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originally posted by: annoyedpharmacist
a reply to: SlapMonkey All proteins are made by transcription of DNA to RNA, and translation of that RNA into proteins. There are some post translational modifications to proteins through enzymatic processes, but that is how all protein is made
The self-templating conformations of yeast prion proteins act as epigenetic elements of inheritance. … Thus, prions broadly govern heritable traits in nature, in a manner that could profoundly expand adaptive opportunities.
The heritable variation that drives new forms and functions is generally ascribed to mutations in the genetic code. We previously proposed an entirely different pathway for creating heritable phenotypic diversity1, through which the inheritance of new traits can precede the genetic changes that ultimately hardwire them. The mechanism for this seemingly paradoxical flow of information resides in epigenetic switches encoded entirely by self-perpetuating changes in protein structure, known as prions.
originally posted by: SlapMonkey
a reply to: soficrow
So, basically, they're the free thinkers of the body and they're out to stage a coup on the man (DNA) as they see fit.
Got it.
originally posted by: annoyedpharmacist
...If they can be passed on without the transcription translation pathway,
The mechanism for this seemingly paradoxical flow of information resides in epigenetic switches encoded entirely by self-perpetuating changes in protein structure, known as prions.
and especially if they can "infect" other agents,
Biochemistry. 2009 Mar 31. Prion diseases and their biochemical mechanisms.
…A growing number of observations support the once heretical hypothesis that transmission of TSE diseases does not require nucleic acids and that PrP(Sc) alone can act as an infectious agent. The view that misfolded proteins can be infectious is also supported by recent findings regarding prion phenomena in yeast and other fungi. One of the most intriguing facets of prions is their ability to form different strains, leading to distinct phenotypes of TSE diseases. Within the context of the "protein-only" model, prion strains are believed to be encoded in distinct conformations of misfolded prion protein aggregates. In this review, we describe recent advances in biochemical aspects of prion research, with a special focus on the mechanism of conversion of prion protein to the pathogenic form(s), the emerging structural knowledge of fungal and mammalian prions, and our rapidly growing understanding of the molecular basis of prion strains and their relation to barriers of interspecies transmissibility.
Mechanism of Cross-Species Prion Transmission: An Infectious Conformation Compatible withTwo Highly Divergent Yeast Prion Proteins
Efficiency of interspecies prion transmission decreases as the primary structures of the infectious proteins diverge. Yet, a single prion protein can misfold into multiple infectious conformations, and such differences in “strain conformation” also alter infection specificity. Here, we explored the relationship between prion strains and species barriers …
that would allow them to bypass the normal mechanism of replication
.......but then this foreign prion would and should be attacked by the immune system.
There is little or no immune response to prion diseases -- that's one of the hallmarks of prion diseases.
2005: Prions Use the Immune System to Spread in the Body
IF they every conclusively prove the prion TSE connection it is something we should be concerned about for sure
Transmissible spongiform encephalopathies (TSEs), also known as prion diseases
originally posted by: lostbook
In summary: * Inherited traits are passed on by prions - with some dating back hundreds of millions of years. As well: * Conscious memories are 'stored' in prions; * Prions are airborne; and * Transmitted human-to-human.
Wow! Thanks for this. This could really change things in our understanding of humans and the world. ... Glad to see you back.
originally posted by: AshFan
I want the Water bear Dsup protein prion please!
WATER BEAR PROTEIN ‘DSUP’ PROTECTS HUMAN DNA FROM RADIATION DAMAGE
I mean, you just stated "time to re-write textbooks" and that "proteins are the product of DNA" thereby admitting to the fact that somewhere somehow studies or experiments involving DNA and/or RNA have been successful
originally posted by: soficrow
originally posted by: ssenerawa
So why have studies and experiments using DNA been successful?
Name some, with links please. And be sure they make a clear distinction between gene products (proteins) and genes (DNA).
originally posted by: ssenerawa
I mean, you just stated "time to re-write textbooks", thereby admitting to the fact that somewhere somehow studies or experiments involving DNA and/or RNA have been successful
originally posted by: soficrow
originally posted by: ssenerawa
So why have studies and experiments using DNA been successful?
