Mad scientists cure mad cows: gene-ious

Mad cow disease(MCD) is a neurodegenerative disease that affects bovines. If infected meat is consumed it can be passed onto humans in the form of Cruetzfeldt-Jakob Disease, which also affects the brain. It is fatal to both.
MCD is caused by the misfolding of a normal cellular protein (prpc), into an infectious protein, a prion.
Due to the fact that everyone (almost) loves a nice steak, MCD in cows is the main problem. Richt et al have used genetics to disrupt the alleles of prpc, producing 12 cloned calves that are prpc deficient. The cows were proved to be immune to MCD after prions were injected into the brain tissue of two of the cows with no effect. The remaining cows were injected with MCD with no effect aswell, but as MCD can lie dormant for several years so, time will tell if they are truly immune.
‘At over 20 months of age they [the cows] are clinically, physiologically, histopathologically, immunologically and reproductively normal’ (Richt et al, 2007).
Aside from reducing/eliminating the occurrence of MCD, these cattle are thought to be beneficial for future drug and prion research. They may also produce favourable, prion free products such as the steak mentioned earlier.
So, no mad cows, no mad people, what’s the problem? Certain issues have been raised by the experiment. Will human consumption of the cows cause side effects? Will reproduction with normal cows cause problems? Is it moral to ‘play god’ by changing and controlling another species mainly for our own benefit?

References:
Primary:
Richt JA, Kasinathan P, Hamir AN, Castilla J, Sathiyaseelan T, Vargas F, Sathiyaseelan J, Wu H, Matsushita H, Koster J, Kato S, Ishida I, Soto C, Robl JM & Kuroiwa Y, 2007, Production of cattle lacking prion protein, Nature Biotechnolgy, vol 25, pp 132-138
Secondary:
Paddock C, 2007, ‘Could Genetic Engineering Eradicate Mad Cow Disease?’, 27th May 2007
Canadian Food Inspection Agency, 2007, ‘BSE Case Confirmed in British Columbia’, 30th May 2007

Not far from a triumphant victory over mastitis in dairy cows

Mastitis in dairy cows causes huge economic loss in the global dairy industry. Despite various measures has been adopted to tackle mastitis, its occurrence has not been declined significantly. A recent research developed a possible solution by creating transgenic cows with the enzyme lysostaphin secreted in their milk. Transgenic cows carrying lysostaphin in the study has shown to be more resistant to S.aureus, a major contagious mastitis pathogen which accounts for 30% of all intramammary infections. While lysostaphin effectively eliminates the pathogen S.aureus, it is relatively harmless to both the cows and the milk consumers compared with commonly used antibiotics. Furthermore, it has minimal effect on milk composition.

To maximize the efficiency in tackling mastitis in dairy cows, major pathogens other than S.aureus need to be dealt with also. Antimicrobials which satisfy a series of criteria, including harmlessness to cows and milk consumers, no biological activity when taken orally and high sensitivity to pathogens, are hard to find. Nevertheless, the development of transgenic cows that secrete antimicrobials in milk is a breakthrough in the field of dairy science and surely of great benefit to the global dairy industry.

Aiming at an increase in milk yield and improvement in milk quality, more dairy science research in creating mastitis-resistant cows are expected to be done in the near future.

Primary source:
Donovan, D.M., Kerr, D.E., Wall, R.J., 2005. ‘Engineering disease resistant cattle’, Department of Animal Science, University of Vermont, Burlington
http://www.springerlink.com/content/u1m28j7732815g68/fulltext.pdf

Secondary source:
Kerr, D.E., Wellnitz, O., 2003. ‘Mammary expression of new genes to combat mastitis’, Department of Animal Science, University of Vermont, Burlington
http://jas.fass.org/cgi/reprint/81/suppl_3/38.pdf

Written by: Kin Fai, Lau
Student number: 41281941

Future of champion stallions

Future of champion stallions

In April 2005 at a press conference in Italy the first ever clone of a champion racehorse was unveiled. Italian scientists cloned Pieraz who had won two world endurance titles. Pieraz had been castrated at a young age like most successful endurance horses. The aim of this clone was to preserve Pieraz genetic heritage.
As Professor Galli leader of the project said “What we have done is to create a clone of a gelding that is a stallion, to preserve the genetic heritage of an exceptional champion. This gives us an unprecedented opportunity to breed from the best animals.” To clone Pieraz a sample of cells from the champion was taken in 2002 and stored in liquid nitrogen after an agreement between Ms Kanavy the owner and Cryozootech, a biotechnology company based near Paris. Scientists from Cryozootech and CIZ a breeding animal company then cloned Pieraz. The horse was cloned using the cell nuclear transfer technique which was developed at the Roslin Institute, near Edinburgh. This is the technique which led to the birth of Dolly the cloned sheep. Although Pieraz-Cryozootech-Stallion the cloned foal was born perfectly healthy there is no guarantee that he will perform as well as Pieraz. If this clone appears to be able to breed it can lead to a new generation of cloned champion stallion.

