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Author | Topic: Mutation and its role in evolution: A beginners guide | |||||||||||||||||||||||
kuresu Member (Idle past 2514 days) Posts: 2544 From: boulder, colorado Joined: |
those deers in africa?
they're called antelopes. you know, "where deer and the antelope reign" (are those the lyrics?) now, as to specific names, god knows. Antelopus grassus could work, for a good fake name (after all, Carolus Linneaus is the latin for Carl Linne. spelled wrong, but then, I never was any good at writing in swedish). good explanation, though. All a man's knowledge comes from his experiences
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AnswersInGenitals Member (Idle past 151 days) Posts: 673 Joined: |
Perhaps this confusion can be cleared up with a simple but very important example. As we all know, human females have two X chromosomes while males have just one X chromosome. That one X in males has to be sufficient to make the correct amount of whatever proteins are encoded by that chromosomes for males to survive. That means that females would get too much of a good thing, which for some proteins could be lethal.
But when the female's egg first forms, one of the Xs is shut down by the methylation process (and some other similar processes) that has been discussed in this thread. This methylation inhibition of one of the two Xs is passed on to all the female's cells throughout her life. The mechanism for achieving this methylation (not well understood at this time, but undergoing extensive research) is also passed on to her daughters, so that it is inherited. In principle, it is possible for the female's two X chromosomes to have identical base sequences, so that the methylation can be considered a form of mutation - it changes the genetic function of the affected DNA - but it does not change the actual base sequence. (The 'base sequence" is just the sequence of As, Ts, Cs, and Gs in the chromosome.) It is helpful to remember that (almost) every gene on each chromosome has associated with it another nearby stretch of DNA that acts as a variable control region. Specific molecules, usually certain proteins called transcription factors, can attach to this associated stretch of DNA to turn on or inhibit the processing of the gene to make its target protein, RNA, or whatever it produces. This stretch of DNA is referred to as the operon or cis control region for the particular gene. ('cis', usually italicized, just means 'nearby') To me, this is very similar to the way factories control production by issuing works order sheets that require a variety of authorizing signatures to be effected. Epigenetic processes like methylation and acetylation can be looked upon as just another type of gene control. Regards, AnInGe______________________________ Remember, All of Noah's grandchildren married their first cousins. A lot of human history makes sense given that fact.
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Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
The only difference, although a very important one, between this example of AnInGe's and the mouse example I gave is that in the case of the mice the inheritance operated transgenerationally rather than simply being inherited in the differing somatic lineages of the organism.
A particularly well studied epigenetic mutation is associated with the Agouti viable yellow allele which affects coat colour in mice. While epigenetic inheritance at this locus has previously been ascribed to methylation (Morgan et al, 1999) a recent paper suggests that in fact the allele is demethylated during early embryonic development and that the actual inherited epigenetic mark is something else (Blewitt et al, 2006). It may be that the actual transmitted epigenetic marker at the Axin-fused locus is similarly something other than the methylation but it is the methylation which is mediating the effect and the marker is still thought to be epigenetic rather than genetic. TTFN, WK
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Hawks Member (Idle past 6147 days) Posts: 41 Joined: |
An often overlooked concept that has the potential to cause genetic changes in organisms is horizontal gene transfer (HGT). Rather then just letting organisms undergo single-base mutations, duplications and such, HGT allows for the transfer, from one organism to another, of anything from short stretches of DNA up to hundreds of genes - all in one go. Mechanisms/vectors such as homologous recombination, plasmids and integrons have been shown to sometimes be the most important ways bacteria adapt to environmental change, such as exposure to antibiotics.
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Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
Bumping this for TheWay should he return.
