Transparent Frogs Reduce Dissections

Dissections of animal have become a controversial issue as they are inhumane and cruel to the animals. Recently, the lead researcher Masayuki Sumida, professor at the Institute for Amphibian Biology at Hiroshima University announced that his team has created transparent frogs which their organs, blood vessels and eggs can be observed without performing dissections. Apart from observing the functions of organs, research of cancer can be carried out as the development of cancer can also be observed from the transparent frogs. Besides, we can also observe the effect of toxins on the frogs’ bones, livers and other organs and it is a cost-effective method. To produce the transparent frogs, Sumida’s team crossed the frogs with two kinds of recessive genes which can cause the frog to be pale through artificial insemination. As a result, the skins of the frogs are transparent from the tadpole stage. The transparent frogs can reproduce offspring with same traits. However, their grandchildren will die shortly as they have two sets of recessive genes and the genes will be soon kicked in by natural selection. Lastly, Sumida suggested that genetic engineering could also produce transparent and even illuminating frogs in the future by injecting an illuminating protein into the transparent frogs.

Link to original article:
http://www.abc.net.au/news/stories/2007/09/27/2045617.htm

Swee Kee Tan
41936175

"DNA Sudoku"

DNA and Sudoku. What could possibly be the link between the very basis of all known living organisms and a 2,000-year-old Chinese math theorem used in the popular game today? CSHL Professor Gregory Hannon, PhD. and his team have cleverly devised a new approach to genome sequencing, called "DNA Sudoku”. This strategy allows thousands of combined DNA samples to be sequenced all at once, rather than restricting to only sequencing single DNA samples at once in past methods.

“DNA Sudoku” is currently best suited for genotype analyses that require only short segments of an individuals genome to be sequenced to find out if the individual is carrying a certain variant of a gene or a rare mutation. The pooling strategy has similar logic and combinatorial number-placement rules used in the popular game. This strategy replacing the previous individual bar code tagging method “minimizes the number of pools and the amount of sequencing”.

It was developed to overcome the limitations of the previous multiplexing process and increase levels of efficiency, ultimately reducing costs dramatically from $10 million down to approximately $50,000 to $80,000. Further improvement in sequencing technology and integration with this new method will open up future doors for diagnosis in autoimmune diseases, cancer, and for predicting the risk of organ transplantation.


Ariel Kim, 41811281
Link to Original Article: http://www.sciencedaily.com/releases/2009/06/090624153112.htm

Transgenic plants

Recently, scientists have genetically engineered transgenic crop plant to release neurotoxins to kill insects and grubs that are now very resistant to insecticides. They have been looking to using funnel web spider venom where the peptide toxin(atracotoxin) which stops the release of calcium ion in the synapse of the nerves which antagonises the synaptic transmission where the peptide chain form intrachain disulfide bridges which has been shown to inhibit the insects and kill them. The toxin has been cultured in bacteria where the strain has been inserted in the plant's genome so the plant can produce the toxins to kill the pests. This has been useful form cotton as the has been used to stop grubs from eating the cotton bulb of the plant and ruining the plant. The toxin doesn't harm mammals so it does affect human and it's a natural solution so its environmentally friendly. They are now looking into finding a toxin from spiders that is less specific than what has currently been used so it can be used more widely for alternative uses.

Itch No More!

Was it the ant or an allergic reaction? Do you ever wonder why your skin gets itchy? The creams and herbal remedies work, but what triggers this itchy sensation? Researchers have found that specific nerve cells are responsible for the itchiness. Although we have various treatments for eczema, infections, allergies and other chronic itching conditions they are only partially effective. With rapid advances in scientific knowledge a discovery for future treatments for skin conditions or management of chronic itching.

Why nerve cells? Researchers at Washington University and Peking Univeristy performed experiments on mice showing they have nerve cells that convey only an itch sensation. By killing their itch-specific neurons they created itch-free mice. This has contradicted the common idea that itch and pain are closely related. In 2007 they found an itch gene active in the spinal cord called gastrin-releasing peptide receptor (GRPR). In an experiment, using a toxing that binds to GRPR and injecting it into the spinal cords of mice, it destroyed nerve cells that had active GRPR. However, instead of scratching when exposed to things that caused an itching reaction the mice felt pain. This discovery results in suggesting that there is an itch-specific neuronal pathway in the spinal cord. By treating various diseases, such as eczema, could consequences such as pain arise?

http://psorialess.us/blog/?page_id=275


Posted By:
Michelle Phan 42053127

Lengthy Illnesses? Genes to Blame

Have you ever wondered why you seem to be sick all the time? Or even considered why your next door neighbour seems to recover from illnesses within a few days? Well, you might want to blame your genes for that.

