This group is a platform to discuss and share information about epigenetics and related methods.
Questions related to Epigenetics
We are measuring methylation at the POMC gene on human DNA.
We are getting good results with out PCR but are consistently having issues with low peak height and baseline drift on the sequencing step.
The option appears to be to increase PCR product though the manual says the maximum is 10ul. We have tried 15ul and this shows some improvement but does not resolve the issue entirely.
Does anyone have experience of the machine and can you put more product in?
Any suggestions much appreciated.
Toby
Cytosine methylation, histone acetylation, etc. represent distinct epigenetic mechanisms of gene regulation. Which example is most likely to account for transgenerational effects, such as grandparent effects, etc.?
I am acid extracting total nuclear histones from plasmodium parasites. I precipitate the acid extracted histones using 20% TCA and then washing the pellet with ice-cold acetone. The final pellet is resuspended in ultra pure water. When I estimate the protein usign BCA or bradford method the amount varies eratically between BCA or Bradford and is not matching with protein amount loaded on the SDS-PAGE (Visual estimation). Which method is best for estimating the protein concentration of histone preparations?
Can epigenetic modifications affect various aspects of sperm development, function, and fertilization?
I am trying to find a correlation between fetal macrosomia and hypertension during pregnancy from CDC data. But there have been a lot of studies on the epigenetics of the underlying relationship without analyzing real patient data. Then, is my original study considered novel?
Limitation:
1) target specific gene:
2) do epigenetic modification:
According to epigenetic science, does it play a role in discovering genes that contain different amino acids that cause the appearance of characteristics or behaviors in people who eat meat and milk from imported animals? Which lived in a special nature other than that in which the importing country lives?
I'm using epitech bisulfite kit (qiagen) and even starting with huge amount of starting material (up to 2 micrograms) I'm unable to recover DNA. Does anyone have similar experiences?
Trying to find the relationship between epigenetic and cancer more deeply.
Jaques Monod Albert Camus et l’affaire Lyssenko.
1) Molecular genetics: A revolutionary meeting of minds
2) Jacques Monod Quelques pages inédites de sa vie.
Trofim D. Lyssenko, né à Kiev, devient ingénieur agronome. Sa carrière fulgurante le conduit en 1938 à la tête de l’Académie des sciences agronomiques de l’URSS. Sa doctrine scientifique, basée sur la transmissibilité des caractères acquis, devient une idéologie.
Quant à Jacques Monod, il n’a aucune hésitation et publie dans le journal Combat que dirige alors Camus, un article au titre éloquent en première page : “la victoire de Lyssenko n’a aucun caractère scientifique” et termine de façon radicale : “En définitive ce qui ressort le plus clairement de cette grotesque et lamentable affaire, c’est la mortelle déchéance dans laquelle est tombée en URSS la pensée socialiste”
Trofim D. Lysenko, born in kyiv, became an agricultural engineer. His dazzling career led him in 1938 to head the USSR Academy of Agricultural Sciences. His scientific doctrine, based on the transmissibility of acquired characteristics, becomes an ideology.
As for Jacques Monod, he had no hesitation and published in the newspaper Combat which Camus was then directing, an article with an eloquent title on the first page: “Lysenko's victory has no scientific character” and ended radically: “ Ultimately what emerges most clearly from this grotesque and lamentable affair is the deadly decline into which socialist thought has fallen in the USSR.
Peut-on aujourd’hui exclure la transmissibilité des caractères acquis ?
Can we exclude today the transmissibility of acquired traits ?
Dear All.
If a researcher wont to conduct an article to evaluation an axpected noval epigentic compound, what is the most essential steps of techniques that should followed to optimised his work,rather thant measurring the cytotoxicity of the compound
thanks in advance.
Hello,
Is it possible to silence all kinds of epigenetic modifications in a cell by using gene or inhibitor?
Thank you.
What are the epigenetic drivers behind the formation and progression of pediatric brain tumors?
I intend to explore the integration of computational biology and artificial intelligence (AI) with laboratory and experimental work, encompassing animal models, cell culture, clinical trials, and molecular studies. As a clinical biochemistry student with a keen interest in AI, I believe this interdisciplinary approach holds immense potential for advancement and innovation.
However, I face the challenge of identifying relevant literature in this emerging field. I would greatly appreciate guidance on effective keywords and search strategies to navigate this landscape of research and achieve my research goals.