TTFN, WK
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Fosdick  Suspended Member (Idle past 5500 days) Posts: 1793 From: Upper Slobovia Joined: |
WK writes:
OK, so epigenetic material is heritable "...in the differening somatic lineages of the organism." Is all that verbosity necessary? It's a genetic deal and it's heritable. Nuff said. Lot's of alleles operate transgenerationally. So what? I assume epigenetic material physically survives crossing-over and other genetic dispersions of meiosis and makes it all the way to fertilization and a zygote. Then, in the new organism, this epigenetic stuff has certain controls over the expressions of certain alleles. But why is this any different from other genetic inheretances? So the epigenes are switches. But so are certain other genes, inherited in the same way. So what's the big deal? Why isn't the propagation of this epigenetic stuff understood simply as genetic heritability? Should it come as a surprise to anyone that histones and methyl groups ride along those meiotic pathways? ...the inheritance operated transgenerationally rather than simply being inherited in the differing somatic lineages of the organism. I notice two things: 1) Epigenes don't change a allele's expression beyond what it is already capable of. The epigene works only on what has been genetical disposed. 2) Epigenes don't come in from the side or over the top of a meiotic or fertilization event to affect "differeing somatic lineages of the organism." They have to use the same molecular routes traveled by genes. When all is said and done it's still purly genetic business, isn't it? ”HM
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Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
Hoot I can't tell from this if you even have the faintest idea what you are talking about. There is no such thing as an epigene nor epigenetic material. histones and methyl groups clearly don't undergo the same processes as nucleotide bases during meiosis or mitosis.
If your point is that these are concerns of molecular genetics then it is a trivial one. If you don't think that there is a useful purpose in distinguishing between genetic factors centred around the primary sequence of DNA and epigenetic modifications of genetic material then you need to provide some rationale for why you don't see the distinction.
Epigenes don't come in from the side or over the top of a meiotic or fertilization event to affect "differeing somatic lineages of the organism. What is your evidence for this? In fact what does this even mean? the whole point about the somatic lineages was that those were changes ocurring in a developed organism, not an embryo. How can it make any sort of sense to talk about somatic lineages following from fertilization, anything affecting the genetic makeup of a newly formed zygote is clearly going to affect all of the subsequent cells in the body. TTFN, WK Edited by Wounded King, : No reason given. Edited by Wounded King, : No reason given.
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Fosdick  Suspended Member (Idle past 5500 days) Posts: 1793 From: Upper Slobovia Joined: |
WK, I don't mean to be impertinent, but I have an allele-centric POV. If epigenetics explains certain modifications of allelic expression, then what has been explained other than more things about how the alleles express themselves on not? Histones and methyl groups are just part the genetic ensemble, with the critical aspect always coming down to allelic expression. Please, I'm sincere, is there more to it than the show ultimately put on by alleles? Can those mythyl groups and histones do anything on their own?
”HM
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Wounded King Member Posts: 4149 From: Cincinnati, Ohio, USA Joined: |
Can you explain, since you are so allele centric, just what you think an allele is? Because from what you are saying it sounds like you are using it in a very bizarre way.
TTFN, WK
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Fosdick  Suspended Member (Idle past 5500 days) Posts: 1793 From: Upper Slobovia Joined: |
An allele is a variant of a gene. Allelic centricity (my term) would assert that all heritable phenotypic traits, and changes in those traits, ultimately can be accounted for by alleles. Epigenetics is to alleles what paint is to a barn. You can change its tint, its hue, and even its color, but afterwards it's still a barn.
”HM
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Fosdick  Suspended Member (Idle past 5500 days) Posts: 1793 From: Upper Slobovia Joined: |
WK, let me use this definition of epigenetics from Wikipedia to focus my question:
quote:Simply put: Do those epigenetic features participate in biological evolution on their own, or does biological evolution require those epigenetic features to first affect changes in the alleles? ”HM Edited by Hoot Mon, : No reason given.
