Tuesday, 25 September 2012

Cows Producing Human-Like Milk

Scientists in Argentina and China have claimed to have engineered cows to produce human-like milk

In Argentina, Scientist from the Institute for Biotechnology Research, the National Institute for Agricultural Biotechnology and the National University of San Martin have engineered a cow to produce human-like milk.  They achieved this using Genetic Modification.  Human genes were implanted into a cow embryo containing two specific proteins.  One protein of which is completely absent in cows’ milk, and the other of very low levels.  These modified cells were cloned, and then implanted into a surrogate cow. 

Genetic modification

Genetic modification refers to the altering of genes within an organism.  Traditionally, two organisms with favourable traits would be bread together to produce tailored progeny.  The favoured traits are bread in, while the unfavourable traits would be bread out.  And since offspring inherit both the favoured and non-favoured traits of their parents, this process happens over a number of breeding cycles. These traits can range from an organisms colour and height to a plants capability to survive under drought conditions.  Genetic modification is similar, however it uses genes from one organism (which in some cases are artificially altered) and directly inserts them into another, or an organism may have its own genes modified.   

As a result of the project in Argentina, the calf, Rosa-Isa was born in April 2011.   It’s quoted that “The aim is to produce a highly nutritional, baby-friendly cow's milk with enhanced iron and anti-bacterial properties, they said.”  And Julian Domnguez, Argentina's agriculture minister, ‘says that the development of baby milk in cows fulfils a "significant social goal."’

Why human milk is more beneficial to babies

In cases where a new born baby for various reasons is unable to receive its mother’s breast milk, cow’s milk is commonly a substitute.   Although these products have much in common, cow’s milk baby formula is discouraged by health nutritionists for a number of reasons.  Protein has a higher presence in cow’s milk, however it is not so easily absorbed in the human gut.  This is because it lacks a number of accompanying nutrients, minerals and enzymes that allow maximum absorption.  Cow’s milk also contains higher levels of ion, however during the process of making the formula, Lactoferrin (a protein with iron-binding properties) is destroyed, thus making it harder for the baby to absorb.  Breast milk also contains more whey than curds which is favourable for human babies, and also contains anti-bodies that cow’s milk completely lacks. 

In disapproval of the project, animal welfare groups have questions the well-being of the cows and the safety of the milk.  In response to the safety of the milk, scientist Germn Kaiser dismissed these queries by saying ‘it’s not harmful for humans since our bodies are designed to digest these human proteins.’  A similar project was conducted in China.

Emma Phillips s42587453

Sunday, 23 September 2012

Genomics - Joining the Fight Against Climate Change

If any of you have watched David Attenborough’s ‘Pole to Pole’ in the BBC’s Earth series, you’ll happily join the cause too.

Polar bears, Ursus maritimus, are one of eight members of the family Ursidae. The largest of their cousins, they inhabit the circumpolar north, which is unfortunately their demise (Polar Bears International, 2012). Global warming has many ramifications; one being that it’s increasing the rate at which the Arctic sea ice melts, cutting short the regular hunt/feed/breed cycle of the Polar Bear. The question to their survival is, can they adapt?

Norse poets described the polar bear as the seal's dread, the rider of icebergs, the whale's bane, and the sailor of the floe. They praised polar bears for having the strength of 12 men and the wit of 11”(Polar Bears International, 2012).

© Daniel J. Cox/NaturalExposures.com (Polar Bears International, 2012)

Recent studies of mitochondrial DNA (mtDNA) have dated Polar Bears to have had diverged from their closest cousin, the Brown Bear, Ursus arctos, in the late Pleistocene less than 111-166 thousand years ago (Hailer, et al., 2012). This “potentially indicate[s] rapid speciation and adaption to arctic conditions”(Hailer, et al., 2012, p. 344) for such a ‘young’ species. However, a recent study conducted by Frank Hailer and colleagues of Germany’s Biodiversity and Climate Research Centre suggests otherwise (Hirschler Reuters, 2012). Through the analysis of multiple loci of the brown, black and polar bear nuclear genome, they conclude that Polar Bears evolved much earlier, in the middle Pleistocene about 600 thousand years ago (Hailer, et al., 2012).

Hailer and his colleagues argue that the maternal inheritance of mtDNA creates a biased representation of Polar Bear evolution, as it may be explained through “introgressive hybridisation” (Hailer, et al., 2012, p. 346). This is certainly possible with recent sightings of Polar/Brown bear hybrids, suggesting it may have occurred multiple times throughout Polar Bears history*. When compared against Hailer’s time scale, geological evidence suggests that Polar Bears have gone through stages of increasing temperature before, bringing the two species within closer range to one another and thus having the opportunity to interbreed. 