Name some, with links please. And be sure they make a clear distinction between gene products (proteins) and genes (DNA).
originally posted by: theantediluvian
a reply to: soficrow
DNA has not been "dethroned"
In summary:
* Inherited traits are passed on by prions - with some dating back hundreds of millions of years.
As well:
* Conscious memories are 'stored' in prions;
* Prions are airborne; and
* Transmitted human-to-human.
Does this information affect your understanding of life? Reincarnation and karma? What else?
nor has it been demonstrated that "inheritance is protein based."
As protein-based elements of inheritance, prions perpetuate not by changing the way that genetic information is transcribed or translated but rather by co- opting the final step in the decoding of genetic information—protein folding.
Here, we examine the breadth of protein-based inheritance ...
...our data establish a common type of protein-based inheritance through which intrinsically disordered proteins can drive the emergence of new traits and adaptive opportunities.
This screen just gives us a taste of the breadth of prions and protein-based inheritance.
What has been known for more than just the last few years is that prion like proteins can encode information for later retrieval and that this information is heritable.
I wrote a thread a while back about how prion like proteins in flowering plants function as a sort of "memory" and it's a fascinating topic and there is much ground being broken
but you're grossly mischaracterizing to the point that this is very woo-isa.
A quick and by no means comprehensive check with Google:
Current Biology - Cytoplasmic inheritance. Prion-like factors in yeast. (1994)
TheScientist - Protein-based Inheritance (2000)
Nature - Prions as adaptive conduits of memory and inheritance (2005)
originally posted by: theantediluvian
a reply to: soficrow
It's been known since before the very first Punnett Square didn't accurately predict the results of breeding that Mendelian inheritance wasn't the whole of the story.
It seems to me that what you're really doing is trying to setup an argument for Jung's "racial memory." If that's where you're going with this, you're going to be greatly disappointed because there isn't enough storage capacity for information in these prion like proteins for that to be even remotely feasible.
originally posted by: yorkshirelad
a reply to: soficrow
Wrong! Please read the science.
originally posted by: VP740
a reply to: soficrow
So, identical twins don't get their similarities from their identical DNA, they just don't have the epigenetic variation most siblings have? Does that mean most identical twins don't have the same DNA?
2005: Identical Twins Exhibit Differences in Gene Expression
Phenotypic differences in genetically identical organisms: the epigenetic perspective
Monozyg otic Twins Exhibit Numerous Epigenetic Differences
Human monozygotic twins and other genetically identical organisms are almost always strikingly similar in appearance, yet they are often discordant for important phenotypes including complex diseases. Such variation among organisms with virtually identical chromosomal DNA sequences has largely been attributed to the effects of environment. Environmental factors can have a strong effect on some phenotypes, but evidence from both animal and human experiments suggests that the impact of environment has been overstated and that our views on the causes of phenotypic differences in genetically identical organisms require revision. New theoretical and experimental opportunities arise if epigenetic factors are considered as part of the molecular control of phenotype. Epigenetic mechanisms may explain paradoxical findings in twin and inbred animal studies when phenotypic differences occur in the absence of observable environmental differences and also when environmental differences do not significantly increase the degree of phenotypic variation.
A twin approach to unraveling epigenetics
…Twin studies have played an essential role in estimating phenotypic heritability, and these now offer an opportunity to study epigenetic variation as a dynamic quantitative trait. …Recent genome-wide epigenetic studies in disease-discordant monozygotic twins emphasize the power of this design to successfully identify epigenetic changes associated with complex traits.
…..Epigenetics today more specifically defines cellular modifications that can be heritable, but appear unrelated to DNA sequence changes, and can be modified by environmental stimuli [2,3]. At present, epigenetic mechanisms typically comprise DNA methylation and histone modifications, but also include many other mechanisms such as ATP-based chromatin-remodeling complexes, Polycomb–Trithorax protein complexes, non-coding RNA mediated gene-silencing, and potentially prions, transcription-factor binding, and other mechanisms involved in generating and maintaining heritable chromatin structure and attachment to the nuclear matrix.