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Genetic Drift?

Grat3fulh3ad

The Voice of Reason
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y
yeh,,,,i agree,, i do think epigenetics is a broad concept!!,, but i also belive an stress mutation is an epigenetic responce,,,,,IMO its all heritable through repoduction!!,,,,sex aswell as grafting:)

by definition, mutation and epigenetic response are two completely different things.

What is commonly referred to as a stress mutation, I definitely think is in reality epigenetic change.
 

englishrick

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enviromental pressure and the "niche" enviroment is the artist,,,,the genetics is just clay,,you can add bit`s and you can take bits away,,form it into whatever you can depict or whatever the "niche" allows:)

i agree with you again Head,,,,but id like to take it 1 step firther and say any phenotipic shift is a epigentic responce:)
 

Grat3fulh3ad

The Voice of Reason
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i agree with you again Head,,,,but id like to take it 1 step firther and say any phenotipic shift is a epigentic responce:)

Apparently not all...

http://www.the-scientist.com/blog/display/57224/

Researchers have identified a possible mechanism by which DNA regions that don't encode proteins can still determine phenotypic traits such as a person's height or susceptibility to a particular disease, researchers report online in Science today.


Image: Wikipedia
The scientists found that certain chromatin modifications often considered to be epigenetic -- meaning, regulated by factors other than genetic sequence -- are in fact determined by a person's DNA.

Moreover, they found that this chromatin variation is associated with distinct single nucleotide polymorphisms, suggesting that the variation may serve as a platform to enable these SNPs -- often found in non-coding regions of DNA -- to influence phenotype.

"This is quite novel," said Emmanouil Dermitzakis, a geneticist at the University of Geneva Medical School, who was not involved in the study. "Epigenetics has been used as a term that is orthogonal to genetics. This study clearly shows it's not."

Genome-wide association studies have linked single nucleotide polymorphisms (SNPs) to particular diseases or characteristics, but how SNPs relate to phenotype has been unclear. Because SNPs often occur in non-coding regions of the genome, researchers have generally thought that what links these regions to phenotype are processes that control how genes are regulated, but such a relationship has never been demonstrated. "What this paper really does is show this to be the case," said Vishwanath Iyer of the University of Texas at Austin, one of study's three lead authors.

The researchers examined two processes involved in gene regulation: chromatin structure -- in particular, whether or not chromatin is open, allowing genes to be transcribed -- and transcription factor binding. Both of these features can be regulated epigenetically -- that is, by factors such as DNA methylation and histone modifications.

They used high-throughput sequencing to analyze cell lines taken from six individuals whose genomes had originally been sequenced within the 1000 Genomes Project -- two parents and their daughter from Utah, of northern and western European ancestry, and two parents and their daughter from Ibadan, Nigeria, of Yoruban ancestry. This pool of six people allowed them to compare these factors across both alleles of genes carried by single individuals, as well as examine familial heritability in the two daughters. "It's the first time someone has looked at chromatin structure throughout the genome in related individuals," Iyer said.

In 10 percent of the sites they examined, they found that chromatin sites that tended to be open in the parents also tended to be open in their daughters, suggesting chromatin structure was heritable. Similarly, many differences in transcription factor binding were maintained across individuals.

But these differences could still be the result of heritable changes in epigenetics, not genetics. So the authors also looked at these traits at at both alleles in single genes in the individuals' genomes. They found that, in a subset of sites, chromatin structure and transcription factor binding occurred differently at each allele, which suggested it was the genetic code at each allele that produced the difference. "We find that it is actually the sequence that matters," said Iyer.

If a non-coding SNP leads to a difference in chromatin structure and/or transcription factor binding, that effect can indeed be inherited, thereby providing a potential mechanism for transmission of phenotypes like disease susceptibility, Iyer said. "What we have is a way to link polymorphisms to phenotypes via things like chromatin structure and transcription factor binding." He stressed that not all forms of chromatin-level regulation were dependent on the genome sequence. "We are looking at one transcription factor and one measure of chromatin structure," he said; other kinds of chromatin variation, however, may be due to mechanisms such as DNA methylation, which are independent of the sequence.

"The paper in itself is not really surprising," said Maxwell Lee, a geneticist at the National Cancer Institute, but the researchers examined variation at many more loci than previous studies have looked at, and also were able to examine variation both at the level of different chromosomes as well as different individuals.

