Japanese researchers report on a protein that protects bones by promoting bone formation and limiting bone breakdown in mice. The authors conclude that if this protein plays a similar role in humans then it may pave the way for the development of therapeutic agents for bone and joint diseases. The lead author is affiliated with The University of Western Australia.

Thanks to our colleagues at the Science Media Centre of Japan for the comment from one of the study’s authors.

The collaboration between the Australian Science Media and the Science Media Centre of Japan is supported by the Commonwealth through the Australia-Japan Foundation which is part of the Department of Foreign Affairs and Trade. These comments have also been translated into Japanese. Please contact us if you would like a copy of the comments in Japanese.

Feel free to use these quotes in your stories.  Any further comments will be posted here. If you would like to speak to an expert, please don’t hesitate to contact us on (08) 7120 8666 or by email.

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Professor Hiroshi Takayanagi is from the Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Japan, and the Centre for Orthopaedic Research at The University of Western Australia. He is one of the authors of the paper.

“Bones may look solid and stable, but like our skin they are constantly metabolizing. A type of bone cell called osteoclasts break down older bones (this is called bone resorption) while osteoblasts create new ones. These two processes help the body’s bones to maintain their strength and flexibility.

A healthy body maintains this balance and ensures the amount of bone remains the same, but factors like advancing age or menopause can lead to an imbalance. When more bone breakdown occurs than bone formation, a person is more likely to develop bone disorders such as osteoporosis. Osteoporosis treatments available today largely involve taking medication which suppresses bone resorption, but these drugs also suppress bone formation. It has been hoped someone can develop a new drug which can control both bone resorption and formation to help recover the normal amount of bone.

Our research team looked at Semaphorin 3A (Sema3A), a protein produced by osteoblasts which controls the development of neuron paths and inhibits T-cells in the body’s immune system. When we treated mice with Sema3A we found the protein was suppressing bone breakdown and speeding up bone formation at the same time.

Without functioning Sema3A, the mice showed a rise in the level of bone breakdown and a drop in bone creation, resulting in an abnormally small amount of bone in the body. We also tried treating mice in which we had opened a hole in their bones – in order to study the rate of bone formation – and mice with osteoporosis with the Sema3A protein. The results found an increase in bone formation and we were able to stop the amount of bone dropping any further.

I hope our discovery will lead to better treatment developments for osteoporosis, arthritis, or bone fractures. I also think Sema3A could be used as a bio-marker for disease diagnosis because we found that in the older mice where the amount of bone was dropping, the amount of Sema3A protein had also decreased.”

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The following comments are from experts who are independent of the study:

Dr Gethin Thomas is Deputy Director of Education and Senior Research Fellow in the Muscoskeletal Genetics Group at The University of Queensland Diamantina Institute

“Osteoporosis, a disease stemming from a weak skeleton frequently resulting in bone fracture, occurs when the activity of osteoblasts (which make bone) and osteoclasts (which degrade bone) gets out of balance. The burden of osteoporosis to the general community is considerable, with half the women over the age of 50 expected to suffer at least one osteoporotic fracture and over two million Australians currently affected.

Most current approaches for osteoporosis therapy decrease the activity of osteoclasts to decrease bone degradation, but the gold standard is to find therapies that can build bone as well as stop bone degradation, as osteoporosis is frequently only diagnosed after the bones have already become very weak. One way to identify such potential therapies is to identify the biological pathways that control the osteoblasts and osteoclasts. This study has identified Semaphorin 3A as a key molecule in that it can stimulate osteoblast activity and inhibit osteoclast activity. Further, Sema3A acts through a receptor, neuropilin-1 (Nrp1). Thus, this presents two options for developing new therapies for osteoporosis either by treating the patient with Sema3A or activating the Nrp1 receptor.

This is a very exciting discovery identifying a completely new bone regulating pathway and one that is potentially very “druggable”, indeed in this study they have shown that treating mice with Sema3A results in increased bone strength.”

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Professor T.J. Martin is Emeritus Professor of Medicine in the Bone Cell Biology and Disease Unit at St Vincent’s Institute of Medical Research and the University of Melbourne

“This interesting science extends the link between the nervous system and bone. It has been known for some years that Sema3A is produced in bone, but this work shows that it is a product of the osteoblast that both promotes bone formation and limits its breakdown. There is much interest in developing drugs that will do just that for osteoporosis, since existing inhibitors of bone breakdown all inevitably decrease bone formation.