Due to the variations in genetics in all human, the period of time in which each one of us having a disease may also vary. Disease experts have discovered that if people carry a high risk gene, they have eight times more chance of obtaining a severe and prolonged disease. 300 immune responses from people who were diagnosed with acute glandular fever and their genetic variations in five cytokines, protein hormone messengers of the immune system were analysed. Around 80 of these people were found to acquire these lengthy diseases more easily and result in spending more time at home trying to recover. In addition, they were unable to perform their normal tasks and duties due to these prolonged illnesses.

Dr Vollmer-Conna, from University of New South Wales, believed that these new findings may assist in identifying people with more vulnerability to illnesses and provide individualised and effective treatments in preventing serious illnesses. In some cases, these findings may even be able to save lives.

The original article can be found here:
http://www.news.com.au/story/0,,24731941-1702,00.html

Posted by Chia-Fen Tu (42022002)

How to Heal a Broken Heart.

Clinical trials are currently underway for stem cell injections to quicken healing of the heart after a heart attack. There are two ways being researched using patches of cardiac cells: the cells staying temporarily in stomach tissue, and using a biodegradable mesh to help the heart rebuild itself.

After a heart attack, the heart muscles is weakened and damaged, so the patch must be able to both cover the damaged area and do the work of the weakened areas. Researchers from Israel wondered if the body could be used to create the patch and so they implanted patches of lab-grown heart cells onto rats’ omentums (a fatty tissue in the stomach that is rich in blood vessels). They left the patches (experimental patches) on the omentums for a week before they transferred them to the rats’ damaged hearts. The patch (initially grown on a mesh scaffold from the heart cells of neonatal rats and other compounds to aid development) was found to have more blood vessels after spending a week on the rats’ omentum compared to the patches that were immediately onto the damaged hearts. The experimental patches were also found to contribute to thicker walls and they integrated into the surrounding heart tissue better than the control patches.

At the University of Arizona, a biodegradable scaffold which gives the heart muscle a 3D frame to grow on (once inside the body) has been developed. This scaffold is important because most injected stem cells don’t survive without a supporting matrix. The new patch is designed to disintegrate after about 3 weeks, leaving only the newly grown tissue. Tests on lab rats have shown that the patch increases the wall thickness and blow flow of the heart and also, when there were enough heart muscle cells, the patch started contractions on its own.

Phase 1 clinical trials are currently being held to test for safety in people.

By Rachel Hur 42183583

(This article can be viewed at the following link: http://www.scientificamerican.com/article.cfm?id=patches-repair-damaged-hearts)

Pains of the head and heart...

Ever been rejected and literally felt your heart hurt? Well, University of California and Los-Angeles researchers lead by Naomi Eisenberger may have found an answer to this-having determined a gene linking one’s physical pain threshold with their sensitivity to social rejection. In their studies they found that a mutation of the mu-opoid receptor gene OPRM1 was more common in people who were more likely to suffer from distress in response to social exclusion as well as physical pain. To back-up their studies, the researchers conducted a study involving the saliva samples of 122 people. Here, the participants were first asked the degree to which they were sensitive to being socially excluded before their saliva was tested for the presence of the variant gene. In their findings, participants with the gene reported higher levels of rejection sensitivity whilst having greater levels of activity in the pain-related brain regions such as the dorsal anterior cingulated cortex and anterior insula. According to Eisenberger, this correlation between one’s physical pain and social pain threshold might have had an evolutionary basis, due to the necessity an individual's social connections. In other words, feeling literally hurt by being given the cold shoulder may have been an adaptative strategy to ensure the existence of our “social attachment system”.

Link to original article:
http://www.medicalnewstoday.com/articles/160995.php

Jessica Sun
s42064150

Design a baby?

Bring your partner, grab a seat, pick up your baby catalogue and start choosing. Will you go for the brown hair or blonde? Would you prefer tall or short? Funny or clever? Girl or boy? With rapid advances in scientific knowledge of human genome and our increasing ability to modify and change genes, this scenario of ‘designing’ your baby could be possible in the near future.

