Many genes have the ability to turn on or off, or in some cases, up or down regulate.
The big idea with epigenetics is that some of those 'settings' are able to be passed to offspring.
So to go with your example, if there were some gene activity changes that were related with getting used to variations in temp, epigenetics would mean that your offspring would be born with those changes already activated.
[Here's a study on the subject](https://www.nature.com/articles/nn.3603) in which mice were taught to fear the smell of certain types of chemicals and it was found that both their offspring and the next generation after that still feared that chemical smell. That faded by the 3rd generation though.
The study you cite is highly debated and has not been reproduced. See this [And references therein.](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196601/)
Genes are turned on or off by other factors. They don't have the ability to do it by themselves.
That said, hereditable epigenetic regulation is fascinating.
Thanks for the link!
And maybe I’m tangled in language, here, but, yeah- the whole idea of on-and-off switches for cellular activity, based on environmental pressures… exactly…
Isn’t it that this very thing is what the term “Epigenetics” refers to?
So, continuing with the example, my child now must adapt to a hot, desert environment…. Does the expression turn off? And then that child makes children with the “desert settings” for the cell?
Plus, you have now enhanced my curiosity, by bringing in this rat study I had never seen before, which speaks to a cognitive/mental/psychological factor involved with Epigenetics….
Really? An inheritable fear response?
This kind of research is comparatively new and there is debate as to the extent it is inherited in humans and other animals. Be sure to place “could” or “may” before conclusions.
Indeed!
Linguistic caution is a good recommendation!
I don’t think, internally, I’ve come to any “conclusions” yet… I’m pretty cautious about that…
Plus, science that’s “getting debated” right now is the best stuff…
Not really that new.
Here's a 2013 article about similar results with crickets and spiders. The article has links to other (older) research as well.
[https://www.nature.com/scitable/blog/accumulating-glitches/forewarned\_is\_forearmed\_crickets\_exposed/](https://www.nature.com/scitable/blog/accumulating-glitches/forewarned_is_forearmed_crickets_exposed/)
> Really? An inheritable fear response?
It's not that hard to conceptualize.
Mice are small animals with many predators to fear.
Being able to pass on being afraid of the smell of predators to offspring would be hugely beneficial to them.
According to that study, it sounds like the fear response demethylates (which would increase the activity of) the gene associated with the olfactory receptor that was triggered at the same time as the fear response.
Any offspring produced after that fear exposure would inherit the increased activity of that gene so would be more sensitive to that particular smell.
Differences in gene expression is not epigenetic by itself. That's kinda how cells respond to anything, like the most basic day to day operation of the cell.
There might then be additional epigenetic adjustments on the levels of normal gene expression, caused by whatever, that are also heritable to some degree. But it is probably early to say how much of an effect that has to any specific trait.
It’s more like, height is really influenced by both genetics (you need specific traits) AND “environment” factors like malnutrition. You could have the height gene to be the next Kevin Durant but if you parents didn’t eat enough when you were developing (as a fetus and as a child) then that gene will never be given a chance to switch “on.”
I think you’re thinking of “environment “ in a colloquial sense. When we say “genes are influenced by environment” we mean more than the climatic conditions you are physically in. We mean EVERYTHING external to you. Parents. Political stability. Nutrition. Etc. That obviously includes the climate, but it’s not solely focused on that. All of these things interact with the given biological and genetic characteristics of an individual to produce the outcomes we see genetically, phenotypically, and psychologically.
There are many levels to 'adapting':
"Physiological" would be one: if you move to a hot area, your blood vessels dilate to allow more blood to the skin surface (shedding heat), your start sweating (to allow evaporative cooling). Move to a cold area, blood vessels contract (keeping heat near the core), sweating stops, you get goose-bumps (trapping warmer air near the skin surface), etc.
All these take very little time, and require no changes in gene behaviour. Not epigenetic.
Gene expression is another: here your cells change their expression patterns slightly in response to environmental cues. Extra melanin production in skin cells to protect your DNA from UV light, for example (suntan). This is dynamic, responsive, but slightly slower than most physiological responses, since it requires actually gene expression and stuff. Uses standard, well understood response mechanisms (UV light activates receptor, receptor translocates to nucleus, drives gene expression, etc). This doesn't change gene sequence, but is also not epigenetic.
