/r/epigenetics

Photograph via snooOG

The study of changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence.

In biology, and specifically genetics, epigenetics is the study of changes in gene expression or cellular phenotype, caused by mechanisms other than changes in the underlying DNA sequence – hence the name epi- (Greek: επί- over, above, outer) -genetics, some of which have been shown to be heritable.

--Wikipedia


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/r/epigenetics

7,356 Subscribers

0

Does taking or workout negatively affect my epigenetic?

4 Comments
2024/06/19
21:22 UTC

2

ACVR1C, good or bad?

I hope this is the right sub, I came across these two papers where one suggests that ACVR1C promotes long term memory formation and the other says that it is implicated in eye cancer, I am not from a biology background and I am confused, can anyone explain the difference please.

  1. https://www.nature.com/articles/s41467-024-47996-w

  2. https://www.nature.com/articles/s41388-018-0543-2

0 Comments
2024/06/11
03:33 UTC

15

Why is amphetamine an antiviral?

How does it work?

"Pseudoephedrine can significantly improve the survival rate of H1N1 virus-infected mice"

"These results give clear evidence that pseudoephedrine is a potential anti-influenza drug by blunting cytokine storms and inhibition of replication of IAV, and following these results, we speculate that it should be tested in the novel coronavirus pneumonia (COVID-19, a severe epidemic in China currently) in which the cytokine storms play a key role"

https://www.clinvirologyjournal.com/articles/ijcv-aid1008.pdf

"COVID-19 infection rate is nearly 50% higher among individuals with unmedicated ADHD" https://www.additudemag.com/adhd-symptoms-coronavirus-risk/

"We report the first evidence that meth significantly reduces, rather than increases, virus propagation and the susceptibility to influenza infection in the human lung epithelial cell line" https://pubmed.ncbi.nlm.nih.gov/23139774/

8 Comments
2024/06/09
15:30 UTC

2

Resisting An Increased Epigenetic Speed Of Aging (14-Test Results)

0 Comments
2024/06/09
11:05 UTC

2

Horvath Epigenetic Age: A Weak Spot, But I Have A Plan (14-Test Analysis)

0 Comments
2024/06/06
19:13 UTC

7

Subreddit on Chromatin

Hi, this is Prof. Paul Knoepfler. I started a new subreddit on chromatin. I've seen many comments here on chromatin over the years so I thought some of you might be interested in a chromatin-specific subreddit. I don't see another one on Reddit. Cheers.

1 Comment
2024/06/05
17:05 UTC

12

Textbooks for epigenetics

I'm about to learn epigenetics in my university in the next semester and I have the urge to get a clear idea about this field. Can anyone recommend a/some text book(s) that are using in universities? Best regards.

2 Comments
2024/06/03
18:53 UTC

11

Sexual trama and epigenetic’s

Anyone have information on this, I feel awful I feel sick to my stomach everyday I think I’ve ruined my life and I don’t know if I wanna have kids anymore

4 Comments
2024/06/01
16:19 UTC

0

Multi-Factorial Cellular Reprogramming for Longevity (MCR-L)?

!Presentation: Everyone hates GPT it seems and reading. Oh well here it is anyway made long and self-promoted, like it's the best, even though I asked it not to make the idea sound like some groundbreaking science. Well it did anyways so ingore the GPT'ness of it.!<

!Title: Multi-Factorial Cellular Reprogramming for Longevity (MCR-L)!<

!Introduction:!<

!MCR-L represents an innovative approach to cellular reprogramming designed to promote longevity and mitigate tumorigenic risks. By integrating a comprehensive array of factors and strategies, MCR-L aims to induce controlled and stable cellular rejuvenation.!<

!Components of MCR-L:!<

!Yamanaka Factors (Oct4 and c-Myc): Initiates reprogramming and enhances pluripotency.!<

!Nanog and Lin28: Complements Yamanaka factors, enhancing reprogramming efficiency and stability.!<

!mTOR Inhibition: Temporarily inhibits mTOR signaling to reduce proliferation rates and tumorigenic risks.!<

  1. !mTOR Inhibition: Temporarily inhibiting mTOR signaling can shift cells into a more quiescent state, reducing their proliferation rate and potentially lowering the risk of uncontrolled cell growth and tumorigenesis. By modulating mTOR activity, you can create a more favorable cellular environment for reprogramming without promoting excessive cell division.!<