References

Henderson, M. 2005, Champion the wonder clone, Times online
http://www.timesonline.co.uk/tol/news/world/article381252.ece (accessed 28/05/07)

Coghlan, A. 2005, First clone of champion racehorse revealed, New scientist.
http://www.newscientist.com/article.ns?id=dn7265 (accessed 28/05/07)

When Neutral Bugs Turn Nasty: Venezuelan equine encephalitis virus

The Venezuelan equine encephalitis virus (VEEV) is responsible for a zoonic disease transmitted by mosquitoes that can cause death in humans and equines (such as horses, donkeys and asses). This disease emerges periodically throughout central and southern America and occasionally even in the USA. In humans it causes flu-like symptoms including severe headaches which usually subside after a few days. Death usually only occurs in immunocompromised people such as the very old or young. In equines the effects are more severe and neurological disorders are often observed. The death rate in equines has been estimated as high as 83% for some strains. In these animals death usually occurs within a week of infection.

It has been hypothesised that VEE epidemics are caused by alterations to the genome of a relatively harmless strain of the virus. This less virulent strain of the virus is carried asymptomatically by many small, forest dwelling mammals throughout the Americas and is only capable of infecting humans who are continuously in close proximity with infected populations. This strain is very rarely passed to equines. It was shown in a recent study that a single mutation of the genome causing an amino acid substitution in the less virulent strain is all that is needed to turn it into an epidemic strain. Because of this, it is believed that these outbreaks of highly virulent VEEV will continue to occur unless mosquito populations are better controlled and more equines are vaccinated.

Written by: Sarah Batt

Student number: 41386015

Primary references:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16549790 Venezuelan encephalitis emergence meditated by a phylogenetically predicted viral mutation

http://en.wikipedia.org/wiki/Venezuelan_equine_encephalitis_virus -general info from wikipedia

Secondary references:
http://arjournals.annualreviews.org/doi/pdf/10.1146/annurev.ento.49.061802.123422 - more in depth info on outbreaks

http://www.cdc.gov/ncidod/EID/vol11no05/04-1251.htm -about reservoirs (forest mammals)

http://www.sciencedaily.com/releases/2006/09/060915203515.htm -bioterrorism threat

The Great Debate – Drumstick or Wing?

Scientists, it seems, have decidedly taken sides with the drumstick lovers and have created a chook with three legs.

They have been working on trying to unravel the genetic sequence of limb development, that is – why is a leg a leg and not a wing? They focused on three genes in particular. Normally, Tbx5 is turned on in the wing, and Tbx4 and Pitx1 are turned on in the leg.

To determine the gene responsible for leg development the scientists stuck Pitx1 into a virus, then sprayed the virus on the would-be wing nub of a chick embryo. Amazingly, the resulting chicken had 3 legs and just one lonely wing!

However, the third leg isn’t a perfect drumstick. While feathers became scales, and the limb was straight, clawed and muscled like a leg, some wing characteristics still remained.

This means that Pitx1, while switching on the ‘leg gene’ (Tbx4) in the wing, had no effect on the actual ‘wing gene’ (Tbx5), being independent of it. Both were switched on, making the limb a wing-leg hybrid. More bizarrely, Japanese researchers have now achieved a complete wing and leg position interchange.

While these odd chooks have caused egg-citement in chook farmers and KFC lovers alike, their creation had a more noble purpose. Scientists believe that by understanding the genes responsible for forelimb and hindlimb development, they could one day be able to correct or prevent limb deformities in humans.

Really though, my vote is for the four winged chook. Less meaty, a little less able to walk, but altogether a major step back towards that airy domain, so that they may fulfill their ancestry and return to their rightful place as lords of the sky.

by Stephanie Clark

41207268

Genetics of a cow gone mad

Mad cow disease, also known as Bovine Spongiform Encephalopathy (BSE) is termed a prion disease and variants of this abnormal protein occur in humans through consumption of contaminated meat as well as other livestock. As the term prion suggests, this disease is a result of polymorphisms in the coding and regulatory regions of the normal prion protein (PRNP) gene localized on chromosome BTA 13 at position q17.