The most substantial evidence supporting their claim is the lack of shared alleles in the nuclear genome of the two species, which one would expect from recently diverged species. Rather, “out of 35 haplotypes in polar bears and 79 in brown bears, only 6 were shared” (Hailer, et al., 2012, p. 346).  This places Polar Bears in a distinct clade, rather than within the Brown Bear clade (Fig 1), indicting that they are a genetically differentiated species(Hailer, et al., 2012).

Figure 1: Comparison of Polar Bear and Brown Bear evolutionary lineage when ordered against Nuclear DNA and Mitochondrial DNA (Hailer, et al., 2012, p. 345).

Speciation, in the case of the Polar Bear, can be inferred as the result of adaption to the Arctic environment, and from Hailer’s study, it seems this was a slower process than previously thought (Hirschler Reuters, 2012). This has implications for the survival of the Polar Bear because it implies this species is highly specialised to its habitat. Rapid environmental change, as suggested by Polar Bears International, is the driving force behind the swift loss in population numbers. The Arctic is at the forefront of the impacts suffered from global warming. It’s causing the summer sea ice to melt before Polar Bears have to chance to hunt and breed. However, as previously mentioned, this new evidence calls attention to the possibility that these bears have endured through phases of increased temperatures before, and obviously survived. This holds hope that these creatures can push on, but as Hailer (in Hirschler Reuters, 2012) points out                the main difference this time is that humans are impacting polar bears as well… If they go extinct in this phase of warming, we're going to have to ask ourselves what our role in that process was".

Thanks for reading!
Sophie Smith 42365763

Works Cited
Hailer, F., Kutschera, E. V., Hallstorm, M. B., Denise, K., Fain, R. S., Leonard, A. J., et al. (2012). Nuclear Genomic Sequences Reveal that Polar Bears are an Old and Distinct Bear Lineage. Science , 336, 344-437.

Hirschler Reuters, B. (2012 йил 20-April). Poler Bears are no new kids on the block. (ABC Science) Retrieved 2012 йил 19-August from ABC Science: http://www.abc.net.au/science/articles/2012/04/20/3482016.htm

Polar Bears International. (2012). Polar Bears. Retrieved 2012 19-August from Polar Bears International: http://www.polarbearsinternational.org

Friday, 21 September 2012

Glowing Potatoes

Hey guys, today my blog will be about glowing potatoes and the genetics involved. Let me start off with telling you how the thought came across. It started about 10 years ago when a bunch of scientists decided to map the genome of a potato. It then diverged into genetically modifying the potatoes into withstanding certain pesticides, herbicides, diseases and stuff like that.

However with the price of water drastically increasing this was a higher demand priority. As you already know plants are not like animals, they can’t really say something and water is given to them. And with potato farming since the potatoes are in the ground it is hard to see how they are growing, so most farmers either over or under water them the produce, which can give bad result.

This was the occurring phenomenon until a Professor of the University of Edinburgy Antony Trewavas said ‘The best-placed organism that can tell you what is happening in terms of environmental insults like dehydration and mineral depletion is the plant itself.’  So with that in mind the researchers tried to accomplish it.

They did this sort of like the techniques we have been doing over the past few weeks, by cutting a gene and inserting it into another cell. Except they cut the gene that produced the Green Fluorescent Protein (GFP) form the Aequorea victoria, jelly fish, and just inserting it into the potato genome. The GFP gene was attached to the potatoes water conserving gene. So when the potato first senses that it is in need of water, and consequently starts conserving water, the inserted process of producing the GFP is also made active. So the potato leaves glow fluorescent green.

This can be seen as a good or a bad advantage. Good because it assists the farmer in when to water the potatoes, which would save money on water, approximately $330 per hectar. And yes that isn’t that much however for a 200 or 300 hectare plantation over say 10 years the benefits would be appreciated.

But also bad because when they go on sale in the supermarket, not many people would like the idea of buying a genetically modified potato.

However this is not the extent of this testing! Researchers are also testing weather if the GFP gene is added to the right parts of the chromosome, whether it can report on the nitrate, phosphate and sucrose status. As well as trying this technique in other plants and vegetables.

By Mitchell Everlyn 42936248

Thursday, 20 September 2012

Judd Higgins 42889492

Vaccines and bacterial vectors.

The main aim of this research is to change the route of delivery and effectiveness of vaccinations to the human population.

Genetics and Biology
·      Using live bacteria as a vector to carry vaccines into the human body
·      Using specific plasmids that create a immune response in the human body and in turn vaccinating and building immunity in humans
·      Using live bacteria as a vector combined with recombinant bacteria using techniques such as PCR and electrophoresis.