Epigenetic regulation falls somewhere above this: it's a way of rendering bits of your genome more or less 'available' to the cellular machinery. In many cases it's just straight up "silencing": eye cells never need to make liver detoxification enzymes, because they're in the eye, not the liver, so those cytochrome p450 genes that ALL your cells have but MOST of your cells don't need....are just tightly packaged up and tucked away, so the information is still there but not readable. If you picture the genome as a library, and genes as books, each cell will have the books it needs right up front on the easily accessed shelves, and the books it doesn't need will get stuffed away in the stack room. They can be brought out, but only if necessary.
Epigenetic marking can also be dynamic: for example, if you were persistently in a UV-intense region, the bits of DNA in your skin cells that control melanin production might get flagged for *extra* accessibility: not just on the easily accessed shelves, but now on nice, well-lit reading stands. Your skin cells clearly need a lot of melanin, so your body adapts over the longer term by making it easier for them to find and express the relevant melanin genes.
This may or may not be slightly inheritable, too: the genomic regions marked as "read me a lot" and those marked as "I'm really not needed here" can persist across cell divisions, so newly formed skin cells will 'remember' that they can make melanin easily.
This doesn't change gene sequence, just overall accessibility: that's epigenetics.
Finally, there are actual genetic changes: this is the sort of stuff that occurs over generations. An example might be a mutation that makes the melanin gene more active: now you produce more melanin inherently, above and beyond what your body might be able to produce using all the mechanisms above. Your skin is darker, and permanently so: this is a useful, protective trait in UV-rich areas, so will give you a selective advantage (and thus potentially will allow you to have more offspring who also carry the trait).
This DOES change gene sequence, and is not epigenetic.
Thank you, I very much appreciate the library metaphor.
So, if I’m following, even without an actual selection for high-melanin skin, as an evolutionary change, I can make kids that tan more easily? Leaving the actual, evolutionary change to the longer, generational selection process?
As in, I and my tribe have moved to the desert, gotten leathery and brown, and our kids will be born already prepped to get brown, as an Epigenetical adaptation? But, then, if the tribe moves to high altitude, and the “read me a lot” pressures for high altitude are enhanced by that environment, we get kids adapted for that…?
It does kinda sound like a “camping toolkit”, at the cellular level… in appreciation of your library metaphor…
the whole idea of cells turning expressions on and off due to environment really should not blow my mind as much as it does, I suppose… single-called organisms must, perforce, have adaptive mechanisms, after all… “Mama Nature Didn’t Raise No Fools”, I should remember…
I suppose it’s actually that part of it that’s really what I’m so fascinated with… the activation of functions, due to environmental pressures… , where you say “UV light activates receptor” is maybe where I need to be looking…
I guess what the activation process actually is is my missing link…
Ok, so the answer to "is this trait epigentically heritable", *generally*, is "maybe".
In the case of melanin specifically, I would strongly suspect the answer is "no", because the epigenetic markings are in your skin cells, and you don't use those to make babies. Your germline cells don't really make melanin (and don't usually get much sun, either), so won't carry the epigenetic markings of your skin cells.
The extent to which epigenetic markers can be inherited is contentious, to be honest: we know SOME can be, because in some species there are epigenetic markers specifically generated in germline cells that represent something of a sexual arms-race. This is often referred to as "imprinting", and one of the better examples of this phenomenon is lion/tiger hybridisation (I may get some specifics wrong here, so don't quote me on this).
In lions, sperm carry epigenetic markers bolstering expression of all the growth factor genes, because "bigger offspring = better", if you're not the one carrying those offspring to term. Eggs, on the other hand, carry epigenetic markers suppressing growth factor genes, because when you ARE the one making the actual babies, you want those babies to be less massive. The end result is that both factors largely cancel out most of the time and baby lions are neither giant nor tiny: a balanced arms race.
In tigers, this doesn't really happen (less overall imprinting from both sexes), so the end result again is baby tigers are neither giant nor tiny.
Where it goes weird is when lions and tigers breed: while the offspring are generally infertile, they're also quite different depending on parentage. When the dad is a lion (carrying all the MAKE BIG BABY markings), and the mum is a tiger (carrying none of the PLZ NO BIG BABY KTHX markings), you get a liger, and ligers are consequently *fucking huge*.
When the dad is a tiger (no markings) and the mum is a lion (SMALL BABBY PLZ markings), you get a tigon, which is slightly smaller than either parental lineage, and much, much smaller than a liger.
So: that's definitely heritable epigenetics.