!Genetic Modifications: Includes CRISPR-mediated edits or epigenetic modifications to enhance genomic stability and modulate aging-related pathways.!<

!Key Features and Benefits:!<

!Comprehensive Approach: MCR-L integrates multiple factors and strategies to achieve controlled and stable cellular reprogramming.!<

!Precision and Control: Offers precise control over reprogramming process, minimizing off-target effects and optimizing outcomes.!<

!Risk Mitigation: Reduces tumorigenic risks associated with traditional reprogramming methods through targeted interventions.!<

!Therapeutic Potential: Holds promise for regenerative medicine and anti-aging interventions, offering novel strategies for combating age-related degeneration.!<

!Conclusion:!<

!MCR-L represents a scientifically grounded approach to cellular reprogramming, leveraging the synergistic effects of key factors and interventions to promote longevity and cellular rejuvenation. With further research and development, MCR-L has the potential to advance our understanding of aging-related processes and contribute to the development of innovative therapeutic strategies.!<

!Using Multi-Factorial Cellular Reprogramming for Longevity (MCR-L) should offer several advantages over the default Yamanaka reprogramming method, primarily in terms of safety, precision, and effectiveness. Here's why MCR-L may be preferred:!<

  1. !Safety:!<

!Reduced Tumorigenic Risk: MCR-L incorporates Nanog and Lin28, which have been associated with lower tumorigenic potential compared to Sox2 and Klf4, traditionally used in Yamanaka reprogramming. Additionally, temporary mTOR inhibition further reduces the risk of uncontrolled cell growth and tumorigenesis during the reprogramming process.!<

!2. Precision and Control:!<

!Fine-Tuned Reprogramming: MCR-L allows for precise control over the reprogramming process by integrating multiple factors and interventions. This enables researchers to optimize reprogramming outcomes while minimizing off-target effects and potential complications associated with genetic manipulation.!<

!3. Efficacy:!<

!Enhanced Stability and Longevity: By promoting genomic stability and modulating aging-related pathways, MCR-L aims to create reprogrammed cells that are more stable and functionally rejuvenated. This may lead to improved efficacy in lifespan extension and age-related disease mitigation compared to traditional Yamanaka reprogramming.!<

!4. Therapeutic Potential:!<

!Broader Applications: MCR-L holds promise for a wide range of therapeutic applications beyond cellular reprogramming, including regenerative medicine, disease modeling, and anti-aging interventions. Its multifactorial approach provides versatility in addressing diverse age-related conditions and disorders.!<

!Conclusion:!<

!Multi-Factorial Cellular Reprogramming for Longevity (MCR-L) represents a scientifically grounded and innovative approach to cellular reprogramming, offering several advantages over the default Yamanaka method. By prioritizing safety, precision, and efficacy, MCR-L has the potential to advance our understanding of aging-related processes and pave the way for new therapeutic strategies aimed at promoting longevity and enhancing human healthspan.!<

  1. !Tumorigenic Risk Reduction:!<

!Enzymatic Mechanisms: Nanog and Lin28 have been associated with maintaining stem cell pluripotency and self-renewal through intricate regulatory networks involving various enzymes, including transcription factors and epigenetic modifiers. These factors are known to promote a more controlled and stable cellular state compared to traditional Yamanaka factors like Sox2 and Klf4, which have been linked to increased tumorigenic potential.!<

!Biomechanistic Insights: Nanog and Lin28 regulate key signaling pathways involved in cellular proliferation, differentiation, and genomic stability. By modulating these pathways, they help maintain cellular homeostasis and reduce the risk of aberrant cell growth and tumorigenesis during the reprogramming process.!<

!2. Precision and Control:!<

!Enzymatic Mechanisms: Temporary mTOR inhibition, achieved through the modulation of various enzymatic cascades involved in the mTOR signaling pathway, promotes a state of cellular quiescence and metabolic dormancy. This controlled metabolic state allows for more precise manipulation of cellular reprogramming without inducing excessive cell proliferation or metabolic stress.!<

!Biomechanistic Insights: mTOR inhibition suppresses the activity of downstream effectors involved in protein synthesis, cell growth, and proliferation. By temporally regulating mTOR signaling, MCR-L provides a window of opportunity for efficient reprogramming while minimizing the risk of off-target effects and aberrant cell behavior.!<