The study was done in the context of the ENCODE Consortium, a large-scale project conducted by the National Human Genome Research Institute that aims to understand all the functional elements in the human genome. The next step, said Iyer, is to examine this type of variation in a much larger set of people to determine when it is functional, and exactly how it drives phenotype.


Read more: "Epigenetics" drives phenotype? - The Scientist - Magazine of the Life Sciences http://www.the-scientist.com/blog/display/57224/#ixzz0kf06jjL5
 

Grat3fulh3ad

The Voice of Reason
Veteran
Epigenetic response or not, something immediate is involved most likely, and not some major shift of the genome. Lights, air, medium, feed....and then find out what I am doing that anyone else that sees the same problem may be doing too. Seems to me that it would be some major shifting going on to cause a plant to totally change character "out of nowhere". And what could bring about such a major shift so fast?

I agree. nothing occurred to indicate a shift in the genome. That's why I thought mutation as an answer to be so off base. By saying epigenetic response, it is somewhat implied that the response is a result of some stimuli. That is the nature of responses after all , there must be a something to respond to.

when that thing ( Lights, air, medium, feed....) does something to the cut which sticks with it through multiple clonings, then by all indications epigenetic change is immensely more probably than mutation as the condition.

You are absolutely correct that I did nothing to attempt to provide a solution or direction to proceed, only a statement as to the probable non-genetic nature of the problem.
 

Greyskull

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when that thing ( Lights, air, medium, feed....) does something to the cut which sticks with it through multiple clonings, then by all indications epigenetic change is immensely more probably than mutation as the condition.

and pests!!!!
dont forget the fucking goddamn pests...
 

hoosierdaddy

Active member
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And imo, Greyskull has brought up a very important point. We know that there are chemicals that we can stress the plant with, and we generally understand how these work.
What we may not have a full on grasp of are how the acids and fluids that pests may produce are effecting the triggers of a shift. Surely the plant reacts to the physical damage that a pest provides, but it also may be reacting at the molecular level to amino acids, etc.
Surely another variable.
 

Grat3fulh3ad

The Voice of Reason
Veteran
Indeed, i.e. spider mites excrete enzymes which retard the flowering process... no telling what all effects insects /pathogens may be having... We are "drifting" a bit from the original topic, imho, but i guess it is good to list many different variable external stimuli which might cause or contribute to changes which are heritable and not related to genetic mutation (a.k.a. epigenetic changes).
 
I am interested to hear if anyone comes up with a final explanation. My hubby says he has heard of this happening. We're lucky we don't have anything like this yet, but we are also always jonesing to get new strains going, so I imagine that when/if it does happen, we'll be ready to start something else. My soft side hates to see anything go to waste, however, and thus far there are a couple of our strains that are so yummy and yield so well that I'd cry if we lost them.

I'm assuming that although we have another grower running backups of all our current genetics, that this kind of drift would occur there, too, if/when it happens here, since that seems to be the case with others who are suffering from it . . . .
 

Grat3fulh3ad

The Voice of Reason
Veteran
Healthy plants will produce healthy cuttings which are identical to the original mother in perpetuity almost always. If your clone changes then 99% more likely than not it is something other than the plant which caused the change.

I've seen clones of clones go on for decades with no change.
Fucked up environments are what fuck up clones.


IMHE
 

englishrick

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Grayskull brings a good point ,,but this is all part of the "niche"

Modifications Brought about by Domestication Are, in Many Cases, Loss-of-Function Changes ,,,i wonder what could be considerd a Constitutive Gain of Function??,,,:):)


CropScience said:
the inheritance of domestication traits has been investigated many times since the rediscovery of Mendel's laws at the beginning of the 20th Century. Initially, the traits were analyzed as Mendelian traits because many of them display qualitative variation and discrete phenotypic segregation classes. More recently, these same traits have been analyzed by quantitative trait locus (QTL) approaches, which are more powerful because they allow a genome-wide analysis of influence on several traits at the same time (Lee, 1995; Tanksley, 1993). Such approaches have been applied to a limited number of crops, including maize (Doebley et al., 1990), common bean (Phaseolus vulgaris L., Koinange et al., 1996), tomato (Lycopersicon spp., Grandillo and Tanksley, 1996), rice (Oryza sativa L., Xiong et al., 1999), and pearl millet [Pennisetum glaucum (L.) R. Br., Poncet et al., 1998, 2000].