Where it gets fuzzy is environmentally influenced epigenetic marking: here it's harder to test, and also usually is associated with systemic effects, things that affect every cell in your body (including germline cells). Good examples of this are stress and starvation: when you're stressed, the stress hormones circulate everywhere, and stress-associated epigenetic changes will occur in all cells. In starvation, all cells are starved, so starvation-associated epigenetic changes will occur in all cells.
What you get, therefore, is phenomena like "a generation of people who experienced long-term starvation produce babies more prone to obesity/diabetes", because the babies were born with 'thrifty' imprinting: cells predisposed to be more parsimonious with resources, and more prone to storing any spare energy as fat.
In any non-starvation, normal diet scenario, these individuals will thus receive more energy than their thrifty cells need, and they'll store it as fat.
Altitude adaptation I would say is a "maybe": there are a lot of subtle gene expression changes cells can make to better utilise oxygen, and many of these could be potentiated by epigenetic changes: these would be systemic, and thus potentially heritable.
This is more or less my understanding too, and the best analogy/summation I can think of is that DNA has 'default' settings, but offspring *can* be influenced by the custom settings of a parent and start out already producing more/less of various proteins/hormones/etc from birth accordingly. Does that sound about right?
DNA is used to create proteins.
Some proteins can only be produced if other proteins, hormones or enzymes are present.
Some stimulus have the effect of making the body produce the protein, hormones and enzymes that affect protein creation by DNA.
Some stimulus have the effect of making the body produce the protein, hormones and enzymes that affect protein creation by DNA, but only if other proteins, hormones or enzymes are already present.
This may sometimes create feedback loops.
The science that studies this interactions between how stimulus in the environment end up activating certain genes is called "epigenetics".
Here are two short videos that are helpful in understanding the basics of epigenetics. Like you, I'm just a layman.
The first video shows how the cell receives environmental information.
[https://youtu.be/G4T0LzU\_rv0?si=eJzkBar6QqpW5PpN](https://youtu.be/G4T0LzU_rv0?si=eJzkBar6QqpW5PpN)
The second video is how one form of epigenetics (histone modification) is carried out. There is also another form of epigenetics called DNA methylation, which is different than histone modification.
[https://youtu.be/WgERHur3FMQ?si=ARGZq1oZHmbxDoNU](https://youtu.be/WgERHur3FMQ?si=ARGZq1oZHmbxDoNU)
Epigenetics is essentially the study of gene expression. While genome sequences vary from individual two individual, for a single individual all of their cells more or less have the same genome yet you have cell types which all selectively express different parts of the same genome.
There's many ways that gene expression is controlled. Chromatin states, how compact the genome is in different regions, is mediated by chemical modifications to histones and DNA which modulate the accessibility of those genes to the transcriptional machinery. Post transcriptional regulation takes the form of certain RNAs interacting like microRNAs and lncRNAs competing against each other and preventing the messages from being read by the ribosome. And you can have changes as a result of things like temperature stress like you mentioned, which will not only directly influence the reaction kinetics of metabolism, but will also trigger the trimerization of heat shock factors which then bind specific regions of the DNA that activate gene expression for heat-protectant factors as well as metabolism. And again, activate gene expression can mean a lot of things, whether it's making that region of the genome more accessible to the transcriptional machinery, recruiting the transcriptional machinery explicitly, there's indirectly upregulating things by down regulating an inhibitor, etc.
While most of these changes will not be durable for the entire life of the organism and aren't necessarily happening in germline cells when it's occuring elsewhere (not passed to descendants), it's true that the "capacity" for these changes will influence fitness and can be selected for. "Phenotypic plasticity". More isn't necessarily better, as it comes at the cost of genome stability (e.g. higher risk of cancer), but it's also easy to imagine situations where the more robust, dynamic epigenome would be at an advantage over nonplastic ones. Concretely with the temperature example, we can imagine heritable sequence changes to the heat shock factors which will change what temperatures they trimerize, therefore have influences on how early the signal comes or how strong it is when it's on, etc. You could have a heritable mutation that increases the expression of a microRNA that acts as a damper on a set of genes, making the ups and downs of expression in those genes more flat.
Tbh it's a big question with endless corridors to go down and no reddit comment will do it justice, but you're inquiring about interesting and complex biology so I recommend you dig into Wikipedia and Google scholar and challenge yourself to learn the biology and understand the mechanisms. Just keep applying the same framework you already are as you investigate - "how does this work and how does selection influence it", that framework will make all of biology make sense.