I am currently trying to express Turritopsis dhornii TET enzyme with a 6x HIS tag in a BL21 E.coli host. Every time I purify my protein it shows double bands on SDS-PAGE, when testing its activity on ELISA there seems to be no activity. My lysis buffer contains 50mM HEPES ph 7.5, 30 mM imidazole, 500mM NaCl, and 1mM DTT. I purify with 800uL of Nickel Sepharose beads. Are there any adjustments I could make to stop this double band from showing?
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?
how yoga is affecting the epigenetics and is there any mechanisms available?
On 21-22-23 June 2023, the Milan Medical School of Ambrosiana University promoted an International Conference in streaming, on the subject:
The paradigm change of medicine: the epistemological and scientific basis
of Person-Centered Medicine
This conference is aimed to underscore the urgent need for overcoming Medicine's current wrong and obsolete deterministic-mechanistic-biological paradigm based on the linear causality toward the assumption in Medical Education, Clinics, and Public Health of the right indeterministic person-centered paradigm of human nature, Medicine, medical science, and health.
Call for papers on the following topics:
EPISTEMOLOGY AND MEDICINE, ALLOSTASIS PHYSIOLOGY, EPIGENETICS PSYCHO-NEURO-ENDOCRINE-IMMUNOLOGY, PSYCHOPHYSIOLOGY, NEUROBIOLOGY, MEDICAL ETHICS, PERSON-CENTERED MEDICINE, PERSON-CENTERED HEALTH, PERSON-CENTERED PSYCHIATRY, MEDICAL EDUCATION, WHO and HEALTH DEFINITION, SOCIAL PSYCHIATRY
If you have an interactionist approach to behavior and affectivity quality, PNEI, neuromodulation, and epigenetics you are welcome.
Deadline: June 10, 2023
Registration and abstract forms on
Giuseppe R.Brera
Rector of Ambrosiana University
Director of the Milan School of Medicine
Dear colleagues! I've tried to estimate the histone variants enrichment of several arabidopsis genomic sites but every time my enrichment result looks like the added screenshot. What am I doing wrong?
The running function is:
enr.df <- enrichment(query =gr_list[[1]], catalog = anno, shuffles = 24, nCores = 12)
anno is remap2020_histone_nr_macs2_TAIR10_v1_0.bed,
catalog is a GRanges of sites of interest of A.thaliana (all 5 chromosomes).
There are no warnings after function execution.
Hi, I'm studying the epigenetic changes in genes. For this I have the primer sequences and I need to identify the corresponding target gene sequences. Can someone help me out?
Where can I find this information? thanks a lot!!!!
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?
I am trying to insert a 60 bp shRNA into the pLKO.3G plasmid (variant of pLKO.1), yet nothing is working.
I digest with EcoRI and PacI, anneal the oligos at 95 for 4 mins then 70 for 10 mins, then cool down to room temperature gradually. And I do quick ligation for 10 mins at room temperature, and transform into HB101 competent cells. However, nothing is growing on the ampicillin plates. Any suggestions?
I followed the protocol they have on Addgene, but it did not work.
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:
GSE64491_datSignal_tissue.csv.gz
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.
Thank you
The relevance of the Microbiota-Gut-Brain axis to Alzheimer’s and neurodegenerative diseases needs extensive analysis. The various articles indicate that there are various questions with relevance to microbiota-gut-brain axis that are relevant to the pathology, pathogenesis and treatment of neurodegnerative diseases.Several mechanistic studies are required to determine the underlying mechanisms for effective and safe probiotic treatment for AD and probiotic benefits remain to determined. The relevance of gut dysbiosis may induce inflammatory responses that may be the cause of the induction of the pathogenesis of AD and relevance of diet (unhealthy diets), probiotics and gut microbiota should be carefully assessed. The meta-analysis studies indicate that probiotics reduce inflammation and oxidative stress and enhances cognition in AD and MCI individuals. The effects of different types of probiotics on amyloid formation and deposition needs to be evaluated and probiotic mixture therapy may be unsafe. The safety of probiotic therapy for AD patients require investigation with relevance to neuron reprogramming and programmed cell death in AD. The risk of unsafe microbiota and probiotic use may lead to the inactivation of the anti-aging gene Sirtuin 1 and the generation of uncontrolled short chain fatty acid release that promote amyloid beta plaque formation.
