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Re: Prion research and mad cow disease



Tim,
thanks for YOUR explanations and post explanations. YOu were not much clearer than Prusiner, who (I read the URLs, not the entire 56 p Nobel lecture, of course) either did not want to disclose or did not know the whole story what he invented. Nomenclature adds nicely to the consfusion.
Prions are identified mostly by what they are (do) NOT. I don't know why a protein 'should' contain DNA or RNA at all? I thought I have a vague idea about them, not anymore.  What ar they?
(Prion is what prion does, sometime infetious, sometimes not, etc.)
And why do you (does he) call a different folding a misfolding?
Of course conformation can expose or hide specific hooks for action, so a flat (beta) format is acting quite differently from a quadruple helix rod-format.
I like Jamie's biol nanotube metaphor.
Fact is: we know precious little about proteins, they are too big and "complex" for the existing methods of investigation. We notice superficial characteristics and "dream up" possible mechanisms, based on the desultory knowledge we have. Imagine the cure for the black death in the 14th c. Praying. I just heard on TV that in Washington state there were extra praying sessions to avert the mad cow catastrophy.
In the meantime nobody knows how the self-replicating elements of the 'bad' prions survive transition through other animals, pigs, chickens, etc. and revitalize when we eat those animal tissues.
They swiftly found out that it all came from Canada, so the damage will be collectible.
Anyway, thanks for the help and references.
 
John M
 
----- Original Message -----
From: Tim Gwinn
To: ***
Sent: Saturday, December 27, 2003 11:16 PM
Subject: Re: Prion research and mad cow disease

Well, I think I have to amend my remarks. After reading a bit more of Prusiner's work I think I seriously mis-stated when I said that "prion" does not only refer to "misfolded" version of certain proteins. I was getting confused in his usage of the two terms 'prion' and 'prion protein'. :(
 
'Prion' is more like a term referring mostly to function: to what a certain 'some thing' does. 'PrPSc' refers to the specific physical entity which comprises the 'some thing'.
 
So, it appears that Prusiner uses the term 'prion' to refer only to the pathological entity that is composed of the "misfolded" version of a PrP.
 
(from: "Prions in Skeletal Muscles", 2002)
 
Prions cause neurodegenerative diseases, including Creutzfeldt-Jakob disease (CJD), bovine spongiform encephalopathy (BSE), chronic wasting disease (CWD), and scrapie in mammals (1). The only known constituent of the infectious prion is an aberrant isoform (PrPSc) of the normal cellular (PrPC) prion protein (PrP). PrPC is a cell-surface glycoprotein, the _expression_ of which is necessary for the production of prions (2, 3). In animals with clinical signs of scrapie, the highest levels of prions are found in the brain and spinal cord, but other tissues, particularly those of the reticuloendothelial system, exhibit substantial prion titers
Also, from his UCSF website:
Nascent prions are created either spontaneously by mutation of a host protein or by exposure to an exogenous source. Prions are composed largely, if not entirely, of a modified form of the prion protein (PrP) designated PrPSc. Like other infectious pathogens, they multiply but prions do not have a nucleic acid genome to direct the synthesis of their progeny. A post-translational, conformational change features in the conversion of cellular PrP (PrPC) into PrPSc during which alpha-helices are transformed into beta-sheets. Since this structural transition in PrP underlies both the replication of prions and the pathogenesis of CNS degeneration, much of the effort in the laboratory is devoted to elucidating the molecular events responsible for this process. Indeed, prion diseases seem to be disorders of protein conformation.
 
So, this changes several of my remarks as follows:
 
This is just plain wrong:
So, when talking about a prion-caused disease, we should probably not say that "the prion causes x", but rather something like: "PrPSc causes x" or "the pathological isoform of PrP causes x". Otherwise, we would be saying something analogous to "genes cause x" when we really mean that "mutated genes cause x".
 
This is also largely wrong:
When is a protein a prion?
The answer to this is still a bit unclear to me. I speculate from what I read that a protein can be a called a prion based not necessarily on specific amino acid sequence (which varies with species), but on some (mostly) functional criteria:
1) if a protein is coded for in the genome of the species under study
2) and if it can be folded into the two isoforms representing PrPC and PrPSc
3) and if the PrPC isoform is normally occurring and functional in the species under study
4) and if the PrPSc isoform is not functional in that species
5) and if the PrPSc isoform can convert the PrPC in the organism into PrPSc
6) and if the PrPSc isoform is highly resistant to destruction by proteasomes.
 
Sorry for those errors. That's what I get for rushing to post rather than waiting and researching more. :(
 
Tim
 
 
-----Original Message-----
From: ROSEN Forum [mailto:***On Behalf Of Tim Gwinn
Sent: Saturday, December 27, 2003 10:00 PM
To: ***
Subject: Re: Prion research and mad cow disease

Hi JohnM,
 
I was a bit hazy on what 'prion' exactly referred to myself. Here's what I've dug up.
 