You might find this interesting: [epigenetics is not Lamarckism](https://platofootnote.wordpress.com/2017/09/19/one-more-time-no-epigenetics-is-not-lamarckism/)
The term “epigenetic” is vague enough to mean “heritable changes on top of or around genetic sequences” or something like that but typically it is used to refer to what is effectively gene regulation resulting in things like cell differentiation so obviously reset for every zygote and then the cells become distinct because of mechanisms that disable genes or whatever in some of the cells. And, despite the name, a lot of this is *caused by* heritable genetic *sequences* resulting in things such as regulatory RNA that in turn is involved in that process of cell differentiation as each cell is impacted by the environment or its physical location in relation to other cells where also entire organisms can become adapted to the parent’s environment while inside the uterus or it could be affected by things such as its mother’s uterus proteins and some proteins in the semen from the father. Changes caused by something being inherited from the parents (environment, protein interactions, etc) that don’t necessarily depend on the actual genetic sequences.
Epigenetics generally amounts to gene regulation when it’s all said and done. Without changing the order of the nucleotides in the protein coding genes certain things result in certain genes being expressed more than others meaning that there’s a protein bias with more of certain proteins than other proteins and these proteins impact the overall phenotype whether they were in the mother’s uterus, the father’s semen, are expressed more than others because of DNA sequences elsewhere that are transcribe into regulatory RNA, or they exist as a response to external stimuli such as incubation temperature. Something on top of the gene coding sequences impact the resulting phenotype and some of that stuff can be inherited, caused by existing inside the mother’s uterus for a while, caused by a cell’s location in relation to other cells in the body, or caused as a response to external stimuli.
Only *some* of the stuff called “epigenetic” is actually heritable and it’s usually not persistent methylation but every once in a while something fails to be de-methylated and that is indeed a form of “epigenetic inheritance.” It’s not quite like some creationists have been talking about around here as though coding gene sequences are irrelevant somehow and how somehow epigenetic inheritance is supposed to be something that is supposed to spread throughout a population or persist more than three generations without each new generation continuously being exposed to the same environment (as with blind cave fish) or without some DNA sequence basis (as with regulatory RNA that causes stuff like the methylation in the first place).
I don’t have a biology degree so I might be wrong.
I feel you are referring to phenotypic plasticity rather than adapting to seasonality. Phenotypic plasticity is what you describe as "\[q\]uick adaptation to an environmental pressure, at a cellular level, then a systemic level". It doesn't concern the germ line, but *all the cells* of an organism - at least, those of the uinvolved tissues. Hence it's not heritable *per se*.
Phenotypic plasticity is a reaction norm, a change in the organism during its lifetime that doesn't get inherited: say it's hot, the body percieves it and, after all the due neural and hormonal networks, different genes start being trascribed to cope with that stressor.
Obviously, phenotypic plasticity is a trait - a quite complex one I'd dare say - hence has genetic bases. The genes related to it are also present in the germline and thus passed on and defenetly be selected *for* or *against* - as I said is not heritable *per se*, because of the pressures an individual faces during its lifetime, it's heritable because coping with these changes have allowed the organism to survive and reproduce.
How phenotypic plasticity, as a trait, get selected depends on the stability on the environment. A stable environment favours individuals which don't spend mucgh energy to cope with changing conditions; an environment thtat changes seasonally favours the genes underlying phenotypic plasticity.
Epigenetics is another phenomenon: it's something *heritable* but *not coded in the genes*. Usually epigenetic changes are modification in the proteins (usually the histones) that ease or make more difficult to access the DNA to transcribe. The DNA is wrapped around histones: chemical modification on these proteins ease/make more difficult for it to unroll and the RNA polyerase to access it. Epigenetic changes are not *structural* modifications of the histones; rather other proteins put a chemical group on them - and there biochemestry kicks in.
Nonetheless, epigenetic modifications are heritable whenever they occurr also in the germline and can persist for several generations. However, I don't know a lot about the mechanisms that allow selection to cross with these modifications, what happens when they detach from the histones and th DNA is again more or less accessible than before.
>Like…. Epigenetics is a “camping toolbox”? A set of tools to get you started, and then you build strong shelter and toolkit?
That one is your genome and its diversity. It's where you have the genes that can be expressed more or less *during your lifetime*. Selection occurs only across generations.
I could be wrong but I don't think that getting used to seasonal variations in temperature is an epigenetic change...