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molbiogirl Member (Idle past 2642 days) Posts: 1909 From: MO Joined: |
Inherited epigenetic variation - revisiting soft inheritance
Eric J. Richards Nature Reviews Genetics 7, 395-401 (May 2006) In case you don't have access, from the conclusion:
Does the existence of inherited epigenetic alleles that are to some degree independent of genetic variation necessitate a modification of our models of evolutionary change? The neo-Darwinian concept of inheritance posits that the hereditary material is 'hard' and impervious to environmental influences. If the formation of epialleles is random and not initiated or guided by the environment, the generation of epigenetic variation could be equated with random genetic mutation without otherwise altering our current view of evolutionary mechanisms. On the other hand, if the physical or behavioural environment of the cell or organism influences epiallele formation, a mechanistic foundation for soft inheritance exists in which the environment could mould a malleable hereditary material. A growing body of evidence indicates that epigenetic states can be influenced by the environment. For example, prolonged cold-temperature treatments in plants can lead to both chromatin37 and DNA methylation changes at specific genomic loci38. Treatment with DNA damaging agents that are used in traditional chemical mutagenesis protocols can also change epigenetic states39, 40, 41. Indeed, some of the best-studied inherited epialleles in plants were derived originally from chemical mutagenesis experiments42, 43. Some of the most striking examples of environmental modulation of epigenetic states are derived from the recent animal literature. One class of examples involves the alteration of DNA methylation through dietary regimes that alter single carbon metabolism in rodents. In the case of the mouse Avy epiallele (Table 1), dietary supplements (for example, folic acid and vitamin B12) that increase the abundance of the central methyl donor metabolite S-adenosylmethionine elevate DNA methylation of the upstream IAP element and suppress Agouti overexpression44, 45, 46. Another intriguing example of an environmentally induced, mitotically stable epiallele was recently described in rats: nurturing maternal behaviour leads to postnatal remodelling of the epigenetic state of the hippocampal glucocorticoid receptor gene (GR; also known as nuclear receptor subfamily 3, group C, member 1 (NR3C1)), creating a hypomethylated epiallele that persists into adulthood47. Mothers that show poor nurturing behaviour rear individuals with an alternative silent GR gene epiallele. The preceding examples show that epigenotypes can respond to an organism's physical, nutritional and even behavioural environment. Although these examples do not involve meiotic transmission of the environmentally induced epialleles, this is not always the case. A recent publication reported that treatment of gestating female rats with industrial chemicals that disrupt endocrine function can lead to male fertility defects in subsequent generations (F1 to F4), which are correlated with widespread alterations in DNA methylation48. This study resembles an earlier report demonstrating transgenerational effects on gene expression, DNA methylation and growth efficiency that is induced by nuclear transplantation in mice49. All the elements are in place to allow a type of soft inheritance that is based on DNA methylation and chromatin-level silencing: the creation of alternative epigenetic alleles that are biased by environmental inputs; the stability and mitotic propagation of epialleles; absent or incomplete epiallele erasure; and meiotic transmission. There is no reason on mechanistic grounds to reject the possibility that environmentally induced or modified epialleles can be inherited. It might be more meaningful to ask why we are not constantly confronted with the inheritance of environmentally induced phenotypic variation. In the case of mammals, the answer probably lies in a reasonably comprehensive erasure of epigenetic marks and the early germ-soma divergence that ensures that epigenetic alterations in somatic lineages are not transmitted through the germ line. The germ-soma division formed the core of Weismann's rejection in the late nineteenth century of neo-Lamarckian inheritance. These considerations indicate that epigenetic inheritance is unlikely to mediate in mammals the most extreme form of soft inheritance that involves the transmission of adaptive acquired characters (Box 4). However, a less extreme form of soft inheritance is possible that might be based on the transmission of environmentally induced or influenced epialleles that are generated in the germ line. In this case, there is no reason to propose that these epialleles will have any adaptive significance, without resorting to the contortion of invoking a parallel induction of epigenetic changes in reproductive and somatic lineages. However, in organisms in which reproductive lineages or germ lines are derived from vegetative or somatic lineages late in development and epiallele erasure is less extensive, such as plants, both forms of soft inheritance could operate through epigenetic mechanisms. Even if it is conceded that the molecular mechanisms are present to mediate soft inheritance through epigenetic mechanisms, the significance of such mechanisms must be questioned. The variation that has been shown to underlie the developmental and phenotypic differences between species occurs at the genetic rather than the epigenetic level. Among individuals in a population, however, epigenetic variation might have a significant role in controlling phenotypic variation50, 51. In addition, epigenetic variation might have a role as a bridge towards genetic end points by facilitating genetic assimilation of characters (for example, accelerated genetic decay of hypermethylated epialleles)52, 53, 54. Future directions
There are many questions to address about the mechanistic aspects of epigenetic inheritance and the significance of inherited epialleles. Several continuing lines of enquiry will be important in resolving these questions. First, it is necessary to continue to flesh out our knowledge of the machinery that orchestrates epigenetic regulation through biochemical and genetic dissection approaches. Second, studies that parallel Johanssen's pure line experiments55 should continue to determine whether alternative epigenetic alleles can be detected or selected in inbred backgrounds with limited genetic variation56, 57, 58, 59. Third, the meiotic behaviour of epigenetic alleles that are created or manipulated by environmental regimes needs to be examined, starting with the better-understood epialleles. For example, do dietary supplements in mice that carry the Avy allele alter the epigenetic state of the epiallele in untreated progeny, as well as the somatic tissue of the individuals that are treated in utero44, 45, 46? Fourth, several epigenomics projects that are currently underway to chart the epigenetic landscape of large eukaryotic genomes will pinpoint new loci that are sensitive to epigenetic modification and variation60. This information will inform systematic efforts to monitor the stability, environmental sensitivity and meiotic behaviour of many epigenetic alleles in different experimental models. Finally, it will be necessary to extend these findings to natural populations to evaluate the role of inherited epigenetic variation in a real-world context.