The results of these genetic studies can be summarized as follows.,,, In spite of the geographically diverse distribution of the domestication centers, a remarkably similar set of traits can be identified that have been selected in widely different crops. These traits jointly make up the domestication syndrome (Hammer, 1984). They result from selection of spontaneous mutations that occurred in wild populations and were selected at various stages of growth of these wild plants (or animals), as well as after harvest (Harlan, 1992). Many traits selected under domestication, because they fit the needs or fancy of humans, are actually deleterious in the wild. As a consequence, fully domesticated crops may not survive in the wild without human intervention in planting and harvesting.

For the sake of this discussion, it is important to point out that many domestication genes represent a loss rather than a gain of function, as indicated by their recessiveness. There are, of course, many more mutations that convert a functional enzyme or structural protein into an inactive one, than there are mutations that give an enzyme or structural protein an entirely new function. There are some exceptions to this pattern, notably the Tb-1 domestication gene in maize, which has recently been characterized at the molecular level (Doebley et al., 1997). The Tb-1 allele of domesticated maize is dominant over the tb-1 allele of teosinte, the wild progenitor of maize, because of overexpression of the gene in maize in comparison with teosinte. Dominant mutations may have been easier to select in an outcrossing species such as maize.


id still say "all phenotipic shifts are epigenetic!",,,even mutations are a result of epigenetic responce to the envitomental pressure`s or "the niche" as some biologist call it,,,,its all heritable through sex or grafting!!,,,,

like charles said and i love to quote this "adaptation is mutation"......<<<i love that quote!!
 

englishrick

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many biologists now view "niche construction" as an important evolutionary process (Day et al, 2003), and acknowledge that each generation of organisms inherits both genes and a legacy of modified selection pressures from the ancestral generation..
 

furious george

New member
id still say "all phenotipic shifts are epigenetic!"
But they're not. As the research Head posted explains.

,,even mutations are a result of epigenetic responce to the envitomental pressure`s or "the niche" as some biologist call it,,,,
No they are not. Have you not read any of the thread you are contributing to?

it's all heritable through sex or grafting!!,,,,
Epigenetic changes are not always heritable.

like charles said and i love to quote this "adaptation is mutation"......<<<i love that quote!!

This quote seems to be misleading you. Darwin is talking about adaptation of a species, not talking on the level of the individual. Don't let the terms confuse you. If you had to start carrying the brick hod all day at work, your body would adapt by developing larger muscles and seriously calloused hands. Would that be a mutation? Also Darwin had no knowledge of epigenetics, which allow adaptation without mutation. Don't want to get down on you rick, because I admire your desire to learn but that last post made it look like you've learned nothing from this thread.

In this thread there's only one person talking any sense on a topic that his has an understanding of (but is clearly not a practicing student/scientist in the field) and that's Head. Then there's Hoosier playing internet catchup, a bit out of his depth, googling every term he reads to try to find something he can pick at.
 

englishrick

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hoos made some good points about maping with twins!...has any1 adressed it?

im just taking a different perspective,,,:),,,im just not 1 to move with the croud:),,,,

new data could change Head`s mind at a later date,,,
 

Sam_Skunkman

"RESIN BREEDER"
Moderator
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Clones don't change, they don't drift. I have clones more then 20 years old that are still the same as year one. Yes in theory it could have a mutation, but that is rare and wont happen to back up copies, if you keep them.
What clones do is pick up viruses and then they can lose vigor and yield. They can be cleaned up of some viruses by fast growing, or special treatments, and then the taking of very small meristems to be grown in-vitro or rooted virus free.

-SamS
 

ROJO145

Active member
Veteran
Clones don't change, they don't drift. I have clones more then 20 years old that are still the same as year one. Yes in theory it could have a mutation, but that is rare and wont happen to back up copies, if you keep them.
What clones do is pick up viruses and then they can lose vigor and yield. They can be cleaned up of some viruses by fast growing, or special treatments, and then the taking of very small meristems to be grown in-vitro or rooted virus free.