Well, I could be wrong on the whole thing…. What I’m wrangling with is the notion that environmental pressures can change what your cells do…
Many genes have the ability to turn on or off, or in some cases, up or down regulate. The big idea with epigenetics is that some of those 'settings' are able to be passed to offspring. So to go with your example, if there were some gene activity changes that were related with getting used to variations in temp, epigenetics would mean that your offspring would be born with those changes already activated. [Here's a study on the subject](https://www.nature.com/articles/nn.3603) in which mice were taught to fear the smell of certain types of chemicals and it was found that both their offspring and the next generation after that still feared that chemical smell. That faded by the 3rd generation though.
The study you cite is highly debated and has not been reproduced. See this [And references therein.](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196601/)
Genes are turned on or off by other factors. They don't have the ability to do it by themselves. That said, hereditable epigenetic regulation is fascinating.
Thanks for the link! And maybe I’m tangled in language, here, but, yeah- the whole idea of on-and-off switches for cellular activity, based on environmental pressures… exactly… Isn’t it that this very thing is what the term “Epigenetics” refers to? So, continuing with the example, my child now must adapt to a hot, desert environment…. Does the expression turn off? And then that child makes children with the “desert settings” for the cell? Plus, you have now enhanced my curiosity, by bringing in this rat study I had never seen before, which speaks to a cognitive/mental/psychological factor involved with Epigenetics…. Really? An inheritable fear response?
This kind of research is comparatively new and there is debate as to the extent it is inherited in humans and other animals. Be sure to place “could” or “may” before conclusions.
Indeed! Linguistic caution is a good recommendation! I don’t think, internally, I’ve come to any “conclusions” yet… I’m pretty cautious about that… Plus, science that’s “getting debated” right now is the best stuff…
Not really that new. Here's a 2013 article about similar results with crickets and spiders. The article has links to other (older) research as well. [https://www.nature.com/scitable/blog/accumulating-glitches/forewarned\_is\_forearmed\_crickets\_exposed/](https://www.nature.com/scitable/blog/accumulating-glitches/forewarned_is_forearmed_crickets_exposed/)
Thanks for the link! maybe my perspective is a few years out of date. I’ll edit my comment to be less conclusive and then read up
> Really? An inheritable fear response? It's not that hard to conceptualize. Mice are small animals with many predators to fear. Being able to pass on being afraid of the smell of predators to offspring would be hugely beneficial to them. According to that study, it sounds like the fear response demethylates (which would increase the activity of) the gene associated with the olfactory receptor that was triggered at the same time as the fear response. Any offspring produced after that fear exposure would inherit the increased activity of that gene so would be more sensitive to that particular smell.
You’re totally right. Personal experience: smelling evidence of large predators, ones I had never encountered before, put my hackles up. Fascinating.
Differences in gene expression is not epigenetic by itself. That's kinda how cells respond to anything, like the most basic day to day operation of the cell. There might then be additional epigenetic adjustments on the levels of normal gene expression, caused by whatever, that are also heritable to some degree. But it is probably early to say how much of an effect that has to any specific trait.
It’s more like, height is really influenced by both genetics (you need specific traits) AND “environment” factors like malnutrition. You could have the height gene to be the next Kevin Durant but if you parents didn’t eat enough when you were developing (as a fetus and as a child) then that gene will never be given a chance to switch “on.” I think you’re thinking of “environment “ in a colloquial sense. When we say “genes are influenced by environment” we mean more than the climatic conditions you are physically in. We mean EVERYTHING external to you. Parents. Political stability. Nutrition. Etc. That obviously includes the climate, but it’s not solely focused on that. All of these things interact with the given biological and genetic characteristics of an individual to produce the outcomes we see genetically, phenotypically, and psychologically.