The pathway to a drug will provide many challenges though. Sema3A is known to play important roles in development of the central and peripheral nervous system and heart. It is one of a family of related molecules that overlap in their effects – including particularly Sema4D – that these same authors showed recently to be produced in bone by osteoclasts and to inhibit bone formation.

The treatment studies in the paper are limited, but the control pathway revealed in the genetic experiments is of great interest, posing many further questions. Although it is not easy to see Sema3A itself as a drug, it provides much that will influence thinking as attempts are made to develop  the “holy grail” of an inhibitor of breakdown that promotes bone formation.”

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Dr Paul Anderson is Senior Research Scientist in the Musculoskeletal Biology Research Laboratory at the University of South Australia

“The authors have identified a molecule in mice, Semaphorin 3A, which appears to play an important role in signalling the control of bone remodelling.

Current and developing therapies for osteoporosis typically target either bone resorption or bone formation but not both. In particular, compounds which reduce bone resorption alone are considered to be effective only in preventing bone loss but cannot be used to increase bone gain, and so there has been a concerted effort by researchers and drug companies to develop promising treatments which can increase bone formation.

If Semaphorin 3A can be shown to play a similar role in humans, this could potentially be a valuable target for therapeutic treatment for reducing bone resorption as well as increasing bone formation.”

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Associate  Professor Yin Xiao is from the Institute of Biomedical Innovation at Queensland University of Technology

“This paper has carefully demonstrated the role of Semaphorin 3A in preventing the activity of osteoclasts (bone resorption cells) and increasing the activity of osteoblasts (bone forming cells), indicating the potential application of this molecule in the treatment of bone loss.

A number of gene knockout animal models and cells have been used to prove the concept. The result is convincing and the phenomenon has been showed clearly in the paper.

However, to translate this research result into clinical application, it still needs more detailed investigation. The receptor for Semaphorin 3A and the subsequent activation of cell signalling pathways have not been unveiled and the mechanisms for this molecule working on bone resoprtion and formation are still largely unclear.

This information from this study is useful for better understand the molecule and the potential side effect upon its application.”

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*Osteoprotection by semaphorin 3A, Hayashi et al., Nature, 18 April, 2012

An Australian scientist has written a provocative opinion piece which looks at the impact of grazing on bushfires, as well as the problem of feral flora and fauna in Australia. It suggests considering all potential solutions, including the introduction of wild elephants to keep introduced grasses under control.

Below the author explains his intentions while other experts in the field respond to the piece. 

Feel free to use these quotes in your stories. If you would like to receive a copy of the embargoed paper or to speak to an expert, please don’t hesitate to contact us on (08) 7120 8666 or by email.

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David Bowman, author of the Comment piece, is Professor of Environmental Change Biology at the School for Plant Science at the University of Tasmania (author comment)

“This piece is intentionally challenging. We are going to be driven, whether we like it or not, to think outside the square, because current approaches to land management in many of our landscape settings – in protected areas and unprotected areas, productive landscapes and outback Australia – are not working. Or the approaches we’ve got are not sustainable. We’ve got some big challenges ahead, that’s the point, and we have to be honest about it. Humans are a very important part of Australian ecology.

What I’m saying can be completely misconstrued and that will be sad if it’s put into a polarising debate. What I’m saying is that these challenges open up really fresh thinking which is what we need.”

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Dr Aaron Petty is from the Research Institute of the Environment and Livelihoods at Charles Darwin University, Northern Territory

“I will speak mostly about Gamba grass, as it is the major focus of this piece and his only rationale for why elephants are needed. What Professor Bowman suggests is that “the usual approaches…are not working”, but the fact is the usual approaches have not even been tried effectively. As far as I know Gamba Grass has not yet been declared a weed of national significance, although that status is pending. In the Northern Territory, Gamba Grass was only recently, in 2008, declared a controlled weed and its sale as hay banned. This came only after the tireless work of a dedicated and small group fighting against intense pressure and lobbying from the cattle industry.