The concerns with relevance to the induction of dyslipidemia and the role of safety of diet-microbiota-brain axis should be carefully assessed with relevance to the cholesterol-AD connections. The prebiotic, symbiotic and probiotic formulations should be carefully assessed for bacterial composition and living microorganisms such as gram negative and positive. The release of bacterial lipopolysaccharides (LPS) from gram negative bacteria needs to be controlled and the content of gram negative bacteria carefully assessed in these prebiotic, symbiotic and probiotic formulations. Unhealthy diets contain end products such as LPS and diets should be carefully assessed for LPS contents since LPS has been associated with the inactivation of Sirtuin 1. The gut microbiota based therapy is in progress and the relevance to the treatment of brain diseases such as AD is limited. The benefits, limitations and safety of gut microbiota and probiotics on Alzheimer’s disease needs to be placed under systematic review with relevance to dietary regulation and postbiotic supplementation that have the implications for amyloidosis and neurodegeneration. The role of probiotic therapies to create a health gut environment by balancing bacterial populations may require the activation of the anti-aging gene Sirtuin 1 to reverse the pathogenesis of Alzheimer’s disease. The literature indicates that yogurt is a prime source for probiotics and provide a healthy balance of live bacteria to provide health benefits to individuals in various countries of the world. However a recent article indicates that within 12 hours yoghurt can grow gram negative bacteria. The gram negative bacteria in yoghurt depending on daily or weekly intake can generate high levels of plasma LPS with relevance to prebiotic, synbiotic and probiotic quality products and ill health. Yoghurt products may need to be assessed for gram negative bacteria populations and LPS to determine the quality control of these products for international communities.
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RELEVANT REFERENCES:
A. Marzban A, Rahmanian V, Marzban A, Ramezani Siakhulak F. The Role of Probiotics in Improving Alzheimer's Disease. JNFS. 2022; 7 (2) :136-138.
B. de Rijke TJ, Doting MHE, van Hemert S, De Deyn PP, van Munster BC, Harmsen HJM, Sommer IEC. A Systematic Review on the Effects of Different Types of Probiotics in Animal Alzheimer's Disease Studies. Front Psychiatry. 2022 Apr 27;13:879491.
C. Guo L, Xu J, Du Y, Wu W, Nie W, Zhang D, Luo Y, Lu H, Lei M, Xiao S, Liu J. Effects of gut microbiota and probiotics on Alzheimer's disease. Transl Neurosci. 2021 Dec 27;12(1):573-580.
D. Ji HF, Shen L. Probiotics as potential therapeutic options for Alzheimer's disease. Appl Microbiol Biotechnol. 2021 Oct;105(20):7721-7730.
E. D’Argenio V, Sarnataro D (2021) Probiotics, prebiotics and their role in Alzheimer’s disease. Neural Regen Res 16(9):1768-1769.
F. Bonfili L, Cuccioloni M, Gong C, Cecarini V, Spina M, Zheng Y, Angeletti M, Eleuteri AM. Gut microbiota modulation in Alzheimer's disease: Focus on lipid metabolism. Clin Nutr. 2022 Mar;41(3):698-708.
G. Naomi, R.; Embong, H.; Othman, F.; Ghazi, H.F.; Maruthey, N.; Bahari, H. Probiotics for Alzheimer’s Disease: A Systematic Review. Nutrients 2022, 14, 20.
H. Arora K, Green M, Prakash S. The Microbiome and Alzheimer's Disease: Potential and Limitations of Prebiotic, Synbiotic, and Probiotic Formulations. Front Bioeng Biotechnol. 2020 Dec 14;8:537847. doi: 10.3389/fbioe.2020.537847.
I. Peterson CT. Dysfunction of the Microbiota-Gut-Brain Axis in Neurodegenerative Disease: The Promise of Therapeutic Modulation With Prebiotics, Medicinal Herbs, Probiotics, and Synbiotics. J Evid Based Integr Med. 2020 Jan-Dec;25:2515690X20957225.
J. Kincaid HJ, Nagpal R, Yadav H. Diet-Microbiota-Brain Axis in Alzheimer's Disease. Ann Nutr Metab. 2021;77 Suppl 2:21-27. doi: 10.1159/000515700.
K. Alessio Vittorio Colombo Rebecca Katie Sadler Gemma Llovera Vikramjeet Singh Stefan Roth Steffanie Heindl Laura Sebastian Monasor Aswin Verhoeven Finn Peters Samira Parhizkar Frits Kamp Mercedes Gomez de Aguero Andrew J MacPherson Edith Winkler Jochen Herms Corinne Benakis Martin Dichgans Harald Steiner Martin Giera Christian Haass Sabina Tahirovic Arthur Liesz. (2021) Microbiota-derived short chain fatty acids modulate microglia and promote Aβ plaque deposition. eLife 10:e59826.