Prion - short for "proteinaceous infectious particle", specifically ones that lacks nucleic acid (see quote below). The term was coined by Stanley Prusiner at Univ. of Cal. Med School in 1982. Prions are proteins and contain no RNA or DNA. he won a Nobel Price for his work on prions in 1997.
 
PrP - short for "prion protein".
 
From what I read, neither "prion" nor "PrP" automatically imply that they refer only to the "misfolded" version of the proteins. However, many websites talk about prions as if the term 'prion' did refer only to the "misfolded" versions. Those sites appear to me to be incorrect.
 
Prusiner's Nobel lecture (in PDF form):
 
Prusiner's paper in "Science" (1997, No. 5336, Oct., p. 245-251) is available free at:
 
In the Science paper, footnote 1 is as follows:
Prions are defined as proteinaceous infectious particles that lack nucleic acid. PrPC is the cellular prion protein; PrPSc is the pathologic isoform. Amino-terminal truncation during limited proteolysis of PrPSc produces PrP 27-30 (so named because this protease-resistant core of PrPSc migrates at ~27 to 30 kD).
Further on in the paper:
PrPSc is the major, and very probably the only, component of the infectious prion particle. PrPSc formation is a posttranslational process involving only a conformational change in PrPC
 
So, when talking about a prion-caused disease, we should probably not say that "the prion causes x", but rather something like: "PrPSc causes x" or "the pathological isoform of PrP causes x". Otherwise, we would be saying something analogous to "genes cause x" when we really mean that "mutated genes cause x".
 
I am uncertain if all currently identified pathological isoforms of prions are termed "PrPSc", or if there are other terms (for pathological isoforms of PrP found in some other species, for example), but I believe it does refer to all forms, even though the "Sc" in "PrPSc" apparently initially was a reference to scrapie (the sheep version of BSE). From the Nobel lecture:
"The amino acid sequence of PrPSc corresponds to that encoded by the PrP gene of the mammalian host in which it last replicated. In constrast to pathogens with a nucleinc-acid genome that encodes strain-specific properties in genes, prions encipher these properties in the tertiary structure of PrPSc." (p. 4)
 
When is a protein a prion?
The answer to this is still a bit unclear to me. I speculate from what I read that a protein can be a called a prion based not necessarily on specific amino acid sequence (which varies with species), but on some (mostly) functional criteria:
1) if a protein is coded for in the genome of the species under study
2) and if it can be folded into the two isoforms representing PrPC and PrPSc
3) and if the PrPC isoform is normally occurring and functional in the species under study
4) and if the PrPSc isoform is not functional in that species
5) and if the PrPSc isoform can convert the PrPC in the organism into PrPSc
6) and if the PrPSc isoform is highly resistant to destruction by proteasomes.
 
 
Other "what is a prion?" sites:
 
 
 
 
Regards,
Tim
 
 
 
-----Original Message-----
From: ROSEN Forum [mailto:***On Behalf Of John M
Sent: Saturday, December 27, 2003 7:23 PM
To: ***
Subject: Re: Prion research and mad cow disease

Tim and All,
I told several times that I am a virgin-minded layman (=stupid) in the biology-related sciences up from the macromolecules. Question:
in superficial reading I got the impression that "PRION" is used as the specific villain in mad cow disease. I thought it is a 'small' piece of proteinatious molecule with an inorderly folding. Maybe the latter is pertinent to MCD only and prions can be 'orderly folded protein
midgets' with RNA only, as well? Many other animals (fish, etc.) have prions, do they spread mad fish disease? I don't think so.
I find it unreasonable to 'wait 30 months' or any, since infected remnants (mentioned are: placentas) of MCD cows stay for years in pastures ready to infect deer, hare etc, which then do the favor for the coyotes, wolves, people and other predators. That is pertinent to PA, NJ, NY, MN, and all other states as well, not only the West.
 
Agribiz - as any other successful biz does not care beyond making money today. That's why that stupid law was concocted in the US.
Suicidal behavior? for the others. Not for "me". The government owning oligarchy will feed safely on their private (organic) sources of their food staple, even if millions fall over like mad cows.
 
Protein folding is big deal. I made experiments myself (El Micr.-ly controlled) "straightening out" protein (and the like) molecules, froze them in unfolded state, then restored the mobility and it reformed the orig. folding perfectly, no matter in what 'changed' environment. So a "misfolding" is more than an esthetic nuisance.
It forms the joining sites (or hides them) for enzymes, etc., so the conformation is a fundamental adage to the "life processes".
 
I asked the question in the 1st par because it seems that we have mixed info and I don't have the time to study along books on the proteinatious materials of recent. The old ones I know do not include the word prion. Just as the recent ones do not include words which will be coined in the future, when we (hopefully) will learn more about nature. We can use more knowledge.
 
I hope the US science will come up with a better SAFE solution than cremating 45million cows (and bulls!). It's a mad mad world.
 
John M