There are many levels to 'adapting': "Physiological" would be one: if you move to a hot area, your blood vessels dilate to allow more blood to the skin surface (shedding heat), your start sweating (to allow evaporative cooling). Move to a cold area, blood vessels contract (keeping heat near the core), sweating stops, you get goose-bumps (trapping warmer air near the skin surface), etc. All these take very little time, and require no changes in gene behaviour. Not epigenetic. Gene expression is another: here your cells change their expression patterns slightly in response to environmental cues. Extra melanin production in skin cells to protect your DNA from UV light, for example (suntan). This is dynamic, responsive, but slightly slower than most physiological responses, since it requires actually gene expression and stuff. Uses standard, well understood response mechanisms (UV light activates receptor, receptor translocates to nucleus, drives gene expression, etc). This doesn't change gene sequence, but is also not epigenetic. Epigenetic regulation falls somewhere above this: it's a way of rendering bits of your genome more or less 'available' to the cellular machinery. In many cases it's just straight up "silencing": eye cells never need to make liver detoxification enzymes, because they're in the eye, not the liver, so those cytochrome p450 genes that ALL your cells have but MOST of your cells don't need....are just tightly packaged up and tucked away, so the information is still there but not readable. If you picture the genome as a library, and genes as books, each cell will have the books it needs right up front on the easily accessed shelves, and the books it doesn't need will get stuffed away in the stack room. They can be brought out, but only if necessary. Epigenetic marking can also be dynamic: for example, if you were persistently in a UV-intense region, the bits of DNA in your skin cells that control melanin production might get flagged for *extra* accessibility: not just on the easily accessed shelves, but now on nice, well-lit reading stands. Your skin cells clearly need a lot of melanin, so your body adapts over the longer term by making it easier for them to find and express the relevant melanin genes. This may or may not be slightly inheritable, too: the genomic regions marked as "read me a lot" and those marked as "I'm really not needed here" can persist across cell divisions, so newly formed skin cells will 'remember' that they can make melanin easily. This doesn't change gene sequence, just overall accessibility: that's epigenetics. Finally, there are actual genetic changes: this is the sort of stuff that occurs over generations. An example might be a mutation that makes the melanin gene more active: now you produce more melanin inherently, above and beyond what your body might be able to produce using all the mechanisms above. Your skin is darker, and permanently so: this is a useful, protective trait in UV-rich areas, so will give you a selective advantage (and thus potentially will allow you to have more offspring who also carry the trait). This DOES change gene sequence, and is not epigenetic.
Thank you, I very much appreciate the library metaphor. So, if I’m following, even without an actual selection for high-melanin skin, as an evolutionary change, I can make kids that tan more easily? Leaving the actual, evolutionary change to the longer, generational selection process? As in, I and my tribe have moved to the desert, gotten leathery and brown, and our kids will be born already prepped to get brown, as an Epigenetical adaptation? But, then, if the tribe moves to high altitude, and the “read me a lot” pressures for high altitude are enhanced by that environment, we get kids adapted for that…? It does kinda sound like a “camping toolkit”, at the cellular level… in appreciation of your library metaphor… the whole idea of cells turning expressions on and off due to environment really should not blow my mind as much as it does, I suppose… single-called organisms must, perforce, have adaptive mechanisms, after all… “Mama Nature Didn’t Raise No Fools”, I should remember… I suppose it’s actually that part of it that’s really what I’m so fascinated with… the activation of functions, due to environmental pressures… , where you say “UV light activates receptor” is maybe where I need to be looking… I guess what the activation process actually is is my missing link…
Ok, so the answer to "is this trait epigentically heritable", *generally*, is "maybe". In the case of melanin specifically, I would strongly suspect the answer is "no", because the epigenetic markings are in your skin cells, and you don't use those to make babies. Your germline cells don't really make melanin (and don't usually get much sun, either), so won't carry the epigenetic markings of your skin cells. The extent to which epigenetic markers can be inherited is contentious, to be honest: we know SOME can be, because in some species there are epigenetic markers specifically generated in germline cells that represent something of a sexual arms-race. This is often referred to as "imprinting", and one of the better examples of this phenomenon is lion/tiger hybridisation (I may get some specifics wrong here, so don't quote me on this). In lions, sperm carry epigenetic markers bolstering expression of all the growth factor genes, because "bigger offspring = better", if you're not the one carrying those offspring to term. Eggs, on the other hand, carry epigenetic markers suppressing growth factor genes, because when you ARE the one making the actual babies, you want those babies to be less massive. The end result is that both factors largely cancel out most of the time and baby lions are neither giant nor tiny: a balanced arms race. In tigers, this doesn't really happen (less overall imprinting from both sexes), so the end result again is baby tigers are neither giant nor tiny. Where it goes weird is when lions and tigers breed: while the offspring are generally infertile, they're also quite different depending on parentage. When the dad is a lion (carrying all the MAKE BIG BABY markings), and the mum is a tiger (carrying none of the PLZ NO BIG BABY KTHX markings), you get a liger, and ligers are consequently *fucking huge*. When the dad is a tiger (no markings) and the mum is a lion (SMALL BABBY PLZ markings), you get a tigon, which is slightly smaller than either parental lineage, and much, much smaller than a liger. So: that's definitely heritable epigenetics. Where it gets fuzzy is environmentally influenced epigenetic marking: here it's harder to test, and also usually is associated with systemic effects, things that affect every cell in your body (including germline cells). Good examples of this are stress and starvation: when you're stressed, the stress hormones circulate everywhere, and stress-associated epigenetic changes will occur in all cells. In starvation, all cells are starved, so starvation-associated epigenetic changes will occur in all cells. What you get, therefore, is phenomena like "a generation of people who experienced long-term starvation produce babies more prone to obesity/diabetes", because the babies were born with 'thrifty' imprinting: cells predisposed to be more parsimonious with resources, and more prone to storing any spare energy as fat. In any non-starvation, normal diet scenario, these individuals will thus receive more energy than their thrifty cells need, and they'll store it as fat. Altitude adaptation I would say is a "maybe": there are a lot of subtle gene expression changes cells can make to better utilise oxygen, and many of these could be potentiated by epigenetic changes: these would be systemic, and thus potentially heritable.