-SamS
Thanks Sam for clearin that up.You called it furious george,Rick will never get it,an asshole in every thread,just like his new catch up buddy who will prolly be sellin beans soon!!!Got plural degrees ya know:tiphat:
 
R

RNDZL

Clones don't change, they don't drift. I have clones more then 20 years old that are still the same as year one. Yes in theory it could have a mutation, but that is rare and wont happen to back up copies, if you keep them.
What clones do is pick up viruses and then they can lose vigor and yield. They can be cleaned up of some viruses by fast growing, or special treatments, and then the taking of very small meristems to be grown in-vitro or rooted virus free.

-SamS

I had to re read this because at first i was confused

I gather the point Sam is making is that in his practical experience all plant health decline is due to plant health decline, not a epigenetic trigger or genetic trigger that tells a plant to die or lose vigor after a certain age or due to some influence.

I do think in this case in response to the OP it may be whats occurring to his parental stock.

What I would really like to clarify, and I think it has some relevance is how easily is marijuana effected by epigenetic triggers, if at all on the plant so triggered by epigenetic influence

I think that if a parent plant can be effected epigenetically then that bias would be passed to its clones, perhaps there are other examples of this in the horticultural world

Once we can ascertain this real threshold of epigenetic response we can try to establish what percentage of maladies are due to it

I dont think epigenetic infuences are prevalent to a current plants pathological influences than it does its progeny's

I feel epigenetic triggers occur and can be expressed rapidly in subsequent generations from triggered parental stock.

Epigenetic cues and resultant effects seem to be relevant to the most cursory levels of evolution (adaptive traits not macro evolution) and seems to be the measure in which breeding organisms adapt to a rapidly changing environ

that being said, it could be a possibility that a parent plant could produce 10 clones, each which is raised to adult hood in different environments with different variables and be exposed to the same pollen and each clone parent could possibly have a different epigenetic influence

To be completely honest the answer is probably available in our collective experiences if people could dilute the topic less critique on content and more critical thinking
 

Grat3fulh3ad

The Voice of Reason
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Well said Skunkman. Mutations are among the rarest causes of issues. I have read recently of virus causing epigenetic changes in some cases.

Host epigenetic modifications by oncogenic viruses


Epigenetic Modification of Plants with Systemic RNA Viruses

RZNDL, sam only addressed genetic change, not epigenetic response. When the issue is epigenetic there is zero change in the actual genome, and epigenetic responses are temporary. Epigenetic response would not be considered "changed" since it is reversible. I don't think sam intended his reply to address epigenetic response at all. If I am off base, hopefully he'll chime back in, so's we can discuss it.


George, all epigenetic responses are heritable. Heritability is integral to the definition of epigenetic.

Rick, you can still say that all phenotypical variations are epigenetic, but according to the criteria used by those who are involved daily in that field of study, there are phenotypical variations which are most definitely not epigenetic, so you'd be disagreeing with the experts.

According to my understanding of the things I've read, your trying to make phenotype and epigenetic response synonymous is carrying the concept past it's realities.
 
R

RNDZL

RZNDL, sam only addressed genetic change, not epigenetic response. When the issue is epigenetic there is zero change in the actual genome, and epigenetic responses are temporary. Epigenetic response would not be considered "changed" since it is reversible. I don't think sam intended his reply to address epigenetic response at all. If I am off base, hopefully he'll chime back in, so's we can discuss it.

im really trying to understand the relevance of genetic/epigenetic influences on cannabis and the subsequent relativity to the growers

if triggers can be effected on either an epigenetic or genetic level, how does that influence the plant?

I would think that most epigenetic or genetic triggers do not bring forth change to the current organism but has a bias on the makeup of the progeny only, except for the rare instant genetic mutation, which I know too little about to comment

many of the mutations that occur seem to have a cause other than genetic (i.e. disease, environment conditions, ect)

I guess in a nutshell, if i get this correctly, triggers to the genome are of interest to the breeding community but not necessarily a factor of concern to the cultivator

if this is indeed the case that being said, how can epileptics be used to influence adaptive traits in subsequent generations

for example, is there a trigger for earlier flower production in subsequent generations

say an early rainy season or some other environmental influence in the natural environment; or more practically say you are growing a plant in a foreign environment that it finds stressful and you breeding it in that environment, what percentage of its offspring will be effected to adapt to the environment its parent found stressful


this seems to be were the real meat of genetic influence is
 

furious george

New member
Epigenetic changes are not always heritable.