Prof. Bowman is quite correct in his concern about Gamba Grass as it has the potential to irreversibly alter the structure of our northern savannas. He is also correct that only chemical treatment and physical clearing of the landscape can control it. However, the proportion of the landscape at present invaded by Gamba grass is large, but a tiny proportion of our northern savannas. Containing the spread of Gamba grass will be costly, but tiny compared to, say, recent money applied to prop up the car industry.

Likewise, Prof. Bowman claims that efforts to control buffalo are ineffectual. Yet this is not so, the Brucellosis and Tuberculosis Eradication Campaign (BTEC) was immensely successful in eradicating buffalo from Kakadu National Park, rapidly repairing wetlands that were severely damaged from buffalo overpopulation. So, in short, we are not out of ideas, we merely lack the political will to implement the steps needed to control our environmental problems.”

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Professor Richard Hobbs is an Australian Laureate Fellow with the School of Plant Biology at The University of Western Australia

“Dave Bowman has rightly suggested that we need to consider new and varied approaches to tackling Australia’s ecological management conundrums. He points out that existing approaches have largely failed to make an impact on the massive problems of wildfires, feral animals, weeds and so on. I agree that we need to think broadly about alternatives – but we need to do this sensibly and with an eye on the lessons of the past.

Dave provides a wide spectrum of potential strategies, some of which have more merit than others. The Nature article contains some interesting contradictions: in one sentence Dave highlights the importance of controlling the ad hoc release of non-native animals and plants, but in the next advocates the introduction of predators to control feral animals and herbivores to graze the flammable grasses.

Does bringing elephants and komodo dragons into Australia make ecological sense, given the unforeseen circumstances generated by earlier introductions (usually carried out with the best of intentions)?  Species introduced to solve one ecological problem frequently end up causing more and often worse problems themselves. The Nature article mentions fire in both the north and the south of Australia but doesn’t differentiate between the different systems and factors at play. Elephants are unlikely to make any difference to the occurrence of forest fires in Victoria, even supposing Victorians were happy to have elephants running around their state, but they do have the potential to wreak ecological havoc in any ecosystem they are introduced to.

Maybe we need to come to terms with the fact that some of our ecosystems may remain changed because of the species we’ve already introduced, rather than introducing more in the hope that they can fix things for us.

In amongst the more outlandish suggestions lurk ideas that are less risky and can work – indeed some are already being implemented, such as the reinstatement of Aboriginal fire management in the north. Programs such as the Australian Wildlife Conservancy’s fire management in the Kimberley are having great success. These in themselves are radical innovations, but ones based on sound ecological understanding.

While I agree that the full spectrum of options needs to be canvassed, discussion of bringing elephants to Australia is probably more of a useful ploy to get people’s attention than a serious option for the future.”

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Dr Ricky Spencer is a Senior Lecturer with the Native and Pest Animal Unit at the University of Western Sydney

“Professor Bowman is obviously trying to raise some very important issues that we face in Australia; the problem is that his comments are careless given recent proposals for the establishment of game reserves in NSW and introduction of new potential feral animals into these reserves. His comments about introducing more dingoes to control other feral animals are also irresponsible because the science behind meso-predator release or suppression is in its infancy and at best correlative. If we did go down the road of introducing elephants to Australia, we had better develop the technology to clone saber-tooth tigers to eventually control the elephants.”

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Professor Patricia Werner is a Visiting Fellow at the The Australian National University’s Fenner School of Environment and Society

“Professor Bowman is the same fellow that made the headlines in the Northern Territory News about five years ago when he advocated introducing African large grazing mammals to rid the place of introduced grasses (i.e. gamba grass, mentioned in this article). So, this is not new.

As for elephants and rhinoceroses, these are browsers, not grazers (as are various types of antelope, cattle, etc.). They eat not only grass but leaves, twigs, fruits, roots they dig up, and even bark. An adult elephant can eat 150 – 300 kg of vegetation a day, only about half of which is grass. They digest only about 40 per cent of what they eat, so have to rely on volume to get enough food to sustain themselves.

There are countless studies in Africa showing that when elephants are removed from an area, tree cover increases. That is, elephants reduce/keep down trees, eating juvenile trees, stripping bark, etc. Are we in Australia prepared to try yet another landscape-scale “experiment” as we did with foxes, rabbits, etc, and merely hope that the elephants don’t find our native Australian trees tasty?  Can we somehow command them to eat only introduced African grasses?  And would we mind seeing our wooded savannas turn to a more grassy-savanna such as those that dominate in Africa – match any rainfall area to ours and you will find less woody cover than we have.”