!3. Efficacy:!<

!Enzymatic Mechanisms: The integration of Nanog, Lin28, and mTOR inhibition with Yamanaka factors enhances the efficiency and stability of cellular reprogramming by synergistically modulating multiple enzymatic pathways and cellular processes. This multifactorial approach promotes a more comprehensive and robust rejuvenation of reprogrammed cells.!<

!Biomechanistic Insights: Nanog and Lin28, in conjunction with mTOR inhibition, orchestrate complex enzymatic and biomechanistic processes involved in reprogramming, including chromatin remodeling, gene expression regulation, and metabolic reprogramming. By targeting these pathways, MCR-L creates an optimal cellular environment for successful and sustainable rejuvenation.!<

!Conclusion:!<

!Multi-Factorial Cellular Reprogramming for Longevity (MCR-L) offers a scientifically grounded approach to cellular rejuvenation by leveraging the intricate enzymatic and biomechanistic mechanisms underlying cellular reprogramming. Through the integration of Nanog, Lin28, and temporary mTOR inhibition with Yamanaka factors, MCR-L provides enhanced safety, precision, and efficacy compared to the default Yamanaka reprogramming method. This nuanced understanding of enzymatic and biomechanistic processes informs the rationale behind choosing MCR-L as a promising strategy for promoting longevity and mitigating tumorigenic risks in cellular reprogramming.!<

!Is someone/somewhere/someplace trying something like this? Or would this be worse in truth than the normal Yamanaka factors? For all those that feel the need to comment on the fact it's GPT generated....I promise I get it..... buck up for the future because it's only going to progress until most of our content is AI generated or touched by an AI/method in some way. Sorry if it bothers you.!<

My main question being would a change in the factors as purposed be at all viable? if no, an explanation would be much appreciated.

0 Comments
2024/05/22
17:56 UTC

4

How is epigenetic methylation heritable after post fertilisation demethylation?

Mitosis epigenetic heritability is enabled through DNMT1.

After fertilisation, the male and female genome undergoes active and passive demethylation respectively.

How are similar epigenetic markers then reinstated afterward, similar to that which were on the parents genome, if it has all just been stripped via 2 different methods?

1 Comment
2024/05/13
16:40 UTC

4

Is my appearance, personality, and way of thinking a combination of my ancestors traits?

Im part of a rarer ethnic group, and I find it interesting to look at all of my relatives and consider how similar we all are, in appearance and attitudes towards life? How much of that is due to our culture and how we’ve been raised, and how much is genetics? Same with appearances we all have similar features that would qualify us as conventionally attractive, but still dynamically unique looking. Do we all just share traits from our ancestors, and certain things like cheekbones, lips, noses, are renditions of our ancestors’ features?

0 Comments
2024/05/12
08:05 UTC

24

DNA changes caused by trauma

I’m interested in studying how DNA is changed by trauma and also how this works. It would be nice if you guys could refer me to as many good sources as possible or where you got your information on this topic.

16 Comments
2024/05/06
19:45 UTC

12

Bioelectricity and epigenetics - skepticism?

Hi everyone!

I've always been intrigued by cell biology, and my journey of self-education recently led me to explore the concept of cell communication. Along the way, I stumbled upon the fascinating field of bioelectricity. As I went deeper, I became particularly interested in the work of Michael Levin on bioelectricity and its role as a conduit for biological information. From what I've gathered, bioelectricity is more than just a biological curiosity; it intersects with the realm of epigenetics, showing potential for controlling gene expression by tweaking bioelectric profiles.

Perhaps my background as a molecular physicist/engineer, a field quite distinct from cell biology, amplifies my fascination with how bioelectricity can manipulate gene expression in ways that seem almost science fiction. I might also be capturing the wrong picture here, so my apologies in advance.

Moreover, I've noted that epigenetics, despite its significant contributions, had faced skepticism until about 60 years ago when perceptions began to shift. This historical context makes me wonder if bioelectricity's relatively low profile compared to more buzzworthy topics like gene editing and CRISPR is due to a similar phase of emerging credibility.

I'd love to hear your thoughts on this. Is bioelectricity on the cusp of becoming a mainstream topic in biology, medicine, and genetics, or does it still need to overcome a hurdle of skepticism akin to what epigenetics faced in its early days?

Ps.: I posted this on /physiology too.