L. Anti-Aging Genes Improve Appetite Regulation and Reverse Cell Senescence and Apoptosis in Global Populations. Advances in Aging Research, 2016, 5, 9-26
M. Appetite Regulation and the Peripheral Sink Amyloid beta Clearance Pathway in Diabetes and Alzheimer’s Disease. Top 10 Commentaries in Alzheimer’s Disease (e-book). 2019;2:1-11. www.avidscience.com
N. Single Gene Inactivation with Implications to Diabetes and Multiple Organ Dysfunction Syndrome. J Clin Epigenet. Vol. 3 No. 3:24.
O. Sirtuin 1, a Diagnostic Protein Marker and its Relevance to Chronic Disease and Therapeutic Drug Interventions”. EC Pharmacology and Toxicology 6.4 (2018): 209-215.
P. Nutritional diets accelerate amyloid beta metabolism and prevent the induction of chronic diseases and Alzheimer’s disease. Photon ebooks. 2015.
Q. Wassenaar TM, Zimmermann K. Lipopolysaccharides in Food, Food Supplements, and Probiotics: Should We be Worried? Eur J Microbiol Immunol (Bp). 2018 Aug 21;8(3):63-69.
R. The Future of Genomic Medicine Involves the Maintenance of Sirtuin 1 in Global Populations. Int J Mol Biol . 2017. 2(1): 00013.
S. Bacterial Lipopolysaccharides and Neuron Toxicity in Neurodegenerative Diseases. Neurology Research and Surgery. 2018; 1(1): 1-3.
T. C.J. Hervert, N.H. Martin, K.J. Boor, M. Wiedmann. Survival and detection of coliforms, Enterobacteriaceae, and gram-negative bacteria in Greek yogurt, Journal of Dairy Science, Volume 100, Issue 2, 2017, Pages 950-960.
U. Fisberg M, Machado R. History of yogurt and current patterns of consumption. Nutr Rev. 2015 Aug;73 Suppl 1:4-7.
In Evolutionar Biology, Epigenetics has become part of the explanations for changes in the phenotype across generations. But can these changes directed to specific phenotypic traits along many generations be converted into DNA mutations?
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?
Thank you.
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.
I'd like to know the different type of post translational modifications that occur in a mammalian cell ?
Few examples from my side are :
- Glycosylation.
- Phosphorylation.
- Ubiquitination
- Epigenetic modifications.
In case of transcription factors in Cut&Tag (cut and tag), is there any way if a particular antibody works or not before going for sequencing. Has anyone tried qPCR after library preparation? What antibodies did you validate for Cut&Tag (cut and tag) in your experiments?
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.
Antibody recommendations
Can anyone recommend a Myc-tag antibody that works well in ChIP or ChIP-seq for detection of a tagged TF?
We have tried to perform ChIP-seq against a Myc-tagged TF of interest [using Cell Signalling 71D10] but have not had success in achieving specific pulldown (ChIP-seq results shows ubiquitous binding across all open chromatin without any correlation to the binding motif of this TF family).
This antibody has not performed well in Western blotting either according to several colleagues who have tried (but then performance of an Ab in a Western is rarely predictive of performance in ChIP/ChIP-seq, anyway).
Any suggestions (preferably with your results attached) would be greatly appreciated so I can try another antibody with a better chance of success!
Hi,
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?
Chromatografy is recommended for epigenetic studies with organisms lacking a reference genome
I wanted to measure methylation of a single gene promoter using DNA extracted from whole blood samples. What would the most cost effective and reliable method be? I have a total of 36 samples. I have come across a handful of ways people quantify methylation, but am unsure which is best for my project.
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???
what about your think is the best target to analyze the certain genetic effects in human disease?
study the
- gene sequencing or
- specific SNP or
- mRNA or
- the end product (protein measure) or
- microRNA or
as I think to measure the protein levels as the end product of all genetic processes from gene transcription to translation take in account the effect of epigenetic at the same time
because it's easy, high accurate, can be recommended as routine work, and more sensitive?
what about your think
Metabolic rewiring and epigenetic remodeling, which are closely linked and reciprocally regulate each other, are among the well-known cancer hallmarks. Studies have reported use of Onco-metabolites to metabolically reprogram the epigenetic of cancer. I was wondering what might be major limitations of such techniques?
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??
Plant research (Genomics, epigenetic, proteomics)
Dear PIs,
If you have any projects in the field of molecular biology and/or epigenetics, please let me know
Thanks in advance ☺
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.
