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hope
11-03-15, 16:42
Here is a very nice study that has been done via joint research by the Department of Pharmacology and Therapeutics and the Department of Biology, at McGill University, Canada.
Together the team have been conducting epigenetic experiments on Camponotus ants, with regard to size. As there is little genetic influence regarding size in the worker ants, being as they are so closely related, the team were able to focus on the effects of epigenetic factors creating size variation.
They say by increasing the degree of DNA methylation of a gene involved in controlling growth called Egfr, they were able to create a spectrum of sizes in the worker ants, despite the lack of genetic difference between them. The more they methylated the gene the larger the ant.
Sebastian Alvarado PhD co-author of the study said, "By modifying the methylation of one particular gene, that affects others, in this case the Egfr gene, we could affect all the other genes involved in cellular growth. We were working with ants, but it was a bit like discovering that we could create shorter or taller human beings."
Rajendhran Rajakumar, first co-author, said for other complex traits, whether they are involved in the growth of cancer cells in humans or fat cells in chickens, what we now know is, in each case, once we have discovered the key genetic position that is affected by epigenetic factors we can influence how much or how little the gene is expressed, with potentially far reaching results.

I keep being logged out from here so have to write quickly but here is the link for anyone who wishes to read further.

http://www.mcgill.ca/newsroom/channels/news/honey-i-shrunk-ants-how-environment-controls-size-243448

Angela
11-03-15, 18:42
Here is a very nice study that has been done via joint research by the Department of Pharmacology and Therapeutics and the Department of Biology, at McGill University, Canada.
Together the team have been conducting epigenetic experiments on Camponotus ants, with regard to size. As there is little genetic influence regarding size in the worker ants, being as they are so closely related, the team were able to focus on the effects of epigenetic factors creating size variation.
They say by increasing the degree of DNA methylation of a gene involved in controlling growth called Egfr, they were able to create a spectrum of sizes in the worker ants, despite the lack of genetic difference between them. The more they methylated the gene the larger the ant.
Sebastian Alvarado PhD co-author of the study said, "By modifying the methylation of one particular gene, that affects others, in this case the Egfr gene, we could affect all the other genes involved in cellular growth. We were working with ants, but it was a bit like discovering that we could create shorter or taller human beings."
Rajendhran Rajakumar, first co-author, said for other complex traits, whether they are involved in the growth of cancer cells in humans or fat cells in chickens, what we now know is, in each case, once we have discovered the key genetic position that is affected by epigenetic factors we can influence how much or how little the gene is expressed, with potentially far reaching results.

I keep being logged out from here so have to write quickly but here is the link for anyone who wishes to read further.

http://www.mcgill.ca/newsroom/channels/news/honey-i-shrunk-ants-how-environment-controls-size-243448

Very interesting, Hope...I think we will discover that epigenetic factors have a great deal to do with whether a certain bit of genetic code is expressed or not, which would give scientists another avenue of attack against certain deleterious mutations.

Oh, and welcome back from your hiatus.:smile:

hope
11-03-15, 21:04
Very interesting, Hope...I think we will discover that epigenetic factors have a great deal to do with whether a certain bit of genetic code is expressed or not, which would give scientists another avenue of attack against certain deleterious mutations.
Absolutely Angela. I know epigenetics is still a little controversial with some but I believe the more studies and results are replicated the better and this is what is being seen more often.

Oh, and welcome back from your hiatus.:smile:
What a lovely welcome...thankyou ..:smile: I must confess however, only half my break was due to life, the other half was due to posting trouble..gremlins no doubt...:laughing:

LeBrok
12-03-15, 05:09
Absolutely Angela. I know epigenetics is still a little controversial with some but I believe the more studies and results are replicated the better and this is what is being seen more often.


Hey Hope.
Where I find epigenetics doubtful is when people want it to be a nurturing influence over gene. For example, when a mother leads good and proper life she will produce good and proper offsprings. Or if mother prays a lot she will get a saint child, etc. Not exactly my best examples, but here they are.
Till today the only example of epigenetic is in rats, still controversial, was to producing nervose offsprings if mother was under the stress for a long time, before or during pregnancy.