·      What you are essentially doing is infecting a host with bacteria leading to research into suitable bacteria.
·      One option is using GRAS (generally recognised as safe) bacteria. Which don’t readily replicate once in a mammalian host. These are readily used in the food industry to preserve food products.
·      Lactobacillus is one of the bacteria used by the food industry and is considered a GRAS bacteria. Some lactobacillus strains are know to colonise in the human gut, exhibiting probiotic health-promoting activities. This has a disadvantage that producing a immune response in the guts is physiologically difficult.
·      Enteric pathogens have shown promise and most of the research has been in this area. Were there is a higher surface area, the potential create a sufficient immune response.
·      Currently there is one recombinant bacterium that is successful in creating immunity for tuberculosis. This bacterium is known as BCG bacteria (Bacille Calmette-Guerin). Which can delivered nasal or orally and has been proven to work. Which then leads to bacteria colonizing in the lungs preventing future infection.
·      There are lots of others that are undergoing testing and clinical trial, but shows that this is all possible.

Pros and cons
·      Cheep – theoretically once this is possible it will require no health professional to administer vaccinations.
·      Save’s time - Vaccines can be cultured/grown in about two weeks, currently takes about a month to produce vaccination
·      Convenient – its can be as simple as going to your pharmacist with a script from the doctor and ingesting recombinant bacteria from the routes of administration available. Oral, intranasal, rectally.
·      Essentially what you are doing is infecting patient with live recombinant bacteria, negative side effects will occur
·      From this there will be lots of safety requirement and guidelines for suitable bacteria
·      There are known side effects with a live vector bacterium. Therefore a risk benefit for human health needs to be established, choosing bacteria that will produce minimal side effect but can still produce the desired immune response, this is the biggest obstacle at the moment. 

Wednesday, 19 September 2012

Gene Therapy for Duchenne Muscular Dystrophy

Duchenne Muscular Dystrophy (DMD) is a recessive X-linked lethal childhood disorder (1/3300 boys) characterised by progressive muscle wasting and degeneration (Eppie & Kornberg, 2008).  It is caused by mutation in the gene within the X chromosome that provides instructions for the formation of the structural dystrophin protein (Figure 1). The dystrophin gene is the largest gene in the human genome, consisting of 75 exons and 14,000bp and this large size makes it prone to recombination events (Van Deutekom & Van Ommen, 2003). In DMD patients, the majority of mutations result in the deletion of exons (typically exons 45-47) causing a premature termination and producing a dysfunctional dystrophin protein (Eppie & Kornberg, 2008).

Dystrophin binds to the skeletal muscle membrane, anchoring contractile proteins in the cytoskeleton to those in the fibre membrane and acting to maintain the structure of muscle cells (Van Deutekom & Van Ommen, 2003). Absence of functional dystrophin causes disruption of the cytoskeleton, membrane instability and increased susceptibility to mechanical stress during muscle contraction, manifesting in degeneration and necrosis of muscle fibres.  This progressive muscle loss leads to skeletal deformities and impaired motor skills where patients are confined to a wheelchair by the age of 12 and die by their early twenties due to respiratory or cardiac failure (Gregorevic et al, 2006).


In a study by Gregorevic et al (2006), gene therapy using an adeno-associated virus (AAV) vector (which is a nonvirulent, single stranded DNA virus) is currently being explored as curative treatment to DMD. Gene therapy (Figure 2) to correct cellular deficiency of dystrophin involves exploiting the virus lifecycle where viral DNA inserts into the hosts chromosomes, causing the host cell to express proteins coded by the viral DNA (Reece et al, 2012). Due to the large size of the dystrophin gene, prior studies identified certain domains of the dystrophin gene which were non-essential for proper functioning of dystophin so could be shortened or removed (Gregorevic et al, 2006). This enabled the engineering of a micro-dystrophin gene (3, 800 bp) which still produced functional dystrophin, yet was small enough to be packaged into and delivered into the host cell via an AAV vector.

 In the Gregorevic et al study, mico-dystrophins were cloned into recombinant AAV vectors and injected into dystrophic mice. It was found that dystrophic mice treated with the recombinant AAV had increased muscle mass by more than 90%, a considerably extended life-span and an overall reduced DMD phenotype (Figure 3) due to the ability of the micro-dystrophin gene to successfully integrate into the host’s chromosome 19 and the consequent production of dystrophin via transcription and translation (Gregorevic et al, 2006). These findings assert that the administration of AAV vectors carrying the micro-dystrophin gene restore expression of dystrophin, thereby improving muscle function and extending lifespan without serious pathogenic effects in dystrophic mice. Although this evidence suggests that gene therapy has potential benefits for treatment of DMD in humans, gene therapy for DMD is still in the early stages and more studies and assessment of side-effects are required before this technique can be implemented in a clinical setting.