BSE is not a viral or bacterial infection because the alteration in the DNA sequence is brought about by an infectious prion protein acquired primarily from contaminated feed. Furthermore, scientists have proven that only cows which are genetically susceptible are affected. So far, studies have shown that this susceptibility factor is highly associated with the expression of other genes in chromosomes 5, 10 and 20 in addition to the PRNP locus.

In a case study where they compared the genes of healthy and infected cattle, they found that diseased cattle across different breeds were characterized by a higher frequency of insertion/deletion polymorphism within the open reading frame of the PRNP gene.

The body naturally has normal prion proteins within its cells which the infectious prion converts into a form identical to its own after entering. The accumulation of these indigestible proteins leads to chronic degeneration of the central nervous system. Clinical symptoms include ‘nervousness’, kicking, abnormal walking and pelvic limb ataxia.

Despite these advances, scientists are still working to uncover the puzzling mechanism behind the concept of an infectious ‘protein’.





References
Primary source –

Zhang, C., de Koning, D-L., Hernandez-Sanchez, J., Haley, C.S., Williams, J.L. & Wiener, P. 2004, ‘Mapping of Quantitative trait loci affecting Bovine Spongiform Encephalopathy’, Genetics Society of America [online] Available at: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15342524 (accessed 28/05/07)

Secondary source –
Czarnik U, Zabolewicz T, Strychalski J, Grzybowski G, Bogusz M, Walawski K. 2005, Deletion/insertion polymorphism of the prion protein gene (PRNP) in Polish Holstein-Friesian cattle [online] Available at: http://www.ncbi.nlm.nih.gov/sites/entrez

Jeong BH, Sohn HJ, Lee JO, Kim NH, Kim JI, Lee SY, Cho IS, Joo YS, Carp RI, Kim YS. 2005, ‘Polymorphisms of the prion protein gene (PRNP) in Hanwoo (Bos taurus coreanae) and Holstein cattle’, Ilsong Institute of Life Science [online] Available at: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16284424 (accessed 28/05/07)

For more information -
http://www.mad-cow-facts.com/about.htm
http://www.cbc.ca/news/background/madcow/science.html
http://science-education.nih.gov/home2.nsf/Educational+Resources/Resource+Formats/Online+Resources/+High+School/D07612181A4E785B85256CCD0064857B

by Agnes Meredith
41099744

Fainting Goats, No Kidding!

If you don’t believe me, take a quick look at this video.

Selective breeding can produce humorous results, but studies of these genetic mutants can further veterinary knowledge. The Myotonic, or ‘fainting’ goats’ most characteristic feature is the fact that they display a autosomal dominant, genetic condition called myotonia congenita. When they become frightened or excited, it causes the muscles in their legs to contract: they become stiff. There is a lag of about 10-15 seconds before their muscles relax and they are again able to move. Often, this stiffening of the leg muscles causes the goat to fall over, hence earning them the name ‘fainting goats.’

To allow normal muscle use, the muscle cell rapidly changes its membrane’s permeability to certain ions, creating spikes of electrical discharge, allowing it to contract. Myotonic goats however have a mutated form of the gene CLCN-1 that encodes for the permeability of chloride. It was found that this gene’s output differed between myotonic and normal goats only by one amino acid: proline is substituted in the Myotonic goats for alanine. This involves the change of one nucleotide base pair in the DNA sequence: codon CCC instead of codon GCC; affecting the gene’s abilty to function normally.

While such a trait could be seen merely as entertaining, the condition actually enhances muscle development. The determination of the genetic code responsible has allowed scientists to look into its use in other production animals, and to further understand the condition which can occur naturally in other animals including the Chow Chow dogs.

Emily Stevens – 41440999

Further information:
The International Fainting Goat Association [Click here]
Wikipedia: Fainting Goat [Click here]
Tennessee Fainting Goats [Click here]

Primary Reference:
Beck, C. L., Fahilke, C., George Jr, A. L. 1996. Molecular basis for decreased muscle chloride conductance in the myotonic goat. October Vol. 93, pp. 11248-11252 [Click here]

Secondary References:
Myotonia Congenital, Autosomal Dominant [Click here]
All Creatures, One Medicine [Click here]
Mytotonic, The breed or Displaying Myotonia? [Click here]