Having said that, I'm in total agreement with the cited by you paper. Epigenetic, so far is about methylation, which tells the genome which gene will be expressed in cells. Not all the genes are expressed during our lifetime, and different genes are expressed in different cells.
I have to go back to this paper, when times allows, to see what methods they used to increase methylation. Did they oversaturated DNA with methyl molecules? Did they install extra methylation bonding sites on genes, to attract methyl and stop expression?



It would be great to develope a test to check for proper methylation of our genome. This might be the key to understand why some people get cancer, and others with similar probability and cancer prone gens will not. The trick might be the proper methylation. If methylation gets screwed up with time, infection or radiation, the cancer gene might be expressed and lead to a sickness.

hope
12-03-15, 23:14
Hey Hope.
Where I find epigenetics doubtful is when people want it to be a nurturing influence over gene. For example, when a mother leads good and proper life she will produce good and proper offsprings..
Hey LeBrok ..
Certainly we all know and accept that if you smoke when pregnant, this can affect your baby`s weight or increase the chance it may develop asthma. Also we know a poor diet when pregnant is not good for the baby. These are things we all know about and accept. This is why many women try to eat healthy and stop smoking when they are thinking of having a child. Even so, this does not guarantee you will not have a baby with a disease, unfortunately. There are women who do what they consider "proper" when they become pregnant and yet have had a child with a disease, in some instances of a type they believed was not in the family line. What has happened?
This is where I think epigenetics starts to be of use. Through this study we are learning how and which things can affect the way genes express themselves The more study.. the more knowledge.. the sooner we can begin making effective drugs. I think cancer cure may be a way off yet, it is certainly the one many researchers are aiming for however.


I have to go back to this paper, when times allows, to see what methods they used to increase methylation. Did they oversaturated DNA with methyl molecules? Did they install extra methylation bonding sites on genes, to attract methyl and stop expression?

I had a look this evening LeBrok but couldn`t find anything with more detail or the methods used..perhaps it will come online in a day or so..no doubt behind a paywall :annoyed:
Here is what ScienceDaily has, not a lot more in this and the link they give takes us back to the link I posted yesterday.
http://www.sciencedaily.com/releases/2015/03/150311081258.htm

Sorry my answer is short but am trying to post before timed out.. I am like Usain Bolt of the keyboard to-night..:laughing:

Aberdeen
13-03-15, 01:39
Welcome back, Hope. Your ideas are always interesting, but I'm afraid this discussion is a little too science heavy for me. I understand language, law and social constructs but my mind doesn't do heavy science.

hope
13-03-15, 02:10
I'm afraid this discussion is a little too science heavy for me.

Now you know how I feel on the DNA sections...:confused2:


Your ideas are always interesting,
Aberdeen,I think you might have me mixed up with somebody else.....:laughing:...:laughing:

LeBrok
13-03-15, 05:43
Hey LeBrok ..
Certainly we all know and accept that if you smoke when pregnant, this can affect your baby`s weight or increase the chance it may develop asthma. Also we know a poor diet when pregnant is not good for the baby. These are things we all know about and accept. This is why many women try to eat healthy and stop smoking when they are thinking of having a child. Even so, this does not guarantee you will not have a baby with a disease, unfortunately. There are women who do what they consider "proper" when they become pregnant and yet have had a child with a disease, in some instances of a type they believed was not in the family line. What has happened?

Yes of course, mother can easily impact health of her baby during pregnancy. This is done directly, through unhealthy compounds which affect growth and correct formulation of child's body and nervous system.

In my clumsy way with words, I was talking about hereditary epigenetics. Action of mother before pregnancy effecting future babies genetic expression. Or certain father's diet will make kids taller.

I can agree that our extreme behaviours, malnutrition, strass, drugs can potentially reprogram or devastate sperm or eggs. Hower this will negatively affect whole genome and can cause many maladies in a child. I don't think we could link a certain behaviour of parents and see only one epigenetic change, especially a positive one, in future kids. Sort of leading our lives to genetically program our future kids to be better. I don't think such hereditary epigenetics positive programing exists.