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Dr Don Driscoll is a Fellow at The Australian National University’s Fenner School of Environment and Society

“Professor Bowman makes two critical points in his paper with which I agree. Australian ecosystems are in a desperate state of degradation due to invasive plants and animals. Invasive species have wiped out much of Australia’s natural heritage, they continue to destroy what we have left, and international trade combined with pressures to increase agricultural productivity worsen the problem. The second critical point that Bowman makes is that, because of this ongoing environmental catastrophe, we need to put all of the management options on the table to try to find ways of reducing the rate at which our biodiversity succumbs to the impacts of invasive alien species.

We should therefore consider introducing elephants and rhinoceros to Australia. We should also reconsider widely implemented practices such as culling dingos or burning forests to reduce fuels in southern Australia as an asset-protection measure. Introducing elephants to Australia would likely be rather quickly rejected as a method for controlling invasive gamba grass. The cost of fencing, the effectiveness of controlling the problem (think cane-toads and cane-beetles), and the risk of adverse impacts (e.g. elephants have a tendency to push trees down) would, I suspect, quickly render the elephant option less attractive than alternative actions for controlling gamba grass.

On the other hand, evidence is mounting that dingos have enormous environmental benefits with little increased risk to the cattle industry, and wide-spread fuel reduction in forests has negative environmental and water quality impacts, while having little influence over the risk of house loss in wildfires. It is crucial to consider all of the management options for dealing with invasive species (even ideas that might seem crazy at first), and it is just as crucial to consider their cost and the evidence of the kinds of impacts that each option will have on a range of societal objectives.”

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*Bring elephants to Australia?, Bowman., Nature, Vol 482, 2012

In a comment piece, international scientists argue that added sweeteners pose dangers to health that justify controlling them like alcohol. Here  Australian experts puts the arguments into context for Australian readers.

Feel free to use these quotes in your stories.  Any further comments will be posted here. If you would like to speak to an expert, please don’t hesitate to contact us on (08) 7120 8666 or by email.

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Prof Kerin O’Dea is Director of the Sansom Institute for Health Research in the Division of Health Sciences at the University of South Australia

“I agree with Lustig et al that added sugars in western diets are problematic.  I am quite comfortable with dietary sugars if they come from whole foods (i.e. fresh fruit and some vegetables) – as the sugar is diluted with water, fibre and a range of other nutrients.

With added sugars (in many drinks and an ever larger number of processed foods) the sweeteners are extra calories.  Sucrose is a disaccharide comprised of one molecule of glucose and one molecule of fructose. Glucose is an important energy source for most cells in the body. In contrast, fructose is taken up primarily by the liver  – and if you are over-consuming energy then it is converted efficiently to fat.  If you do not over-consume energy then fructose is not a problem.  However, added sugars are mostly in energy-dense processed foods or added to drinks, and frequently are over-consumed.

Much used to be made of the fact the fructose does not elicit significant insulin or leptin responses (low GI)  – however, it is now recognized that these two hormones are important satiety signals for the brain. Because of this I argue that fructose ‘gets under the satiety radar’.”

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Prof Leonie Segal is Foundation Chair of the Health Economics & Social Policy Group at the University of SA, with an international profile in the economics of nutrition. She was a member of the Ministers Preventative Health Taskforce

“A focus on added sugar is most timely, with increasing evidence of its negative health effects.

The public health arguments for intervening are indeed strong, with perhaps the most important consideration, not highlighted by the authors, the imperative of governments to protect vulnerable members of society, especially where the capacity for well-informed decision making is limited or non-existent.

Because eating habits and taste tend to be influenced by what we eat as infants and young children, an unhealthy habituation or addiction to sugar, which influences lifetime health, can be established from a very young age when the ability and capacity to make informed eating choices are simply unavailable. This provides a strong case for governments to intervene to encourage healthy food choices, by children and thus families. And as the authors argue excess sugar is a crucial aspect of current poor food choices and thus an important focus of such policies.

While at its extreme alcohol may have more damaging effects than sugar, excessive consumption of sugar is considerably more prevalent than excessive alcohol consumption, part of the reason why population level strategies make sense.”