Early this year, an US clinic offers parents the chance to select traits like the eye and hair colour of their baby. This trait-selection is based on a technique called pre-implantation genetic diagnosis (PGD). A technique of genetic screening that has already being used since 1989. For PGD, parents are require to provide a number of fertilised embryos created through In Vitro Fertilisation (IVF). The embryo grows for a few days before a single cell is removed, and tested to find out if abnormal genes are present. Only those free of certain disease are implanted in the mother’s womb. Similarly, in trait-selection, the doctor will select an embryo with the desired physical traits such as blonde hair and blue eyes – to continue the pregnancy, and discard any others.

With no doubt, PGD is a sophisticated way to avoid a growing number of genetic diseases, as well as opens up a whole new set of possibilities in genetic alteration. However, the main issue is the idea of treating the child as product for which parents are seeking quality control. So, the question arises: should we be doing this? Should parents be allowed to create their babies? The potential for misuse of this technology could have dire consequences for the human race.


Jacqueline Hu 42061618
http://www.bionetonline.org/English/content/db_cont1.htm
http://news.bbc.co.uk/2/hi/health/7918296.stm

Why DNA Repair Sometimes Fails and the Implications for Huntington’s Disease and Colon Cancer

All life forms on Earth, from prokaryotes to humans, have developed sophisticated DNA repair mechanisms that allows the cells to repair damage to the DNA molecule due to such events as environmental stress or errors during the replication of the genetic code. As cells undergo such processes as mitosis and meiosis, mismatch repair pathways identify and repair irregularities in DNA to prevent the accumulation of mutations, which could possibly result in disease. Recently, researchers from Mayo Clinic have uncovered a greater depth of knowledge regarding these repair pathways and are the first to explain why the correction of specific mutations sometimes does not occur in cells. The sufferers of neurodegenerative diseases such as Huntington’s disease and Friedrich’s Ataxia and even colon cancer may eventually have effective treatments stemming from this discovery. The researchers found that an important protein neglects to recognise a specific form of DNA that is essential in beginning the repair pathway by the recruitment of necessary additional proteins. It is believed that the diseases aforementioned are a result of the cells’ failure to initiate repair and the subsequent formation of toxic aggregates within cells, which inhibit homeostatic cellular functioning.

Cynthia McMurray, Ph.D. lead investigator of the study stated that ‘Since the mutation initiates coding for the defective, toxic protein, we feel that it is likely that a successful effort to stop the steps leading to mutation will likely stop the progression of the disease.’ It was also found that under certain conditions, a specific mismatch repair protein, Msh2-Msh3, was found to damage the cell instead of assisting in repair of the DNA. This occurred when the protein arrived at an inopportune time and location and bound to a section of DNA which altered the homeostatic biochemical activity and thus promoted DNA expansion, as opposed to repair. This expansion is a key feature of diseases such as Huntington’s disease in which the IT15 gene, located on chromosome 4, undergoes a pathological expansion of an unstable CAG trinucleotide repeat within the coding region of the Huntingtin (htt) gene. The normal range of 6-35 is resultantly expanded to 36-121 and disrupts essential cellular processes such as energy metabolism, gene transcription, intraneuronal trafficking, post-synpatic signalling, clathirn-dependent endocytosis and the workings of the ubiquitin-proteasome system. Mitochondrial function and CNS energy metabolism also seem to be affected when the disease comes to fruition. The combined effects therefore result in the loss of neurons and selective neural dysfunction in the striatum, cerebral cortex and other areas of the brain.

The research is now being used to further understand the mechanisms which causes these problems. Dr.McMurray stated, ‘Towards this goal, we are currently dissecting the molecular mechanism by which the aborted function of this repair enzyme attenuates its normal repair pathway. This is crucial information for understanding how to design new drugs or other interventions to help patients.’ If such advances could be made, the longevity of those suffering these diseases could be vastly improved. Currently Huntington’s Disease is a neurodegenerative disorder which is typically fatal within 15-20 years of diagnosis and the condition cannot be stopped, slowed or reversed.

Nick Ravenswood (42005470)

Link to original article -
http://www.sciencedaily.com/releases/2005/10/051010100302.htm

Unravelling AIDS: new technology assists in understanding the virus

AIDS has become one of the world’s major health crisis within the 21st century with statistics revealing that over the past 25 years, nearly 25 million people have died from AIDS.

Could a new technique in drug discovery give hope to the suffering victims of AIDS? The groundbreaking work, conducted by Kevin Weeks and his colleagues at the University of North Carolina, has given researchers for the very first time an insight in understanding the genome of the AIDS virus and its entire gene map. Furthermore, it may also accelerate the creation of a new class of antiviral drugs to combat not only the incurable HIV, but also the viruses that cause influenza, hepatitis C, and the common cold.

The human immune-deficiency virus or HIV uses RNA instead of DNA as its map when carrying out functions. Given that RNA has just a single strand in comparison to the double strands of DNA, the folding patterns and functions are therefore very complex. "There is so much structure in the HIV RNA genome that it almost certainly plays a previously unappreciated role in the expression of the genetic code”, Weeks state. The research team developed a new imaging method called SHAPE to produce an image not only of the RNA’s nucleotides, but of the shapes and complex folds of the RNA strands. What makes SHAPE stand out from other imaging techniques such as X-ray crystallography is its ability to capture and produce high quality images of the precise position of each atom.

Professor Kevin Weeks states, "The hallmark of HIV is its rapid mutation, our study helps us to better understand how this happens, so we can learn how the virus attacks, replicates, evades and lies in wait”, “By stopping the replication of the virus, it may be possible to even attack the virus before it gets a chance to sit idling in the reservoir”.

This discovery will indeed open up many pathways for researchers to find an entirely new class of drugs that may be developed to fight against the shape-shifting RNA viruses and perhaps one day conquer this pandemic crisis.

http://www.newsdaily.com/stories/tre5745kp-us-aids-genes/

Uyen Nguyen 42040239

High yield in flood zones?

Every year floods destroy hundreds of hectares of rice plants in lowland regions of Southeast Asia. These floods force many farmers to grow a variety of rice plants, that have long stems. These plants however have a very low yield compared to the shorter stem rice plant varieties. Scientists at the Nagoya University have recently managed to isolate the genes which give deepwater rice varieties their long stems. The genes are called snorkel 1 and 2

They have discovered that as water levels rise, the deepwater rice plants release a hormone called ethylene which activates the genes snorkel 1 and 2 which in turn causes rapid stem growth. The higher the water rises, the more ethylene released. Scientists 'trialled this by inserting these two genes into non deepwater rice plants and found that they grew longer stems. It is hoped that this breakthrough will help farmers grow high yielding rice species in flood prone regions.

Original article from: http://www.newsdaily.com/stories/tre57i4t7-us-rice-floods/

Derek Ngoo 43054647

Genes at War

Australia’s contemporary social landscape consists of a whirlpool of new ideas and groups that have always been thought to reflect modern thought and principles. Amongst these rapidly emerging sociological trends are the bikie and gang subcultures, characterized within the mainstream community by violence, criminal behaviour and the use of weapons. For years, individuals involved in these categories have been thought to be the result of aggressive environments and other ambiguous sociological factors. However, recent studies conducted by the Florida State University reveal that certain variation of a specific gene, known as Monoamine Oxidase A, plays a significant role in the instigation of antisocial and violent behaviour in men. Functioning in relation to vital neurotransmitters such as dopamine and serotonin which affect behaviour and emotional disposition, the risk allele is hereditary and found more commonly in men from cultures that glorify warfare and aggression. These variants have been used to predict the probability of individual’s pursuing gang membership, and can further distinguish more sadistic members from those less likely to be exceedingly violent.

The monoamine Oxidase A gene is located on the X-chromosome. Thus, men possess only one copy of this gene while women possess two copies. Because the risk allele is recessive, women who possess the variant gene almost always possess another unmodified gene which compensates for it. However, for males, who possess only one X-chromosome and one Y-chromosome, the variant gene is not able to be offset. Therefore, the monoamine Oxidase A effect has been detected only negligibly in women. This may also be an indication of why men, for the most part, are considered more aggressive and likely to engage in weaponry than their counterparts.

Mrinaal Naiker 42016757
Original Article found at: http://www.physorg.com/news163419590.html (2009)

New research has led to the conclusion that prostate and breast cancer is more deadly for African Americans than for whites. It has been reported that black men in the United States are around 60% more likely to develop prostate cancer than white men, and are more than twice as likely to die from the disease. Researchers have used “gene chips” to look for gene activity in prostate tumours, and found significant differences between the two sets of tumours in terms of the activity of over 160 genes, many of which are highly important in regulating the immune system. Given that these genes are involved in producing interferons, a defence against viruses in the body, the higher incidence of prostate cancer in African Americans could be due to a higher rate of infection (probably with an unknown, cancer causing virus).