I was always curious what mechanism controls the timing of turning gene on and off. For example where is the timer to turn off lactose persistent gene during adolescence? How the gene knows to receive a methyl group or histones to become deactivated?

hope
15-03-15, 19:37
LeBrok, first off let me apologise for rather late answer, we had friends staying for a few days and this is truly the first chance I have had to reply..not a case of bad manners.



I was talking about hereditary epigenetics. Action of mother before pregnancy effecting future babies genetic expression. Or certain father's diet will make kids taller.

I can agree that our extreme behaviours, malnutrition, strass, drugs can potentially reprogram or devastate sperm or eggs. Hower this will negatively affect whole genome and can cause many maladies in a child. I don't think we could link a certain behaviour of parents and see only one epigenetic change, especially a positive one, in future kids. Sort of leading our lives to genetically program our future kids to be better. I don't think such hereditary epigenetics positive programing exists.


I was always curious what mechanism controls the timing of turning gene on and off. For example where is the timer to turn off lactose persistent gene during adolescence? How the gene knows to receive a methyl group or histones to become deactivated?

Recall the numerous studies done regarding mice and rats over the years relating to stress, the effects, and also the effects shown in their offspring [ who had not been subjected to stress themselves.] One study, which I actually posted here a few years ago, showed how mice subjected to chronic stress not only showed the effects of it but produced offspring who likewise exhibited
changes in their levels of corticosterone, the mouse equivalent of the human stress hormone, cortisol.

Then the studies were mice were subjected to chemical toxins. Not only did they develop diseases directly from the exposure but their offspring likewise carried the diseases...and so did their offspring.

And we all know the studies with agouti mice and diet showing change in coat colour.

Yes, I know they are all studies with mice or rats but they do make good subjects for study. Plus it would be extremly hard to get a group of humans into a lab to study under strict lab conditions.

However, we could look for instances where similar things have been noted in humans.
For instance, children of Halocaust victims would appear to be prone to developing PTSD...perhaps suggesting their ability to regulate stress has been altered? .. Pregnant women who were involved in 9/11, in particular those in third trimester at the time and suffered PTSD. showed low levels of cortisol in their saliva. The interesting thing is, their babies also registered low levels of cortisol in their saliva. So can we perhaps see a similarity to the stressed mice studies?
The chemical toxins in cigarette smoke causes damage to our DNA with something like 23.000 mutations showing signs of damage because of the chemicals. Women who smoke when pregnant may have babies of low weight, who may also go on to develop diseases, and also show signs of altered DNA methylation.
Regarding diet. I think anyone who has read something about epigenetic studies knows the famine studies of Sweden where seasons of plenty ran with seasons of famine. Effects from that were showing up in grandchildren of those involved [ can be found on google search.]
So while there is still so much to be learned regarding epigenetics and much to yet be proven, for me I think there are cases where we see something is going on and in some cases it seems it is being carried on.

Regarding methyl groups. All living creatures have vast number of tags. Some like methyl molecules attach to DNA directly, other types grab proteins [histone] around which DNA wraps. The contact is called "hugging" and if hugged tightly it gets hidden from view of the cell and cannot be utilized. Our body adds methyl groups to DNA strands to regulate it. Where there is a methyl group, the genes will be silent, and wherever methyl group is removed genes are expressed.
Concerning lactose tolerance. [ As we all know]...we are born able to tolerate lactose due to lactase gene giving the instuction to make lactase enzyme. As babies we get nourishment and anti-bodies from mum via milk. When we get around the age of weaning the body stops producing these enzymes and we stop being able to utilize milk. This is the normal pattern. The mutant pattern, if you like, is lactose tolerance whereby lactase carries on being made. I don`t know a great deal about this LeBrok, because to be honest I haven`t really read too much about it.

Again, sorry for late reply..I just hope I don`t loose this post as I don`t want to rewrite...:annoyed:


EDIT... I`m not sure if this reads correctly..I did get logged out but thankfully I did a paste and copy job.

LeBrok
15-03-15, 23:17
LeBrok, first off let me apologise for rather late answer, we had friends staying for a few days and this is truly the first chance I have had to reply..not a case of bad manners.