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Prof Peter Clifton is Head of Nutritional Interventions at Baker IDI Heart and Diabetes Institute

“Alcohol toxicity is not just metabolic  – it causes violence and road deaths and sugar in any of its forms cannot compete with this statistic. Almost all of the evidence against sugar is epidemiological  – that is association not necessarily causation.

In intervention studies with fructose, up to 10% of calories show no metabolic effects while a few studies with fructose at 25% of energy do show a modest increase in triglycerides but not high enough to cause pancreatitis.

There are no controlled interventions that show feeding fructose or sucrose causes hypertension and none that show that a controlled reduction in sugar alone reduces blood pressure. However, there is evidence to show that increasing sugar-sweetened beverage intake does cause modest weight gain as the liquid calories are not compensated by a reduction in calories from other foods.

Sugar is just another form of over-consumed calories  – easily available and very palatable but no more metabolically deadly than starch or fat calories and certainly not equivalent to alcohol.”

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Dr Alan Barclay is an accredited practicing dietitian and nutritionist, Chief Scientific Officer for the Glycemic Index Foundation Ltd and head of research at the Australian Diabetes Foundation

“This commentary is a provocative piece intended to encourage debate. Many of the statements simply do not apply to Australia and on certain issues there is little evidence to support their views. ‘Sugar’ is not the issue, it is far more complicated than that.

The authors state that over the past 50 years, consumption of sugar has tripled worldwide. However, in Australia sugar consumption has dropped 23% since 1980. Despite this, during that time cases of overweight or obese people have doubled, whilst diabetes has at least tripled.

The authors believe that attention should be turned to ‘added sugar’, which they have defined as any sweetener containing the molecule fructose that is added to food in processing. The authors suggest that fructose can trigger processes that lead to chronic diseases including liver toxicity, however one would need to eat at least 135g, or about 32 teaspoons, of pure added fructose per day on top of what one already eats. Only one per cent of Americans eat more than 100g per day of total fructose. The only disease proven to be related to excess frequent sugar consumption is tooth decay  – a significant problem  – but even then, refined starch is at least equally as cariogenic but is rarely acknowledged as a problem.

Lustig and his colleagues claim that sugar should be regulated like alcohol because it is unavoidable, toxic, has potential for abuse and has a negative impact on society. However, it is certainly not unavoidable, it is only ‘toxic’ in unrealistic amounts and to suggest that consuming sugar is a form of abuse is one of the worst cases of puritanism that I have seen in a while. It’s worth noting that soft drinks and other non-core ‘party’ foods are already taxed (GST) in Australia.

Just like anything else, sugar should only be eaten in moderation. As we continue our research we are finding out more and more about the importance of refined starch and specific fatty acids and the average Australian can do a lot to improve their diet, but casting sugar as the ultimate villain and calling for regulation is misleading, unfounded and unnecessary.”

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[*The toxic truth about sugar, A Comment piece, Lustig et al., Nature, 2012 (482), pp27-29]

Tuesday 23 August at 10.30am AEST at Monash University (also available online)

Australian researchers are announcing the results of their work into modifying and releasing mosquitoes into people’s gardens in a bid to combat dengue fever. The research is published as two papers in the journal Nature and details how they modified the mosquitoes and what happened when they released them into the community in Cairns.

The World Health Organisation ranks dengue as the most important mosquito-borne viral disease in the world. In the last 50 years, incidence has increased 30-fold and there are multiple outbreaks in Queensland each year. Traditional means of controlling dengue have been failing and Australian scientists have turned to a bacterium called Wolbachia that gives mosquitoes some protection from viruses, including dengue.

The following topics were discussed:

• How successful has this been?
• Are mosquitoes in Cairns now resistant to dengue?
• How did you modify the mosquitoes?
• Are these super-mosquitoes and are they now breeding with the local mosquitoes?
• Will this work for other viruses?
• What did the local people think of you releasing mosquitoes at their homes?

Follow the full briefing here (includes powerpoint and audio)

SPEAKERS: (bios available here) | Powerpoint presentation |Briefing audio only

• Prof. Scott O’Neill, Dean, Faculty of Science, Monash University and Program Leader and Chief Investigator of Eliminate Dengue
• Prof. Ary Hoffmann, Centre for Environmental Stress and Adaptation Research, University of Melbourne (Joining online from Germany)
• Prof. Scott Ritchie, Tropical Population Health Unit, Queensland Health and James Cook University, Cairns (Joining online from Cairns)

BRIEFING DETAILS:

DATE: Tue 23 Aug
START TIME: 10.30am AEST
DURATION: 41 min

For further information , please contact the AusSMC on 08 7120 8666 or email us.