Hey,
I recently have a confusion about single cell ATAC-seq integration analysis between samples. I have read many discussions about that issue. So, I summarized them into two solutions as follows:
SOLUTION 1. (data QC ignored here) find the union feature set from different samples -> generate count matrix for each sample -> merge them into one large count matrix -> normalization/Scaling/cell clustering/ cluster annotations……
SOLUTION 2. generate the count matrix for each sample -> normalization/Scaling/cell clustering/ cluster annotations for each sample -> find common features among all samples -> generate count matrix against the selected common features for each sample -> merging data using pipelines, e.g. Signac/Harmony, to perform cell clustering, cluster annotation and other following analysis (which usually with give a new assay for common features).
My questions:
Either one selected, I will have cell clusters now. So the next plan for me is retrieving differential features for each cell type/cluster, which will be the key to the further investigation of biological functions.
Q1. I know that batch effect indeed exists between samples, but for SOLUTION 1, will normalization and scaling for a single large count matrix work for differential enrichment analysis between samples?
Q2. If SOLUTION 1 is not reasonable, SOLUTION 2 will give rise to a new assay only contain the selected common features, based on which the batch effect should be well corrected and the cell might be better clustered. However, how to perform the differential analysis for non-common features in each clusters? (That's to say, will the batch effect correction in the newly integrated assay by SOLUTION 2 will work for total differential feature detection in raw assays at the sample level?)
Thanks and best regards!
Hello everyone,
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.
I need to perform immunofluorescence on mouse hematopoietic stem cells. However, I have multiple mice that need to be sampled, and the sampling time span is relatively large. However, I hope to be able to perform immunofluorescence staining at the same time. In addition, for future experiments, so I would like to ask if there is a way to store mouse hematopoietic stem cells because, after the extraction of HSC, mice are dead, therefore I need to store cells for future analysis. Moreover, I will do epigenetics Observation, so it is hoped that the storage method will not affect the internal physiological characteristics of the cell.
I am currently working on the H3K4me3-related project for gene activation. I am curious about how H3K4me3 is added to the lysine of H3K4. Does H3K4me3 is step by step added by H3K4me1 and H3K4me2? We know H3K4me3 mainly marks the gene promoter and correlates to gene transcription activates. H3K4me1 and H3K4me2 mark both enhancer and promoter and have multiple functions for gene activation according to different complexes. The three histone makers show different patterns but also with some common features. The question is: If the gene is activation and the H3K4me3 is significantly enhanced, does the H3K4me1 and H3K4me2 at the promoter locus need to be reduced? In contrast, for any reason we find the H3K4me1 and H3K4me2 are all reduced, does the H3K4me3 need to be upregulated at the same locus, or does it reasonable? If the H3K4me3 is added from H3K4me2, our observation is something wrong. But if the H3K4me3 can be directly added from H3K4me0, it can explain our result.
Thanks for the help.
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.
Mains functions are emotion, behavior, long-term memory.The limbic system operates by influencing the endocrine system and the autonomic nervous system.Usually affect depressed . I want to reflect on US elections, Capital rival, as other national problems. Because Im aware of reppetions behaviour from thought that create need for emotional stimuli. Should we all first analyse our political( emotional cognitions) before voting? Whats your thoughts on Epigenetics?
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?
I am interested in finding research that evaluates the combined impact of epigenetic factors, prenatal development (for example hormone imbalance) and childhood trauma (such as an impaired attachment bond with one or both parents) in determining sexual orientation.
Thank you!
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.
Beryllium is exceedingly toxic and known to interfere with Human enzymes.
Analysts have developed techniques to measure Beryllium in parts per Quadrillion.
Beryllium is present in Fluoride industrial waste dumped into drinking water supplies in Australia, measured by one supplier to be 95 gram per tonne (see attached analysis).
I wonder if anyone has studied the concentration of Beryllium in drinking water, its absorbed dose range and risk factors for various diseases, including cancers, as a result of this "Fluoridation" waste disposal? What are the effects on the Human foetus?
Hello,
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.
Hi!
I use pyridine borane to react with DNA. I observed that DNA recovery on the purification stage after pyridine borane reaction is very low, at 10%. Therefore, I would like to kindly ask you about the following:
Does pyridine borane fragment genomic DNA?
Does it affect the efficiency of DNA binding to the column bed during purification?
Does anyone recommend a suitable purification method and tested binding buffers or other suggestions to improve DNA recovery?