Recall the numerous studies done regarding mice and rats over the years relating to stress, the effects, and also the effects shown in their offspring [ who had not been subjected to stress themselves.] One study, which I actually posted here a few years ago, showed how mice subjected to chronic stress not only showed the effects of it but produced offspring who likewise exhibited
changes in their levels of corticosterone, the mouse equivalent of the human stress hormone, cortisol.

Then the studies were mice were subjected to chemical toxins. Not only did they develop diseases directly from the exposure but their offspring likewise carried the diseases...and so did their offspring.

And we all know the studies with agouti mice and diet showing change in coat colour.

Yes, I know they are all studies with mice or rats but they do make good subjects for study. Plus it would be extremly hard to get a group of humans into a lab to study under strict lab conditions.

However, we could look for instances where similar things have been noted in humans.
For instance, children of Halocaust victims would appear to be prone to developing PTSD...perhaps suggesting their ability to regulate stress has been altered? .. Pregnant women who were involved in 9/11, in particular those in third trimester at the time and suffered PTSD. showed low levels of cortisol in their saliva. The interesting thing is, their babies also registered low levels of cortisol in their saliva. So can we perhaps see a similarity to the stressed mice studies?
The chemical toxins in cigarette smoke causes damage to our DNA with something like 23.000 mutations showing signs of damage because of the chemicals. Women who smoke when pregnant may have babies of low weight, who may also go on to develop diseases, and also show signs of altered DNA methylation.
Regarding diet. I think anyone who has read something about epigenetic studies knows the famine studies of Sweden where seasons of plenty ran with seasons of famine. Effects from that were showing up in grandchildren of those involved [ can be found on google search.]
So while there is still so much to be learned regarding epigenetics and much to yet be proven, for me I think there are cases where we see something is going on and in some cases it seems it is being carried on.
I don't know, for some reason I'm not too convinced about hereditary epigenetics. If there is an effect it is rather a small one. And IIRC with time, in normal environment, methyl groups can get fixed and epigenetic effect goes away.
Also, all above examples point to a negative role of epigenetic effect. Methyl groups are messed up, genes don't expressed correctly, causing "misbehaviour" of a body. Seems like a damage to DNA more than inheritance of new traits.


Regarding methyl groups. All living creatures have vast number of tags. Some like methyl molecules attach to DNA directly, other types grab proteins [histone] around which DNA wraps. The contact is called "hugging" and if hugged tightly it gets hidden from view of the cell and cannot be utilized. Our body adds methyl groups to DNA strands to regulate it. Where there is a methyl group, the genes will be silent, and wherever methyl group is removed genes are expressed.
Concerning lactose tolerance. [ As we all know]...we are born able to tolerate lactose due to lactase gene giving the instuction to make lactase enzyme. As babies we get nourishment and anti-bodies from mum via milk. When we get around the age of weaning the body stops producing these enzymes and we stop being able to utilize milk. This is the normal pattern. The mutant pattern, if you like, is lactose tolerance whereby lactase carries on being made. I don`t know a great deal about this LeBrok, because to be honest I haven`t really read too much about it. It is pretty much it, but where is the timer? How the cell counts time to turn off lactose tolerance at puberty? How the cell knows to express some genes in a brain but not in skin? I think scientists are still trying to get to the bottom of it. If you find a future research in this regourd let me know. :)


Again, sorry for late reply..I just hope I don`t loose this post as I don`t want to rewrite...:annoyed:
No problem, I don't expect you rushing to answer my posts. Whenever you have a moment to talk to friends is great.

EDIT... I`m not sure if this reads correctly..I did get logged out but thankfully I did a paste and copy job.[/QUOTE] On longer posts I copy them too before pressing the post button. Learned painfully in the past.

hope
15-03-15, 23:39
It is pretty much it, but where is the timer? How the cell counts time to turn off lactose tolerance at puberty?

Everything is in constant state of maintenance and refurbishment. Genes, except for household genes go off/on as they are needed. The body will not use precious energy on anything it does not need to have running.
Perhaps, but I`m not sure, that when we get weaned and start introducing other food into our system chemical reaction sends this info off to lactase gene and it begins turning down the production of lactase enzymes, eventually shutting them down completely. Does this make sense do you think ?


On longer posts I copy them too before pressing the post button. Learned painfully in the past.
Oh I so know that pain.....:laughing: