Thursday, 31 May 2012

Controlling Dengue Fever with Genetically Modified Mosquitoes

Controlling Dengue Fever with Genetically Modified Mosquitoes

Every year more than 50 million people are infected with Dengue fever, a viral disease that causes fever and acute joint pain. Of these millions who become infected, 25 000 die from the disease annually. Mosquitoes in tropical and subtropical parts of Africa, Asia, South America, the Caribbean and Australia spread dengue fever, which means that 40% of the world’s population, a staggering 2.5 billion people, are at risk(Oxitec Limited, n.d.).

There is no known cure for Dengue fever, nor any vaccine, therefore the effective control of this disease is done through control of the mosquitoes that carry it. Common methods for dealing with mosquito populations include the removal of egg-laying habitats and using insecticides, however, recent research by the Cayman Islands Government in conjunction with British bioengineering company Oxitec has unearthed a new potential mosquito population management strategy. This development involves cultivating a strain of the Aedes aegypti mosquito with an altered genome (Bredow, 2012). Modified mosquitoes are bred and released into wild populations where they interbreed. The progeny inherit the altered genes and these genes inhibit the development of the larvae to the point where they die.

In a normal mosquito cell, a repressor chemical acts to prevent most of a specific gene that produces a protein named tTA from binding to a corresponding binding domain called tetO. Conversely, the genetic modification in the mosquitoes removes the repressor and allows the tTA to bind to the tetO binding domain. This binding causes more tTA proteins to be produced and to bind with tetO to create a cycle of continuous production of the tTA protein. This protein is harmful and damaging to the cells of the mosquitoes and henceforth causes the larvae to die(Oxitec Limited). The following image shows the differences in the tTA gene cycle for repressed and unrepressed binding:

Figure 1: tTA protein production cycle (Oxitec Ltd, n.d.)

When none of the larvae survive to adulthood, they cannot replace the previous generation and the entire population is reduced as a result. A trial was done in the Cayman Islands, where 3.3 million genetically modified (GM) mosquitoes were released over a period of six months in batches of 50,000 animals. By the end of the trial period the number of mosquito eggs being laid was down to 10% of its original volume (Coghlan, 2010). This trial was regarded as a success, and the techniques for controlling mosquitoes in this way are being further explored before widespread use of the technology.

Whilst both males and females with modified genes are needed for the breeding of the genetically modified (GM) insects, only male mosquitoes are released. This is done to prevent any genetically altered mosquito biting a human so that there is no possibility that any of the mosquito’s modified genes could be transferred into humans. Also, because this genetic modification of the mosquitoes causes the offspring to die when still in the larval stage, they do not reach maturity before the genetically altered cells fail thereby preventing them from further reproducing. These considerations are significant for scientists who are using GM organisms because of the ongoing ethical and safety concerns with this technology.


1.         Bredow, R. v. (2012, January 2). Genetically Modified Pests - The Controversial Release of Suicide Mosquitoes. Retrieved March 17, 2012, from Spiegel Online International:,1518,812283,00.html

2.     Coghlan, A. (2010, November 10). Genetically altered mosquitoes thwart dengue spreaders. Retrieved March 16, 2012, from New Scientist:

3.         Department of Health - Communicable Disease Prevention and Control Unit. (2012). Dengue Fever Fact Sheet. Retrieved March 17, 2012, from Better Health Channel:$File/Dengue_fever.pdf

4.          Oxitec Limited. (n.d.). Dengue Fever Information Centre. Retrieved March 17, 2012, from Oxitec:

5.   Oxitec Limited. (n.d.). Molecular biology. Retrieved March 17, 2012, from Oxitec:

6.      World Health Organisation. (2012, January). Dengue and Severe Dengue. Retrieved March 17, 2012, from World Health Organisation:

The Interesting Relationship Between Bees and Humans

Recently, studies have linked two unlikely organisms by comparing their instinctive behaviours and activities. It has been discovered that the neurotransmitters that give humans the thrill-seeking feeling to go and discover new places are also the chemicals that bees release to risk it all to find new food sites. The closest relative to these species are the ocean dwelling flatworms and interestingly enough, they show no signs of “scouting” activities. This means that bees and humans were able to develop similar genes.

As commonly believed, bees within a colony are all categorised under certain “occupations” following orders from the queen bee. New studies have shown that individual bees, such as scout bees go off on their own initiative to leave and forage for more food supplies (and possibly new dwellings). These female bees may search within tree trunks, holes and cavities and may take hours scanning and deciding whether it would be a suitable new location. Once a food site is spotted, the scout will return to her colony and perform a special bee dance, informing other bees of the new discovered location. After her performance, she will leave and hunt down another food site.

Entomologist Gene Robinson and graduate Zhengzheng Liang led the research with the funding provided by institutions such as the National Science Foundation. Studies involved placing bees within a man-made habitat and leaving them for a few days to adapt. When observations began, it was clear to them which bees were the scouts. As Liang added more food sites, only the scout bees would take the initiative, risking themselves to source out the new areas. After looking inside the scout bees, it showed that they presented different gene activities that are also found in thrill-seeking humans. The main focuses were the neurotransmitters – dopamine and glutamate and the increase of messenger molecules (mRNA) in scout bees.

Dopamine and glutamate are substances that send signals between neurons that are found in our brains.  Dopamine drives us to go out and explore but also makes us addicts to substances like drugs. It is in charge of a variety of functions like observing our food consumption and our emotions, signalling positive feedback. Glutamate is a neurotransmitter that is actually the most abundant amino acid found in the brain. Its roles are involved in metabolism including energy production and protein synthesis. Glutamate is also in MSG which is added to food for better flavour and presentation.

Liang also added glutamate and octopamine to the non-scouting bees and observations showed that these bees were beginning to seek out the new food sites, acting as scouts. Inhibiting dopamine in bees also stopped their seeking behaviour.

Robinson’s explanation for these similar genetics in humans and bees was narrowed down to their “evolution of behaviour” explaining how the same molecules have been involved consistently in evolution. The two separate pathways have also allowed organisms to also present contrasting behaviours.

So even though their common ancestor was the marine flatworm which showed no sign of scouting behaviour, bees and humans who follow different pathways have evolved having similar genes due to similar molecules necessary for the thrill-seeking behaviour.

Junk DNA

In 1953 Watson and Crick were the first to discover the 3 dimensional helix shape that we now know is DNA. They determined the role of DNA is to transfer heritable features from one generation to the next.  (Campbell, et al. 2009) However within DNA there is a section they called Junk DNA.  This is an area of non-coding nucleic acids called introns. (Campbell, et al. 2009)
Initially Watson and Crick thought the Junk DNA had no real use and dismissed it as non-coding proteins.  However scientists now believe that the non-coding DNA that makes up 95-98% of the human genome has a much more important role than originally thought.

In recent years more and more research is being performed investigating the real role of the junk DNA and these findings are conflicting with original assumptions.  In 2010 scientist set out to explore the relationship between a non-coding stretch of chromosome (9p21) and heart disease. They said that individuals with a nucleotide mutation along this stretch of DNA are at greater risk of suffering from the disease.  The non-coding stretch of DNA was deleted in a group of mice. The results showed the mice that had the DNA deleted actually died earlier or developed tumours when compared with mice that had the stretch of DNA intact.  They concluded that the genes that may have been deleted on the stretch of DNA may control or ultimately inhibit cell proliferation in heart and other tissues. Meaning that without these genes, cells in arteries divide faster which build up causing restriction of blood flow to the heart which causes heart disease. (Visel et al, 2010)

Another idea of the possible functions Junk DNA performs comes from research done on the genomes of fruit flies. The genome of the fruit fly is approximately 80% junk DNA and it seems that the rate in which the flies DNA mutates is far less than what was expected. This means that because of no mutations the evolution of the fly has effectively come to a halt. Furthermore, they go on to say humans and mice have similar genomes, each consisting of around 30,000 genes.  However the species are hugely different. They think that it’s not the genes that separate the species but in fact the junk DNA. Humans have one of the largest proportions of junk DNA out of all species. This may explain the complexity of our species. (Andolfatto, P.  2005)

From recent research it seems to be emerging the idea that junk DNA plays a more important role in human existence than first thought. Whether or not experiments on animals can be applied to humans is yet to be seen. The nature of this type of work has many ethical issues and may take years until experiments on humans are possible. Could it be that one day junk DNA will be considered no longer trash and instead treasure? Only time will tell.

Andolfatto, Peter (2005) Adaptive evolution of non-coding DNA in Drosophila. Nature. Issue 437, Page 1149-1152
Axel Visel, Yiwen Zhu, Dalit May, Veena Afzal, Elaine Gong, Catia Attanasio, Matthew J. Blow, Jonathan C. Cohen, Edward M. Rubin & Len A. Pennacchio (2010) Targeted deletion of the 9p21 non-coding coronary artery disease risk interval in mice. Nature. Issue 464, Page 409-412
Campbell, N. A., J. B. Reece and N. Meyers (2009). Biology. French Forest, NSW, Pearsons Education Australia.
Carol Guze,(2005) The Human Genome Project. Image available online at
National Human Genome Institute. Image accessed on March 19th 2012. Available online at.

Wednesday, 30 May 2012

Genetics and Bacterial Resistance

By Megan Saunders

Bacteria have many mechanisms for adapting to their environment and they certainly use them when responding to adverse conditions. In particular, bacteria such as Eschericha coli go through many genetic mutations when building resistance to various antibiotics (Toprak et al. 2012). A team of scientists at Harvard have developed a method for recording and understanding these mutations in an experiment which could have future implications on the way we approach bacterial infections (stealth tactics of bacteria revealed, 2012).

aims to not only record, but understand precisely how bacteria forms a resistance to antibiotics. In order to control the present antibiotic, the concentration of that drug and to record how the bacterium responds, they created the ‘morbidostat’ (stealth tactics of bacteria revealed, 2012). Results have been obtained from E. coli as it was monitored about how it responded to controlled doses of various antibiotics.

The results showed that the bacteria developed resistance to all three of the introduced antibiotics (stealth tactics of bacteria revealed, 2012). Some antibiotics can be faulted by a single gene change, although in this case, like many others, a number of genetic mutations had to occur to obtain the desired phenotype (Toprak et al. 2012). The group of genetic mutations that occurred in this case targeted the bacteria’s susceptibility to each of the antibiotics. The way in which the bacteria responded to the three test drugs separately was a testament to the variability bacteria is capable of. Achaean organisms are widely recognized for their adaptive abilities, which stem from their methods of reproduction. High generational rates are achieved by the ability of the organisms to use binary fission.  Also, plasmids play a role in increasing the genetic material available to the bacteria (Campbell et al. 2009). These mechanisms give reason for the successful rapid mutation of genes measured within the experiment.

The mutations occurring within the bacteria differed between the types of antibiotic it was exposed to (Toprak et al. 2012). The differences between these changes can be applied to the way the bacteria’s resistance developed. But perhaps the most useful data that resulted from this experiment was the congruency between separated test populations.  The genomes of bacteria responding to the same drug, which were measured throughout the test, concluded that “parallel populations evolved similar mutations and acquired them in a similar order.” (Toprak et al. 2012, p101). The patterns that were observed suggests that there are specific pathways of mutation, along which bacteria moved to achieve a goal; antibiotic resistance (Toprak et al. 2012). Now that these genetic pathways have been measured, a more complex set of knowledge can be applied to improving antibiotics and increasing their effectiveness in the future.

A greater understanding of bacteria and it’s mechanisms for coping with its environment is being achieved through many studies being conducted, genetic resistance is a particularly relevant topic and developing improved ways of treating bacterial infections in humans is highly beneficial. The measurement of the response of bacteria to antibiotics has resulted in evidence of mutational pathways for bacteria gaining resistance (Toprak et al. 2012). These results are of great significance to the notions of improving the antibiotic method and overcoming bacterial resistance.

 ‘Stealth tactics of bacteria revealed’, 2012, New Scientist, issue 2844 <>
E. Toprak, A. Verdes, J.B. Michel, R. Chait, D.L. Hartl, R. Kishony, Evolutionary paths to antibiotic resistance under dynamically sustained drug selection, research publication, Nature America, volume 4 <>
Campbell, Reece, Meyers, 2009, Biology, 8th edn, Pearsons

Monday, 28 May 2012

Gorilla genomes are keys to uncover human’s evolution history

Chimpanzees, gorillas and orangutans are always said to be human’s closest relatives. There is a very high possibility that human are the later generation of them. From the existing literature, it is known that chimpanzees share 99% of human’s DNA while gorillas and orangutans share 98% and 97% of human’s DNA respectively (Ghosh, 2012). Moreover, by comparing their genomes, results indicate that the human family divided from orangutans 14 million years ago, gorillas 10 million years ago, and chimps 6 millions years ago. Ghosh (2012) also points out that the most surprising thing is the dates are earlier than many scientists had expected while not the order of events. Recently, a group of scientists did a test which compared the genome of the western lowland gorilla and about 11000 of its key genes with humans, Homo sapiens and chimpanzees. The finding is that both before gorillas separated from the other apes and before gorillas themselves divided into two main groups, a comfortable amount of gene flow or inter-bleeding existed between slightly different genetic strains (ABC Science, 2012).

Gorilla and child
The study shows that humans are more similar to gorillas than previously thought

According to the most recent research in Cambridge, professors have figured out the genetic code of the gorilla. Now they can compare human DNA with that of all other apes or gorillas or chimpanzees. At the same time, scientists point out that researchers can now start to observe the relationships between apes. This is a great step in terms of uncovering genetic mutations. It is also hope that researchers will have greater knowledge about what happened in human’s evolution history and of how those genes affect the  brain and other properties that make us modern humans (Ghosh,2012). Another experiment was carried out by extracting genetic code from a female western lowland gorilla called Kamilah. By analysing that data, Jha (A, 2012) stated that something that is similar in genes involved in sensory understanding, hearing and brain development. Genes combined with proteins (which function is to strengthen the skin) were also especially vigorous in gorillas. It goes some way to explaining the it’s shape and size on gorillas' hands. The human being’s hearing genes’ speedy development was connected to the evolution of language. Kelland (K, 2012) indicates that hearing genes have grown in gorillas at a nearly same speed to those in humans.

gorilla baby
The first full genome analysis has revealed that 15% of gorillas' genetic makeup is closer between humans and gorillas than it is between humans and chimpanzees. Photograph: Luanne Cadd

However, it is very attention-worthy that gorilla is an endangered spice. Their numbers are decreasing significantly in this few decades due to human activities like hunting and city development and habitat loss. Researchers (ABC Science, 2012) states that “the study of the great apes or gorillas link to a time when the existence of human was more slender, as well as teaching about human evolution. These definitely highlighted the importance of protecting and conserving these remarkable species," 

Artificial cell life, an overview of the basics.

The purpose of the Artificial cell project, is mainly self explanatory, the goal being, to create molecular sized partitioned chambers, able to self replicate and capable of not only containing, but propagating Genetic material. The first step of this project was to separate a phospholipid vesicle and integrate it with genetic material. After the initial success, the project begun working on attempting vitro gene expression within their own synthetic vesicles. Yet another success, as while the majority were unable to support life, it was found that certain genetic sequences were able to survive within the vesicles, provided the vesicles environment contained all the necessary nutritional sources. Using the information gathered from these experiments, a design was drawn up, of a synthetic, artificial cell, this cell, would be created from nothing, working from the base elements up. For simplicities sake it was decided that the cell would have a similar structure to that of bacteria. The source of energy for the cells was decided to be ATP and GTP, while the genetic material was to be extracted from existing organisms using external machineries. The size of the cell could be easily determined by the cell wall material, a phospholipid bilayer, used because of it's reaction to aqueous solutions. When submerged into a aqueous solution the phospholipids spontaneously rearrange themselves into molecular vesicles. This reaction takes place because of the hydrophobic nature of the fatty linear chains. Without lipid bilayers, there would be no living systems, as they are necessary for the absorption, and excretion of not only genetic information, but all forms of molecular debris within cells. In this way, water is truly a prerequisite for all life, not only for the creation of vesicles, but also the cell exchanges as well as some parts of protein formation. The use of external transcription and translation tools, allows for large boost in the productivity of a huge amount of genetic material, regardless of their transcription requirements. Because of this, the aim of specific DNA replication, is becoming one of the major problems facing the project. Selecting the self replicating material specifically remains a serious difficulty in the project. Going hand in hand with specific propagation, is the process of self organising genetic material. Once the material is created, the programming of the material to assume certain specific orders and structures remains a severe hurdle. As does the creation of a phospholipid membrane able to support the genetic material and actively support an equilibrium with it's environment. The problems with creating a self replicating artificial cell are as numerous as they are serious, but the project continues forward regardless. With the hope that we may one day be able to complete experiments on the evolutionary processes, to further our understanding of the universe and our own nature.

PGD- Preimplantation Genetic Diagnosis

By: Theresa B├╝gler- Student #42908982
P9- Mark Mayhew

Ironically the social driving force behind the need for infertility technologies was the availability of abortions in the late 1960’s. This coupled with the establishment of single parent benefit which occurred in Australia around the same time significantly reduced the availability of babies for adoption and consequently process’s which allowed infertile couples to conceive were in demand.[1]

Enter IVF ! –

First test tube baby Louise Brown was grown in a JAR

Read more: CLICK HERE

On July 25, 1978, Louise Brown, the worlds first ‘test tube’ baby was born in Manchester. Australia followed closely in 1980 with the 4th IVF ( In Vito- fertilization) baby born in Melbourne [2]

As processes became more advanced, procedures such as PGD (Preimplantation Genetic Diagnosis)[3]were established and the age of designer babies was ‘born.’

GENDER CHOICE – A human Right ????

“Woman aborts healthy twin boys
in pursuit of a girl!!”
(Australia 2011)

Read more: CLICK HERE

When determining the social acceptability of gender selection on the grounds of balancing families or individual choice the jury seems to be out with both camps putting forward strong cases. Groups apposed to gender selection state that selecting the sex of a child is detrimental to the parent-child relationship which should be unconditional acceptance. Gender selection may create sexual prejudice especially in cultures where girls are less valued; this will ultimately affect the social structure contributing to a shortage of women for men to partner.  While Sydney IVF’s data contradicted the preference of male babies[4], this has been proved to be the case in China where males are more valued and therefore, female fetuses were aborted as couples were only allowed one child and wished to try again for a boy, currently there 156 boys to every 100 girls[5] in China. This potentially could imbalance the laws of nature.

Watch the harvest of the Blastomere

Two cells being harvested from the blastomere

Why Use PDG?

Preimplantation Genetic Diagnosis is available for three major categories of diseases: sex linked diseases, molecular disorders, and chromosomal disorders.
Sex Linked:  PDG can be used to identify the sex of the embryo for sex linked disorders An example of this group is Duchenne muscular dystrophy. Molecular disorders: single gene defects such as cystic fibrosis can be identified.

Chromosomal disorders including translocations, inversions, and chromosome deletions can be detected using Fluorescence In Situ Hybridisation (FISH).  Parents who carry a chromosomal rearrangement / alterations may never successful achieve a viable , often resulting in repeated spontaneous miscarriages as a result of unbalanced chromosomes in the embryo.

For the list of possible diseases identified in PGDClick Here


Now let’s make them perfect -->

Designer babies


Through a process known as FISH or Fluorescent in-situ Hybridization the nucleus of the cell is exposed, the cells are then dried on a microscope slides and hybridised or bonded with DNA probes. Each of these coloured probes or markers are specific for part of a chromosome, and are labeled with a fluorochrome which makes the chromosomes florescent and the chromosomes including the X and Y chromosomes are able to be identified. [6]

Image showing FISH (Fluorescent in-situ Hybridization)



[1] BBC News ( July 25,1978). FIRST TEST TUBE BABY BORN  (online) Available: (Accessed
[2] The World Today. 22.06.2010. Australia's first IVF baby turns 30. (online) Available: (Accessed 10.03.12)
[3] Monash IVF,(2011). History of IVF (Online) Available: (accessed 10.03.12)
[4] Monash IVF. 2012. PGD and Gender. (Online) Available: ( Accessed 10.03.12)
[5] Dixon,P. Global 2011. Gender Selection: is it right? (online) Available:      :// ( Accessed 10.03.12)
 [6] Weyers, Kate. Journal article 2010.  Prenatal Torts and Pre-Implantation Genetic Diagnosis
; Harvard Journal of Law & Technology, Vol. 24, 2010 (online) Available: ( Accessed 10.03.12)

Sunday, 27 May 2012

Programming Speech into the Human Genome

By Henry North (42935559)

The genes associated with speech – an ability exclusive to our species – are one of the great mysteries of the human genome. However, ten years ago a race to find a ‘language gene’ was sparked by an article published in Nature, looking at genes associated with chronic language-based disorders (Lai 2001). More significant findings have been made in recent years through research aimed at identifying this genetic factor (FOXP2), allowing geneticists to start looking into how evolution has programmed speech into our genome. The gene’s initial discovery paved the way for this new research.

In 1991, a genetic mutation that induced several severe speech disorders was identified in three generations of a London family referred to as KE.  This case was unusual; the disorders were the result of a mutation of just one gene (Macandrew 2003). The specific effects of the mutation were complex, affecting both facial muscle control and speech-associated neuronal processes (Cheuy 2003; Markus & Fisher 2003). Years later, brain scans of language-related cortical regions confirmed this (Copp et al. 2005). The effect on so many bodily functions associated with speech by the mutation of a single gene suggested that this gene was fundamental to our ability to communicate.

Using DNA samples taken from individuals with this specific disability (including the KE family), geneticists looked for re-occurring ‘markers’ –stretches of DNA that were common to all the affected individuals (Markus & Fisher 2003). On chromosome seven, locus 7q31, the FOXP2 gene was identified as the damaged gene (Cheuy 2007). The FOXP2 gene produces proteins that contain forkhead-box domains (or FOX proteins) through transcription and translation (Markus & Fisher 2003). FOX proteins are part of a group of transcription factors; regulatory proteins that bind to DNA and affect the transcription of specific genes (Reece et al. 2012).  Thus, the FOXP2 gene codes for a transcription factor that, in turn, affects the expression of many other genes involved with human speech. 

Fig. 1 (a) & (b) Geneticists looked at the KE family, using a QTL technique to identify 'markers', thus pinpointing the loci at which the mutation was occurring (Source: Marcus & Fisher, 2006). 

Fig. 2 An illustration of a generic transcription factor and its significance to the genome (source: Myers, 2006). 

Once the gene was identified, its evolutionary origins could be determined. FOXP2 is found in all animals and fungi - just two amino acids distinguish the human protein from the rodent version (Wade 2009). This is not to suggest that this difference is insignificant; two separate studies replaced gorilla and rodent FOXP2 genes with the human version, observing remarkable cellular and behavioural changes in test subjects (Markus & Fisher 2003; Genevive 2009).Genomic comparisons imply recent, rapid evolution of the human gene – likely because of the numerous advantages that speech provided early humans with (Enard et al. 2003). Interestingly, a mathematical analysis of the human and rodent versions of the FOXP2 gene suggests that the gene became fixed in the human genome around 200, 000 years ago – coinciding with estimates made by archaeologists regarding the first human languages (Markus & Fisher 2003).

Discovering the significance of the FOXP2 gene in a study of the KE family allowed further investigation into the genetics of human speech, though researchers insist that there is still much to learn (Trivedi 2004). It is important not to overestimate the role of FOXP2 as some journalists have done, deeming it ‘the language gene’; many undiscovered genes may play a role in providing the requirements for language (Enard 2001). Nonetheless, FOXP2 is clearly one of the most significant genes involved with speech, a behaviour that in many ways defines our species. 


Cheuy, D 2003, FOXP2, Department of Biology, Davidson College, viewed 18 March 2012 <>

Copp et al. 2005, ‘FOXP2 and the neuroanatomy of speech and language’, Nature Reviews neuroscience, vol. 6, no. 131-138, viewed 19 March 2012 <>

Enard, W et al. ‘Molecular evolution of FOXP2, a gene involved in speech and language’, Nature, vol. 418, no. 869-872, viewed 18 March <>

Genevieve, K et al. 2009, ‘Human-specific transcriptional regulation of CNS development genes by FOXP2’, Nature, vol. 462, no. 213-217, viewed 18 march 2012 <>

Lai, et al. 2001 A novel forkhead-domain gene is mutated in a severe speech and language disorder’, Nature, vol. 413, no. 519-523, viewed 18 March 2012 <>

Macandrew, A 2003, FOXP2 and the Evolution of Language, viewed 18 March 2012 <>

Markus, GF & Fisher, SE 2003, FOXP2 in focus: what can genes tell us about speech and language? Cell press, Massachusetts Institute of Technology, viewed 18 March 2012 <>

Reece, JB et al. 2012, Campbell Biology, Pearson Australia, Sydney.

Trivedi, VP 2004, Scientists Identify a Language Gene, National Geographic, viewed 18 March 2012 <>

Wade, N 2009, Speech Gene Shows Its Bossy Nature, New York Times, viewed 18 March 2012 <>


Myers, P, 2006, Transcription factors and morphogens, Pharyngula, viewed 20 March 2012. <>

Markus, GF & Fisher, SE 2003, FOXP2 in focus: what can genes tell us about speech and language? Cell press, Massachusetts Institute of Technology, viewed 18 March 2012 <>