I had a feeling that would set off an alarm.

The context was rick saying “it’s all heritable through sex or grafting”

The point was that epigenetic resetting takes place in gametogenesis and embryogenesis that means only in some circumstances are epigenetic changes heritable through sex (transgenerationally). It matters whether the epigenetic change is somatic or in the germline.

You are right in that for pure clarity I should have typed Epigenetic changes are not always heritable transgenerationally, but I though that the context would have been enough.

Edit: Just saw this which is quite interesting and relevant. In my defense I studied mostly animal biology which is why my knowledge of transgenerational epigenetic effects is tainted!

"In plants, newly acquired epigenetic states of transcriptional gene activity are readily transmitted to the progeny. This is in contrast to mammals, where only rare cases of transgenerational inheritance of new epigenetic traits have been reported (FASEB J 12:949–957, 1998; Nat Genet 23:314–318, 1999; Proc Natl Acad Sci U S A 100:2538–2543, 2003). Epigenetic inheritance in plants seems to rely on cytosine methylation maintained through meiosis and postmeiotic mitoses, giving rise to gametophytes. In particular, maintenance of CpG methylation (mCpG) appears to play a central role, guiding the distribution of other epigenetic signals such as histone H3 methylation and non-CpG DNA methylation. The evolutionarily conserved DNA methyltransferase MET1 is responsible for copying mCpG patterns through DNA replication in the gametophytic phase. The importance of gametophytic MET1 activity is illustrated by the phenotypes of met1 mutants that are severely compromised in the accuracy of epigenetic inheritance during gametogenesis. This includes elimination of imprinting at paternally silent loci such as FWA or MEDEA (MEA). The importance of DNA methylation in gametophytic imprinting has been reinforced by the discovery of DEMETER (DME), encoding putative DNA glycosylase involved in the removal of mC. DME opposes transcriptional silencing associated with imprinting activities of the MEA/FIE polycomb group complex."

http://www.springerlink.com/content/f7382g0836n8377u/
 
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Grat3fulh3ad

The Voice of Reason
Veteran
im really trying to understand the relevance of genetic/epigenetic influences on cannabis and the subsequent relativity to the growers

if triggers can be effected on either an epigenetic or genetic level, how does that influence the plant?

I would think that most epigenetic or genetic triggers do not bring forth change to the current organism but has a bias on the makeup of the progeny only, except for the rare instant genetic mutation, which I know too little about to comment
Epigenetic response affects the organism, not the progeny. It can affect the progeny, but key points to remember are that: heritability does not always mean inherited by progeny. The vast majority of epigenetic changes are not transgenerationally heritable but are heritable in that they last through multiple cell divisions. Epigenetic triggers usually do bring about change in the current organism and not in it's progeny. You cannot "fix" an epigenetic response into a line like you can a genetic trait, though epigenetic responses may remain heritable longer in plants than in animals.
many of the mutations that occur seem to have a cause other than genetic (i.e. disease, environment conditions, ect)
mutation is by definition a change in the genetic structure. If the genome was not altered permanently, then it was no mutation.
I guess in a nutshell, if i get this correctly, triggers to the genome are of interest to the breeding community but not necessarily a factor of concern to the cultivator

if this is indeed the case that being said, how can epileptics be used to influence adaptive traits in subsequent generations
it cant. epigenetic changes are temporary and only rarely are they heritable to the next generation.

Perhaps as we learn more about epigenetic responses there may be ways to guarantee heritability through to a seed generation, but imho it would be of little value, since the epigenetic nature of the "trait" would mean it was easily reversible.

The genetics are not going to change, but the epigenetic state changes with environment.
for example, is there a trigger for earlier flower production in subsequent generations

say an early rainy season or some other environmental influence in the natural environment; or more practically say you are growing a plant in a foreign environment that it finds stressful and you breeding it in that environment, what percentage of its offspring will be effected to adapt to the environment its parent found stressful


this seems to be were the real meat of genetic influence is

In the grand scheme all the average grower need to know about epigenetic response is this: Healthy plants will produce healthy identical cuttings in perpetuity.
 
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