Additionally, I have a question, the pyridine borane solution with DNA is shaken for 16h 850rpm, but I wonder if I can mix with vortex before incubation for better distribution of the substance in the solution?
I will be grateful for all suggestions.
How does the awareness that plants are intelligent can help plant scientists? May it be a new school of thought in realm of plant studies?
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.
Hi,
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,
Grace Russell
What are the Epigenetic signatures on HBV cccDNA and bound proteins that control viral replication and gene transcription?
Hi, I treated the cells with 5-Aza-dc and TSA and analyze a specific gene transcription and found out that the gene was induced due to both treatment(q-PCR) relative to control. Then I preform a western blot and found out that the protein level was reduced. This kind of dis-correlation can happen with DNA methylation and histone actylation inhibitors? can someone give a reference for this kind of dis-correlation?
I used to extract Human Sperm DNA for epigenetic studies.
I have done several protocols but DNA was not free of protein although I used 100 microlitr Proteinase K for 400 microlitr washed semen.
Can anyone guide me or have some hints?
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
Hello everybody, I am new with the meta-analysis in Genome Wide Data so I have this doubt. I have read METAL documentation, which is by far the most used meta-analysis software in both EWAS and GWAS microarray data, but I cannot figure out how would be the input for EWAS analysis. As METAL was originally designed for GWAS, one of the inputs is to provide both the reference and no reference allele. Therefore as EWAS arrays do not rely in allele frequencies but in a quantitative measure, I would like to know how would be the input in METAL regarding this case. Thank you so much in advance for answering this issue (which may be easy, but I certainly do not know)
Which explain different types of epigenetic changes and their relation with gene function and disease states.
Most studies investigating genomic changes due to certain illness report their findings based on assessment done using peripherally withdrawn blood. For disorders related to CNS, how accurate would be the genomic or epigenetic analysis done using blood samples reflects changes taking place in CNS?
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.
Best regards,
Sahar Saberijamal
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.
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 have bam files (3 IP and 3 input) from a RIP-seq experiment. I need to split each unique mapped reads bam file based on read strand in order to calculate then strand-specific read coverage along human genome.
Can anyone help with literature on reactions of Glyphosate, N-(phosphonomethyl)glycine), or its degradation products such as (Aminomethyl)phosphonic acid with Fluoride, HF or Fluorine? Material safety data sheets simply state that they are incompatible with Fluorine. Of interest are reports of complexes of Uranium and Europium where Glyphosate and Fluoride are brought into close proximity. This brings into question the wider subject of Fluoride attack on Phosphorus in biological systems and the basis of observed epigenetic interference with human genes.
I'd like to purchase some custom DNA microarrays, circa 100K spot density and 30mers in length. Would anyone be able to recommend a company?
thanks
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?
If the parent has adpkd1, and it passed down to the child, is the truncating vs. non-truncating characteristic of the mutation passed down too? If the parent has a truncating adpkd1 gene, does that mean that the child will also automatically have the truncating adpkd1 gene? Or is it still possible that the child could still have a non-truncating adpkd1 gene? Trying to understand if truncating is passed on exactly or more of an epigenetics thing where it depends on lifestyle factors.
Hi,
i am currently looking for an experiment alternative to southern blot. I heard that pcr based assays give results quickly ( let's say within few hours). I want to perform sybr green relied pcr to detect copy number of my interested gene in the human genome like in southern blot. however, I couldn't find a proper protocol. If you address a protocol or share your experience, I will appreciate.
Thanks.
As nutrigenetic and nutrigenomic understanding is increasing should resources still be spent on developing population-wide recommendations for longevity, prevention of chronic disease and treatment of chronic disease?
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'm developing a MethyLight assay to verify a specific CpG site in a promoter region of my interest gene in rats. Unfortunately, I don't have a lot of choices to design the probe and primers, since I have a specific target. Besides that, after the treatment with bisulfite, the DNA lost the complexity because of the cytosines unmethylated turning in thymine, leading to a lack of cytosine in the sequence. Thus, the Tm of my primers and probes are low (45°C for primers and 55°C for probes). Is possible the qPCR still work with these parameters?
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.
References
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.
As described above.
I think this is a most intriguing issue in terms of better understanding of many human diseases.
I will perform a MethyLight assay with DNA of brain rats tissue. Wich control should I use to normalize de methylation percent of reaction? We found inventoried controls for humans, but not for rats.
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?
Thanks.
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.....
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!!!
I am currently mining epigenome data available on line to describe the epigenetic changes of certain gene loci in cancer cell lines.