Reference List

Eppie, Y & Kornberg, A 2008, ‘Duchenne muscular dystrophy’, Neurology India, vol. 3, no. 56, pp. 236-237

Gregorevic, P, Allen, J, Minami, E, Blankinship, M, Haraguchi, M, Meuse, L, Finn, E, Adams, M, Froehner, S, Murry, C & Chamberlain, J 2006, ‘rAAV6-microdystrophin preserves muscle function and extends lifespan in severely dystrophic mice’, Nature Medicine, vol. 12, no. 7, pp 787-789

Reece, JB, Meyers, N, Urry, LA, Cain, ML, Wasserman, SA, Minorsky, PV, Jackson, RB & Cooke BN 2011, Campbell Biology, 9th edn (Australian version), Pearson Education, Australia.

Van Deutekom, J & Van Ommen, G  2003, ‘Advances in Duchenne muscular dystrophy gene therapy’, Nature Reviews Genetics, vol. 4, pp. 774-783

Tuesday, 18 September 2012

Gene Therapy in Nicotine Addiction

Gene Therapy in Nicotine Addiction

Figure 1-Australian Government (2012)

According to the Australian Institute of Health and Welfare (AIHW), 7.8% of Australia’s total health burden is contributed by tobacco smoking, which is also the highest single preventable cause of Australia’s death and diseases1

Nicotine is a very small molecule found in cigarettes that readily diffuses through skin, lungs and mucous membranes and eventually travels into the bloodstream reaching the brain. The nerve cells in the brain communicate through neurotransmitters which bind to a receptor on the surface of nerve cells. The chemical structure of nicotine is similar to the chemical structure of the neurotransmitter acetylcholine2. Due to the close resemblance in structure, nicotine is capable of activating cholinergic receptors usually stimulated by acetylcholine. These receptors are located in the brain, the heart, muscles, adrenal glands and other peripheral nervous systems and therefore nicotine largely affects the body systemically. Nicotine causes the release of adrenaline, the hormone responsible for fight or flight responses resulting in an increase in heart rate, blood pressure and constricts the blood vessels reducing blood flow to the heart2. It also increases dopamine levels in the brain, a neurotransmitter responsible for feelings of reward and pleasure. The onset of nicotine effects occurs as fast as 10 seconds after inhalation and withdrawal symptoms such as irritability occur when nicotine levels in the body deplete3. Therefore in order to maintain nicotine levels, users resort to continuous smoking which leads to a cycle of nicotine addiction.
Figure 2-Reardon (2012)

Current smoking cessation methods are nicotine patches, gum and prescription medications. Gene therapy may soon be an alternative treatment to suppress nicotine addiction in smokers due to its incredible therapeutic potential. This therapy was tested in mice and showed effective results in controlling nicotine levels reaching the brain. Ronald Crystal of Weill Cornell Medical College achieved this concept by isolating the strongest antibody against nicotine found in a mouse and inserted it into a common carrier used in gene therapy known as adeno-associated virus (AAV)5. This viral vector is a non pathogenic genome comprised of the expression of the full-length, high affinity, anti-nicotine antibody5. This antibody-containing virus was injected into a nicotine-addicted mouse where antibodies were then produced and released into the bloodstream by the mouse. To test the efficiency, researchers administered nicotine equivalent of two cigarettes into the mouse and results showed that 83% of nicotine was bound by the antibodies prior to reaching the brain5. This is more than seven times greater than that in untreated mice. Nicotine concentrations in the brain of the treated mice were reduced to 15% of those in control mice5. The treatment prevented significant nicotine-mediated changes in heart rate, arterial blood pressure and locomotor activity. As well as showing high specificity and high affinity for nicotine, the antibodies were seen to be able to produce monoclonal anti-nicotine antibodies for duration of eighteen weeks in mice5.
Figure 3-Autismspot

Although AAV gene therapy against nicotine addiction has not been tested in humans, the preceding results suggest a possible solution in aiding smoke cessation.

1.     Australian Government. (2010). AIHW. Risk Factors. [Viewed: 1.09.12]. Available: http://www.aihw.gov.au/risk-factors-health-priority-areas/
2.     Tabitha, M. (2004). PMC. Nicotine as Therapy. [Viewed: 2/09/12]. Available: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC526783/
3.     Martin, T. (2011). About.com. Understanding Nicotine Addiction. [Viewed: 01.09.12]. Available: http://quitsmoking.about.com/od/nicotine/a/nicotineeffects.htm
4.     Australian Government. (2012). Australian Government. Quitting Methods. [Viewed: 3/09/12]. Available: http://www.quitnow.gov.au/internet/quitnow/publishing.nsf/Content/quitting-methods
5.     Reardon, S. (2012). NewScientist Health. Gene therapy curbs nicotine addiction in mice. [Viewed: 1.09.12]. Available: http://www.newscientist.com/article/dn21980-gene-therapy-curbs-nicotine-addiction-in-mice.html
6.     Autismspot. (2010). Autismspot. Lab mice. [Viewed: 6.09.12]. Available: http://www.autismspot.com/tags/Spot-Content-Tags/Lab-Mice