A wide range of genetic diseases are linked to defects in mitochondrial DNA. Mitochondria are often called the “cell’s powerhouses” as they are responsible for producing 90% of the energy needed by our bodies. They have their own DNA which is passed directly from mother to child. The new technique, involves taking the nucleus from an egg which has defective mtDNA and moving it into a donor egg with healthy mtDNA. Three healthy monkeys have now been produced using this technique, and the authors propose that it be adapted for use in human in vitro fertilisation.

Images of the monkeys are available on request.

Feel free to use these quotes in your stories. If you would like to speak to an expert, please don’t hesitate to contact us on (08) 8207 7415 or by email.

Associate Professor David Thorburn is Head of Mitochondrial & Metabolic Research at the Murdoch Childrens Research Institute

“Mitochondrial diseases or diseases, caused by mutations in the mitochondrial DNA we inherit from our mothers, affect about 1 in 5000 births at a minimal estimate. That equals about 50 children born in Australia each year but it has been suggested the real frequency could be up to 1 in 250 so they could be a lot more common. At the moment we have essentially no treatment for these diseases which can cause death in infancy or a whole range of neurodegenerative diseases usually with premature death in childhood or adulthood.

Prevention is difficult. There are some families were we can offer prenatal diagnosis or other approaches like pre-implantation genetic diagnosis. We have just done this for an Australian family but it is only the second time that it has been done internationally, and these options are only suitable for some families. The report in Nature is exciting because it potentially offers a new way to allow any family with mitochondrial disease mutations to have a healthy child in subsequent pregnancies. The approach works by essentially transferring the nucleus from the egg of a mother at risk into an egg with healthy mitochondrial DNA. It is innovative and exciting as it offers the potential to prevent mitochondrial diseases in the future. It is a major advance over previous studies of nuclear transfer because it is the first time anyone has achieved virtually no carry-over of mitochondrial DNA from the donor egg.

There are a few things that need to be done before it could play a role in the clinic and there are some safety issues that need further study but it is a very exciting report.

Some people will be concerned about the ethics of this – that the resulting children effectively have three genetic parents because they have a mix of nuclear genes from their mum and dad and mitochondrial genes from a donor, but personally I don’t see that as a major ethical issue, I see the issues as being about safety. In the context of this study there are a few real issues. This technique would currently be illegal in most countries as most countries have legislation that prohibits nuclear transfer although there is a specific exemption that has been created in the UK for exactly this purpose, namely prevention of mitochondrial DNA disease.

The paper also uses a particular method to fuse the nuclear DNA from the mother with the cytoplast from the donor egg which contains the mitochondrial DNA. They use an extract of Sendai virus and although they have done some studies on its safety, there will be regulatory hurdles to jump through before regulators are convinced that it is entirely safe. There are also some theoretical issues around mixing the cytoplasm from two different individuals – it could have impacts on some genetic processes like imprinting – or there could be issues around the compatibility of the mitochondrial DNA from one person with the nuclear DNA of another. The important thing here is that that they have generated live animals and they are not just mice, they are primates which are much more closely related to humans, so those animals can be monitored to see if these issues pose a problem.”

David has also provided the following information which may be helpful:

For some brief summaries of what mitochondrial disease is like for affected families, there are some moving stories on the website of the Australian Mitochondrial Disease Foundation (http://www.amdf.org.au/education.html ). The AMDF’s mission is to promote research and education for the diagnosis, treatment and cure of mitochondrial disorders, and to provide support to affected individuals and families. Coincidentally, the AMDF is having their first major fund-raising event this Sunday, August 30th, with ambassadors including Wallabies George Smith and Luke Burgess plus the actor John Howard and other members of the cast of All Saints. The event is called “Stay in Bed Day”, (http://www.stayinbedday.org.au/) and is designed to allow patients with mitochondrial disease to be involved, despite many of them having problems with weakness or other issues that prevent participation in more active pursuits. The aim is to raise awareness and funds for research on mitochondrial diseases.