3 Comments
2024/04/08
21:27 UTC

0

Resources for studying biological techniques and their applications

Please suggest resources (YouTube, video lectures or sites) to study different tools and techniques used in molecular biology, biotechnology, cell biology research

It should give a brief idea about the technique and explain how they can be used to solve problems in biology

1 Comment
2024/04/05
08:20 UTC

0

How can i fix my epigenetics

Did anyone one here read about post accutane syndrome We have theory that accutane messed up with our genetics So we have permenant side effects so how to fix or reverse my genetics

2 Comments
2024/04/05
02:05 UTC

1

Guys I Need Help

Hi guys, I know this post is going to feel weird but unfortunately my anxiety doesn’t give me peace.

I suffer from anxiety and obsessive compulsive disorder since a long time and I also study biology at University (1st year).

Unfortunately my studies have mixed with my psychological problems and I’ve unlocked a set of new fears I never had before.

A lot of them are related to my physical appearance.

To sum up, I am scared that the body can modify even as an adult, and my head is convinced that thoughts can drive epigenetic changes that change the bone structure slowly etc.

For example, I have a cousin that is super nice but doesn’t really look that good physically. Yesterday while I was yawning, I inspired a big flux of oxygen and in that moment I was thinking about him (his face, body etc.). From that moment I started thinking that I switched on some epigenetic switch and that I’ll be slowly become like him.

I know it doesn’t sound nice, but I didn’t know how to write it in another way.

These intrusive thoughts are destroying my life, productivity, studies, etc.

Some of them are not rational, but my head still believes them.

What can I do to exit these mental loops? Can anybody tell me if epigenetics can be this powerful and can be triggered by single-hit events?

5 Comments
2024/04/04
11:13 UTC

3

Has anyone used thedesignergene co and “body by design” for epigenetics testing and finding best lifestyle / supplements to thrive? If not, would love to hear used someone else? TIA

4 Comments
2024/04/03
15:16 UTC

9

Addiction Research

Hey there! First time posting here.

I'm a Sophomore in college and recently submitted for publication of a literature review I've conducted on the role of epigenetics in opioid addiction and treatment (which included hypothesizing CRISPR as a treatment). I'm looking for some advice on where to go next. I'm currently attending school online and live in a rural area where I don't have access to Neuroscience labs.

I'm also finding it hard to find epigenetic labs in general, even at the university of washington. Should I try to find a cancer lab to volunteer in to get some experience with epigenetic-centered lab work or should I start working on another review?

Thanks in advance and if you have any other advice for someone looking to enter the addiction research part of this field, feel free to share!

3 Comments
2024/03/29
17:18 UTC

1

Ideal conditions for hormone-targeted epigenetic upregulation?

I recently learned about the effects of HDACis on gene expression --in that they block HDAC from inhibiting transcription-- and I, nootropic fan that I am, have been enamored ever since.

I have been toying with the idea of priming the hormone/neurotransmitter pathways that I hope to change using the classical method (agonizing/inhibiting for up/down regulation) as a stage one.

Stage two would consist of doing the opposite of stage one (agonize or inhibit), alongside a protocol of an HDACi and a methyl donor.

(I have yet to decide on a chemical candidate for these tasks, this could be a slow burn, repeating the process at increasing intensity, starting with increasing butyrate.)

Anyways, cutting to the chase: though it likely varies at the level of individual genes, as a general rule, if I wanted to increase BDNF epigenetically for example I would do things in the following order, right? Is there any good research on this topic?

  1. Downregulate BDNF via agonization.

  2. Inhibit HDAC and provide methyl donors while upregulating BDNF via inhibition.

  3. Stop dosing HDACi and methyl donor BEFORE peak upregulation by dose.

  4. Stop dosing BDNF inhibitor once HDACi has cleared my system.

And the opposite would hold true if I wanted decrease BDNF?

Lastly: any suggestions on HDACis and methyl donors that are easily obtained and useful for my purposes?

Also, I assume this process may be less effective with more delicate systems like androgens, would this protocol still work in these cases?

Downregulated testosterone may provide opportunities to encode for increased testosterone, for example, but wouldn't it also provide just as many opportunities to encode for muscular atrophy and increased estrogen activity? Are there tweaks that can be made to the protocol to get around these issues?

Thanks in advance!

5 Comments
2024/03/22
20:37 UTC

5

What is known about epigenetics and sexual orientation?

What is known about how epigenetics contribute to sexual orientation?

3 Comments
2024/03/19
21:06 UTC

3

How to investigate eary epigenetic event?