African American women, on the other hand, are less likely to develop breast cancer that white women, but in blacks, the disease strikes younger people and is more likely to kill. It is suspected that differences in tumours may again be involved. Research found 65 genes with significantly different levels of activity between the tumours from blacks and whites. Unlike the prostate study, this research found no obvious link to the immune system. Most of these genes had not previously been linked to cancer suppression or tumour development.

What causes these differences between the races is not yet clear. Researchers believe that mutations in genes may be involved. An alternate suggestion is that the differences may be linked to chemical alterations, or epigenetic changes, to the DNA that regulates the genes’ activity. The long term goal is to identify new targets for drugs, which will hopefully be valuable for treating African Americans.

Brodie Grant-Taylor
42063425

Article available at:
http://www.newscientist.com/article/dn13681-gene-activity-may-explain-cancers-racial-divide.html

‘Genome smuggling is a step toward synthetic life’

Dr Craig Venter and his team from the J. Craig Venter Institute have devised a new technique in which to create synthetic microorganisms by “smuggling an ‘alien’ genome into unwitting bacterial cells” (McGuninness 2009) The genome of Mycoplasma mycoides was assembled from quarter molecules by the transformation associated recombination cloning in yeast where it “...is the largest chemically synthesized molecule of defined structure of which we are aware” (Gibson et, al. 2008) This genome will is then being transplanted into a host cell

However, on transplantation the modified genome was destroyed by the recipient cell. Consequently, Craig Venters’ team devised a method that deactivates the enzymes capabilities of recognising and destroying the foreign DNA. The advantage of synthetic DNA is that it allows even more radical changes than an engineered genome, in which “Venter's quest for synthetic life ultimately aims to create purpose-built organisms that can carry out specific roles, such as producing bio-fuels or even making hydrogen”( McGuinness 2009): where avoiding foreign recognition and destruction will be central to the process.
Reference List
Gibson, GG, Benders, GA, Andrews-Pfannkoch, Denisova EA, Baden-Tillson, H, Jayshre Zaveri & Venter, CJ 2008, ‘Complete Chemical Synthesis, Assembly, and Cloning of a Mycoplasma genitalium Genome’, Science, vol. 319, no. 5867, pp. 1215-1220, viewed 21 August 2009, http://www.sciencemag.org.ezproxy.library.uq.edu.au/

McGuinness, L 2009, ‘Genome Smuggling is step towards synthetic lfe’, New Scientist, 20 August, viewed 21 August 2009, http://www.newscientist.com/article/dn17656-genome-smuggling-is-step-towards-synthetic-life.html

J. Craig Venter Instistute 2009, ’Chemical synthesis of the mycoplasma gentalium genome’ J. Craig Venter Institute, viewed 21 August 2009, http://www.jcvi.org/cms/research/projects/chemical-synthesis-of-the-mycoplasma-genitalium-genome/overview/

The Asian Red-Face Syndrome

Have you ever wondered why your closest oriental friends often get a notable red face whist drinking alcohol? Being of Asian descent myself, I too suffer from this condition which is commonly coined “Asian red face”, or on a more clinical tone, Alcohol Flush Reaction.

The reason why this occurs particularly to Asians is due to a genetic mutation of which approximately 50% of all Asians have. Normally, consumed alcohol is broken down (metabolised) into acetalaldehyde. Acetalaldehyde is then metabolised into harmless acetic acid by the enzyme dehyde dehydrogenase-2 (ALDH2). Many Asians lack the dehyde dehydrogenase-2 (ALDH2) enzyme which prevents acetalaldehyde from metabolising and increases its concentration in the blood.

Dr Geoff Chambers of Victoria University states that the build-up of acetalaldehyde causes unpleasant symptoms such as increased blood flow to the face and neck, headaches, nausea and extreme drowsiness. Acetalaldehyde is also responsible for the infamous “hang-over” after a big night out.

However, “Asian red face” is not all bad. Dr. Ting-Kai Li, a professor of medicine and biochemistry at the Indiana University School of Medicine believes that the mutant gene responsible for Asian flush may protect against heavy drinking and alcoholism.

Similarly, researchers interested in genealogy have successfully used this particular genetic marker to identify the oriental origins of the Polynesian people, who also lack the alcohol metabolising enzyme.