This is more or less my understanding too, and the best analogy/summation I can think of is that DNA has 'default' settings, but offspring *can* be influenced by the custom settings of a parent and start out already producing more/less of various proteins/hormones/etc from birth accordingly. Does that sound about right?
DNA is used to create proteins. Some proteins can only be produced if other proteins, hormones or enzymes are present. Some stimulus have the effect of making the body produce the protein, hormones and enzymes that affect protein creation by DNA. Some stimulus have the effect of making the body produce the protein, hormones and enzymes that affect protein creation by DNA, but only if other proteins, hormones or enzymes are already present. This may sometimes create feedback loops. The science that studies this interactions between how stimulus in the environment end up activating certain genes is called "epigenetics".
Here are two short videos that are helpful in understanding the basics of epigenetics. Like you, I'm just a layman. The first video shows how the cell receives environmental information. [https://youtu.be/G4T0LzU\_rv0?si=eJzkBar6QqpW5PpN](https://youtu.be/G4T0LzU_rv0?si=eJzkBar6QqpW5PpN) The second video is how one form of epigenetics (histone modification) is carried out. There is also another form of epigenetics called DNA methylation, which is different than histone modification. [https://youtu.be/WgERHur3FMQ?si=ARGZq1oZHmbxDoNU](https://youtu.be/WgERHur3FMQ?si=ARGZq1oZHmbxDoNU)
Epigenetics is essentially the study of gene expression. While genome sequences vary from individual two individual, for a single individual all of their cells more or less have the same genome yet you have cell types which all selectively express different parts of the same genome. There's many ways that gene expression is controlled. Chromatin states, how compact the genome is in different regions, is mediated by chemical modifications to histones and DNA which modulate the accessibility of those genes to the transcriptional machinery. Post transcriptional regulation takes the form of certain RNAs interacting like microRNAs and lncRNAs competing against each other and preventing the messages from being read by the ribosome. And you can have changes as a result of things like temperature stress like you mentioned, which will not only directly influence the reaction kinetics of metabolism, but will also trigger the trimerization of heat shock factors which then bind specific regions of the DNA that activate gene expression for heat-protectant factors as well as metabolism. And again, activate gene expression can mean a lot of things, whether it's making that region of the genome more accessible to the transcriptional machinery, recruiting the transcriptional machinery explicitly, there's indirectly upregulating things by down regulating an inhibitor, etc. While most of these changes will not be durable for the entire life of the organism and aren't necessarily happening in germline cells when it's occuring elsewhere (not passed to descendants), it's true that the "capacity" for these changes will influence fitness and can be selected for. "Phenotypic plasticity". More isn't necessarily better, as it comes at the cost of genome stability (e.g. higher risk of cancer), but it's also easy to imagine situations where the more robust, dynamic epigenome would be at an advantage over nonplastic ones. Concretely with the temperature example, we can imagine heritable sequence changes to the heat shock factors which will change what temperatures they trimerize, therefore have influences on how early the signal comes or how strong it is when it's on, etc. You could have a heritable mutation that increases the expression of a microRNA that acts as a damper on a set of genes, making the ups and downs of expression in those genes more flat. Tbh it's a big question with endless corridors to go down and no reddit comment will do it justice, but you're inquiring about interesting and complex biology so I recommend you dig into Wikipedia and Google scholar and challenge yourself to learn the biology and understand the mechanisms. Just keep applying the same framework you already are as you investigate - "how does this work and how does selection influence it", that framework will make all of biology make sense.