Hi epigenetics,
I'm investigating changes in epigenetic lendscape on cancer upon treatment, that then drive the chemioresistance.
We have some time points in which we investigate cells with ATAC and CUT&TAG but in your opinion, to have a better understanding of the tumor epigenetics before and immediately after the treatment (24h), just to have a global idea of what is occurring epigenetically, which technique I should apply? Bisulfate conversion? Mass specrtometry on histones? What do you suggest? Thanksss

2 Comments
2024/03/15
08:47 UTC

3

Cann anyone help me understand this? Why is there a correlation. For me it looks like there is 100% no correlation. Link to study: https://www.researchgate.net/publication/41623876_DNA_methylation_of_the_POMC_gene_promoter_is_associated_with_craving_in_alcohol_dependence

6 Comments
2024/03/14
20:54 UTC

2

Help finding this paper (if it exists)

I heard once about a study that went something like this: Some animals (daphnia?) were experimentally stressed and their epigenetic marks reflected that state. Then, either within those individuals over time, or across generations, at some point the organisms went through a period where the epigenetic stress signature was "erased", but then the signature came back later. It implied that the information about the stress state was stored elsewhere and got re-imprinted into the epigenetic marks.

Is this real? Could someone help me find it? Edit: typo

1 Comment
2024/03/12
18:04 UTC

5

Could I be experiencing PTSD from my parents’ trauma? *Trigger warning* CSA

29F In the last few years I’ve been demonstrating PTSD symptoms including dreams, images/impressions, and panic attacks and dissociation triggered by topics of child s**ual abuse and certain touches during intimacy. The thing is, I’ve never experienced CSA; my parents, however, both have. In fact, on my mother’s side it goes back multiple generations. Could this sort of reaction/experience be the result of epigenetic trauma?

Please don’t mention repressed memories, I’ve been down that rabbit hole and don’t want this discussion to become about that.

I’m sorry if this is not the appropriate subreddit for this but I really wanted the opinions of those who are more knowledgeable about epigenetics. Thank you in advance for any insights.

15 Comments
2024/03/11
17:47 UTC

2

Help me formulate a hypothesis please

I’m reading Yuval Noah Harari’s book Sapiens and I have a rudimentary pondering that I’m wondering if it feels even remotely scientifically supported If Homo erectus was the most durable human species, lasted 2 million years and was the species that could best adapt to the cold environment… could we then surmise that humans surviving for generations in hot desert climates will be the ones best equipped to survive climate change?

3 Comments
2024/03/09
21:43 UTC

2

Methyclock R package

Hi has anyone computed the methylclock R package clocks. It's relatively straight forward but the thing is, is that I haven't been able to interpret the age and age acceleration estimates of the clocks because I still don't really understand each clock, having read the papers and computed the estimates. What do they actually show and so I understand Horvath hannumm and kinda phenoage and grimage, but what about DNATL (how is this different to normal telomere length measurements), what about Wu et Al's clock. You know...BLUP clock. Any videos or good resources or simple explanations would really help... Thank you

2 Comments
2024/03/07
14:08 UTC

5

Placental methylome. Is it identical to the mother or fetus? Both? Neither? Please help.

Currently working on my Master’s thesis and am really confused by this. My project is on differential methylation associated with exposure to a water pollutant. The DNA was extracted from tissue from the maternal side of the placenta after birth for 10 subjects. 5 subjects had high pollution exposure and 5 had low pollution exposure.

Whose methylome am I looking at here? Mother or baby? Both? What about the paternal genome, where does that come in?

Does the entire placenta have the same genome and methylome? Or is it different on the maternal side and fetal side?

Please help me 🫠

2 Comments
2024/03/07
01:53 UTC

2

Placental methylome. Is it identical to the mother or fetus? Both? Neither? Please help.

Currently working on my Master’s thesis and am really confused by this. My project is on differential methylation associated with exposure to a water pollutant. The DNA was extracted from tissue from the maternal side of the placenta after birth for 10 subjects. 5 subjects had high pollution exposure and 5 had low pollution exposure.

Whose methylome am I looking at here? Mother or baby? Both? What about the paternal genome, where does that come in?

Does the entire placenta have the same genome and methylome? Or is it different on the maternal side and fetal side?

Please help me 🫠

0 Comments
2024/03/07
01:53 UTC

2

Question about procedure

What kind of procedure could change epigenetics in an adult?

1 Comment
2024/03/02
16:24 UTC

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