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BSE Gene

cedardell

Well-known member
If some of our cattle carry a gene that makes them succeptible to BSE we are capable of testing for that at the packing plant using a gene reader which are in common use now. This reliable test would identify genetics that are suseptible and we could breed around them like we did with dwarfism. Maybe we don't have a lot of cattle with these susseptable genes. Who knows, we don't seem to have very many with BSE. So why is it so necesary to clone GMO cattle and develop strains without this gene if we already have them? I think Kathy is right and we are making a lot of hoopla without knowing the details. Unless of course USDA has been lying to us and covering up some horrendous facts. However, if this was the case I would think we would have found a lot more mad cows by now.
 

Jason

Well-known member
The thing with genes is they aren't labeled. They interact with other genes and biology to give us the differences in animals.

When you talk with those that do embryos or genome work, they tell you there is an intrinsic design and they can only go so far in manipulating that design.

Cloning and GMO aren't necessarilly done to be economically viable entities on their own. It is research to identify if the type of gene exists that would make an animal immune to certian problems.

The big mistake would be to breed for 1 trait, ignoring all others. Some will as it seems to be human nature.
 

cedardell

Well-known member
This is all true but there have been many cases where purebred lines have bred around bad genetics and eliminated problems. Look at dwarfism in cattle. Look at the Impressive line in Quarter Horses. What I am saying is that now it is possible to identify animals carring those genes easily and quickly. So that it would be easier than ever to breed around them. I have a personal feeling that they will be found in French lineage cattle because most of them seem to have a brain problem from day one.
 

mwj

Well-known member
cedardell said:
If some of our cattle carry a gene that makes them succeptible to BSE we are capable of testing for that at the packing plant using a gene reader which are in common use now. This reliable test would identify genetics that are suseptible and we could breed around them like we did with dwarfism. Maybe we don't have a lot of cattle with these susseptable genes. Who knows, we don't seem to have very many with BSE. So why is it so necesary to clone GMO cattle and develop strains without this gene if we already have them? I think Kathy is right and we are making a lot of hoopla without knowing the details. Unless of course USDA has been lying to us and covering up some horrendous facts. However, if this was the case I would think we would have found a lot more mad cows by now.

Tell me all about this gene reader that is in COMMON USE now and how reliable it is!!!!!!!!! When we test all the downers and culls you can decide how much of a prob. we have in our herds.
 
A

Anonymous

Guest
Unless of course USDA has been lying to us and covering up some horrendous facts. However, if this was the case I would think we would have found a lot more mad cows by now.

I'm not saying its happening- but it darn sure could be, when the same Agency (USDA) that is giving all the facts is also the only Agency doing any testing- making the decision on the numbers and type tested- and is controlling/prohibiting any private testing....

Thats the reason their Creekstone decision stinks to high heaven and makes their credibility questionable with the consumer groups........

Too much power in one bureaucracy without enough oversight....
 

Jason

Well-known member
Get out of the USDA for a second and look at what we have found in Canada.

Nearly every animal tested here is older and we have not found them all to be harbouring misfolded prions.

It is crazy to think all animals eventually develop a TSE from natural causes.

Feed bans have been effective in sharply reducing the number of animals found with TSE's, proof positive that feeding TSE infected material is a source of transmission.

If they can show animals that will be resistant to any possible infection that we know about, it stands to reason they would be resistant to any unknown form of aquiring the disease.

Let the researchers do what they do. They postulate theories and proceed to try to proove them. Another researcher may try to disproove the first. Evetually enough evidence is gathered to make a resonably sound decision.
 

Mike

Well-known member
Biology and Pathology of Prion Diseases:
Genetic Linkage of TSE Traits to the Prion Protein Gene



The demonstrated transmissibility of TSEs suggested a contagious spread of the disease; however, some forms of TSEs like GSS and a subset of CJD appeared to be associated with families, resembling a genetic disease. In 1989, Hsiao and coworkers reported the identification of a mutation in the PrP gene which was linked to the occurrence of GSS in an autosomal dominant pattern (Hsiao et al., 1989). Since then, several more mutations in the PrP gene were shown to be linked to the occurrence of GSS or familial CJD (reviewed by Kitamoto and Tatieishi, 1994). When the GSS-associated mutation described by Hsiao and co-workers in 1989 was introduced into transgenic mice, these mice subsequently developed a neurodegenerative disease with detectable, albeit low production of infectivity (Hsiao et al., 1990; Hsiao et al., 1994). Taken together, the above results suggest that certain mutations in the PrP gene are able to trigger a spongiform encephalopathy.

Subsequently, mice homozygous for an ablated PrP gene were shown to be resistant to scrapie (Büeler et al., 1993) establishing that an intact PrP gene is a prerequisite for infection and/or prion propagation.

Genetic linkage to the PrP gene was also observed for the so-called species barrier for infection. Normally, experimental transmission between different species requires high doses of infectivity and results in long incubation times (Pattison, 1965, 1966). Once transmission to a new species has been established, however, subsequent passaging within this species can be done with lower doses and results in shorter incubation times. The infectious agent is therefore specific for the host species it is produced in. When transgenic mice expressing hamster PrP in addition to their own mouse PrP were inoculated with infectious material from hamster, they exhibited much shorter incubation times than wild type mice and produced hamster-specific infectivity (Scott et al., 1989; Prusiner et al., 1990). Subsequent studies established that the species specificity resided within the coding sequence of the PrP gene (Scott et al., 1993).

Differences in scrapie incubation times between different mouse strains have been shown to be linked to the Sinc/Prn-i gene, whose genetic localization has been mapped closely to the Prn-p gene (Dickinson and Meikle, 1971; Carlson et al., 1986, 1993; Bruce and Dickinson, 1987; Hunter et al., 1987). It has not been formally proven, however, that Sinc/Prn-i is identical to Prn-p.

The genetic traits mapped to the PrP gene locus may also be linked to other, unknown genes at the same locus. Goldgaber (1991) and Hewinson and co-workers (1991) provided findings implicating the existence of an ´anti-PrP´ gene on the DNA strand opposite to the PrP coding sequence. This ´anti-PrP´ was suggested to be responsible for properties formerly ascribed to PrP. A subsequent study, presented in this thesis, provided evidence against the conjectured ´anti-PrP´ expression (Moser et al., 1993) refuting the hypothesis that genetic traits mapped to the Prn-p locus may represent inherent properties of an ´anti-PrP´ gene.
 
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