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RAZD Member (Idle past 1405 days) Posts: 20714 From: the other end of the sidewalk Joined: |
A growing body of evidence indicates that epigenetic states can be influenced by the environment. For example, prolonged cold-temperature treatments in plants can lead to both chromatin37 and DNA methylation changes at specific genomic loci38. Treatment with DNA damaging agents that are used in traditional chemical mutagenesis protocols can also change epigenetic states39, 40, 41. Indeed, some of the best-studied inherited epialleles in plants were derived originally from chemical mutagenesis experiments42, 43. If I try to put this into more general (layman?) terminology, is it fair to say that:
Would you still class this as hereditary traits (as in "evolution is the change in hereditary traits in populations from generation to generation") or do we need some new terminology? Should we distinguish this as a different\another kind of evolution? compare Fiocruz Genome and fight Muscular Dystrophy with Team EvC! (click) we are limited in our ability to understand by our ability to understand RebelAAmericanOZen[Deist ... to learn ... to think ... to live ... to laugh ... to share.
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molbiogirl Member (Idle past 2642 days) Posts: 1909 From: MO Joined: |
Short answer?
Yes. Environmental signaling and evolutionary change: can exposure of pregnant mammals to environmental estrogens lead to epigenetically induced evolutionary changes in embryos?Evolution & Development Volume 7 Issue 4 Page 341-350, July 2005 The challenge is to know how an eventual change in DNA methylation patterns could become persistent and evolutionary. Besides, another question arises, regarding the definition of evolutionary change. Is persistence in the conditions allowing the establishment of changed methylation patterns across lineages a sufcient attribute for such changes to be considered as evolutionary, or do such changes need to reach the threshold of mutation at the genomic level? Given the special feature of imprinted genes regarding possessing methylation patterns that are more stable across generations than other genes, persistence could be achieved through changing methylation patterns of imprinted genes. In this view, such changes in imprinted genes could have the same evolutionary value of mutations, given that there is an associated character variation with the changes, and because of the persistence of these changes throughout generations. Thus, the definition of ””evolutionary change’’ at this point becomes blurred. What is true is that persistence through generations could be achieved in alternative ways to genomic mutation. Nevertheless, speaking in terms of genomic mutation, this could be achieved when the persistent change in methylated cytosines bias to specific mutations, as previously mentioned.
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Fosdick  Suspended Member (Idle past 5500 days) Posts: 1793 From: Upper Slobovia Joined: |
molbiogirl, thanks for the article. It hits the spot pretty well. But now I'm left with more questions:
1. What is an epiallele? Is it an intron? 2. When, if ever, does "soft inheritance" turn "hard"? 3. Exactly how could "soft inheritance" turn "hard"? 4. How does mitiosis affect meiosis? How vast is the so-called "germ-soma division"? 5. How come Wounded King doesn't know about epialleles? He said in Message 37:
Hoot I can't tell from this if you even have the faintest idea what you are talking about. There is no such thing as an epigene nor epigenetic material. 6. And once again: Can evolution occur only on an epigenetic level and without the fixation of new alleles? I realize were traipsing around in fronteer territory here. From E. J. Richards:
quote:How much of this epigenetic stuff is speculative and how much has been confirmed empirically? Oh, and one more question: 7. Why don't you post your synthesis of this material rather than quoting someone elses? ”HM
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