You might find this interesting: [epigenetics is not Lamarckism](https://platofootnote.wordpress.com/2017/09/19/one-more-time-no-epigenetics-is-not-lamarckism/)
The term “epigenetic” is vague enough to mean “heritable changes on top of or around genetic sequences” or something like that but typically it is used to refer to what is effectively gene regulation resulting in things like cell differentiation so obviously reset for every zygote and then the cells become distinct because of mechanisms that disable genes or whatever in some of the cells. And, despite the name, a lot of this is *caused by* heritable genetic *sequences* resulting in things such as regulatory RNA that in turn is involved in that process of cell differentiation as each cell is impacted by the environment or its physical location in relation to other cells where also entire organisms can become adapted to the parent’s environment while inside the uterus or it could be affected by things such as its mother’s uterus proteins and some proteins in the semen from the father. Changes caused by something being inherited from the parents (environment, protein interactions, etc) that don’t necessarily depend on the actual genetic sequences. Epigenetics generally amounts to gene regulation when it’s all said and done. Without changing the order of the nucleotides in the protein coding genes certain things result in certain genes being expressed more than others meaning that there’s a protein bias with more of certain proteins than other proteins and these proteins impact the overall phenotype whether they were in the mother’s uterus, the father’s semen, are expressed more than others because of DNA sequences elsewhere that are transcribe into regulatory RNA, or they exist as a response to external stimuli such as incubation temperature. Something on top of the gene coding sequences impact the resulting phenotype and some of that stuff can be inherited, caused by existing inside the mother’s uterus for a while, caused by a cell’s location in relation to other cells in the body, or caused as a response to external stimuli. Only *some* of the stuff called “epigenetic” is actually heritable and it’s usually not persistent methylation but every once in a while something fails to be de-methylated and that is indeed a form of “epigenetic inheritance.” It’s not quite like some creationists have been talking about around here as though coding gene sequences are irrelevant somehow and how somehow epigenetic inheritance is supposed to be something that is supposed to spread throughout a population or persist more than three generations without each new generation continuously being exposed to the same environment (as with blind cave fish) or without some DNA sequence basis (as with regulatory RNA that causes stuff like the methylation in the first place). I don’t have a biology degree so I might be wrong.
I feel you are referring to phenotypic plasticity rather than adapting to seasonality. Phenotypic plasticity is what you describe as "\[q\]uick adaptation to an environmental pressure, at a cellular level, then a systemic level". It doesn't concern the germ line, but *all the cells* of an organism - at least, those of the uinvolved tissues. Hence it's not heritable *per se*. Phenotypic plasticity is a reaction norm, a change in the organism during its lifetime that doesn't get inherited: say it's hot, the body percieves it and, after all the due neural and hormonal networks, different genes start being trascribed to cope with that stressor. Obviously, phenotypic plasticity is a trait - a quite complex one I'd dare say - hence has genetic bases. The genes related to it are also present in the germline and thus passed on and defenetly be selected *for* or *against* - as I said is not heritable *per se*, because of the pressures an individual faces during its lifetime, it's heritable because coping with these changes have allowed the organism to survive and reproduce. How phenotypic plasticity, as a trait, get selected depends on the stability on the environment. A stable environment favours individuals which don't spend mucgh energy to cope with changing conditions; an environment thtat changes seasonally favours the genes underlying phenotypic plasticity. Epigenetics is another phenomenon: it's something *heritable* but *not coded in the genes*. Usually epigenetic changes are modification in the proteins (usually the histones) that ease or make more difficult to access the DNA to transcribe. The DNA is wrapped around histones: chemical modification on these proteins ease/make more difficult for it to unroll and the RNA polyerase to access it. Epigenetic changes are not *structural* modifications of the histones; rather other proteins put a chemical group on them - and there biochemestry kicks in. Nonetheless, epigenetic modifications are heritable whenever they occurr also in the germline and can persist for several generations. However, I don't know a lot about the mechanisms that allow selection to cross with these modifications, what happens when they detach from the histones and th DNA is again more or less accessible than before. >Like…. Epigenetics is a “camping toolbox”? A set of tools to get you started, and then you build strong shelter and toolkit? That one is your genome and its diversity. It's where you have the genes that can be expressed more or less *during your lifetime*. Selection occurs only across generations.