POSTED BY: ALEXANDER LOOK (42034434)
Tutor: PW

References:
* http://www.hsc.wvu.edu/som/cmed/alcohol/metabolism.htm
* http://www.blogsoop.com/blog/is-asian-flush-evolutionarily-adaptive/
* http://twelvestepfacilitation.com/asian-alcoholism-genetics/
* http://www.scoop.co.nz/stories/SC0206/S00038.htm

Cancer and the Genetic Links

Experimental evidence suggests a relationship between the proliferation of cancer and programmed cell death or apoptosis. Apoptosis is a homeostatic function of multi-cellular organisms that culminates in the death of redundant cells or cells whose existence could be detrimental to the organism. These cells are deemed harmful, as in many instances, the DNA molecule has mutated during the cell’s life and therefore could result in the replication of an incorrect DNA sequence or structure.
Apoptosis can be primarily induced by 2 methods: the intrinsic and extrinsic methods. The Intrinsic activation of the apoptotic transduction pathway involves the release of several proteins from the mitochondria within the cell, when receptors within the cytoplasm are activated by a broad spectrum of ‘death’ stimuli such as irreparable DNA damage, such as ionizing radiation. The proteins that are released by the mitochondria are termed nucleases and proteases. These molecules essentially 'cut up' the proteins and DNA of the cell. The extrinsic activation of the apoptotic transduction pathway involves the activation of a cell surface trans-membrane that belongs to a family of receptors known as the tumour necrosis factor (TNF) or commonly known as the ‘death receptors’. The ensuing signal transduction pathway causes the activation of the mitochondria and the subsequent release of proteins from the mitochondria that cause the death of the cell. From these apoptosis activation sequences, should a cell’s DNA become damaged or mutated it could cause a disruption in the signal transduction pathway for the apoptosis to be effective in killing the cell. This means that the damaged DNA of the cell would possibly be able to replicate, thus increasing the numbers of damaged cells. This form of uncontrolled replication as a result from damaged DNA is broadly known as cancer.

Cancer is a disease that is thought to originate from a discrepancy in the apoptosis function of a cell; meaning that the DNA of a cell has mutated in such a way that does not inhibit cellular replication as normally occurs in other cells. This results in the proliferation of mutated cells that can ultimately kill the organism. For example, it has been determined that the C.elegans Ced-4 protein in human melanoma cells is defective, which disrupts the transduction sequence of the apoptotic pathway that would normally culminate in the cell’s death. This defective protein allows the melanoma cells’ to proliferate. C.elegans Ced-4 protein is termed as a ‘death’ protein that when activated causes a transduction cascade, which results in the production of proteases and nucleases that are responsible for the destruction of proteins and DNA of a cell, culminating in cell death.
Currently, research is being conducted into rectifying the apoptosis in cancerous cells such that the cancerous cells can be eradicated without any detrimental effects for other required cells. One such research venture is into TRAIL. TRAIL (Apo2 ligand) is a death protein that essentially induces the suicide signal transduction cascade leading to cell death by an increase in the effectiveness of the pertinent executioner enzymes. TRAIL is currently in early clinical trials and is a promising anti-cancer therapy, especially as it has the potential to be lethal to chemotherapy-resistant tumours.
For more reading check out this article:
Mei Lan Tan, Jer Ping Ooi, Nawfal Ismail, Ahmed Ismail Hassan Moad,
and Tengku Sifzizul Tengku Muhammad, ‘Programmed Cell Death Pathways and Current Antitumor Targets’, 2009, Pharmaceutical Research, Vol 26, No.7, Pages 1547-1560, DOI: 10.1007/s11095-009-9895-1

Aaron Heffernan
4188507

Transparent Frogs Reduce Dissections

The dissection of animals has become a controversial issue as it is inhumane and cruel to the animals. Recently, the lead researcher Masayuki Sumida, professor at the Institute for Amphibian Biology at Hiroshima University announced that his team has created transparent frogs which their organs, blood vessels and eggs can be observed without performing dissections. Apart from observing the functions of organs, research of cancer can be carried out because the development of cancer can also be monitored in the transparent frogs. Besides, we can also investigate the effect of toxins on the frogs’ bones, livers and other organs on top of it being a cost-effective method. To produce the transparent frogs, Sumida’s team crossed the frogs with two kinds of recessive genes which can cause the frog to be pale through artificial insemination. As a result, the skins of the frogs are transparent from the tadpole stage. The transparent frogs can reproduce offspring with the same traits. However, their grandchildren will die shortly as they have two sets of recessive genes and the genes will soon be kicked out by natural selection. Lastly, Sumida suggested that genetic engineering could also produce transparent and even illuminating frogs in the future by injecting an illuminating protein into the transparent frogs.

Swee Kee Tan
s4193617

original text:
http://www.abc.net.au/news/stories/2007/09/27/2045617.htm