Cheesecake makes you fat, but correlation is not causation Genetics Otago Mar 26


Julia Horsfield

I was one of the happy people rejoicing in new gastronomic possibilities after hearing that eating saturated fats may not cause heart disease after all.

Yay! I never could bring myself to opt for that trim latte. Maybe I can even ditch the Olivani in favour of butter. But, as my nutritional friends point out, it’s all how you look at the data. Unfortunately, we mustn’t get too excited, and the best dietary advice is still to stick with omega-3 polyunsaturated fats as part of a balanced diet.

Fair enough, it’s hard not to agree. But I’m an experimental biologist, inordinately interested in the nuts and bolts of how things work. I like cause-and-effect, or as my sons would tell you, ‘consequences’. Stuff you can measure and be unequivocally convinced by. I’ve always been faintly uncomfortable with the nature of the research that encourages folk to burst forth with dietary advice.

In a nutshell, dietary studies look at what people eat, and then determine what happens to them, health-wise, over a period of time. Given enough people, enough time, and some fancy statistics, the studies often conclude that what the people were eating was causative of their health outcomes.

This more than certainly true for simple case studies. For example, eating half a cheesecake a day will make you fatter, worse luck. However, it seems that when the dietary input being measured is just one factor among many (like the type of fat), then the outcome may not be simple. The saturated fat debate outlined above is a good example of where different kinds of analyses show different outcomes, even using the same datasets.

How to establish cause-and-effect? Good old-fashioned biochemistry can sometimes determine the how different foods affect our bodies. Eat enough carrots and you will actually turn orange because of persistence of the carotene pigment (however, I’m told you have to eat an awful lot of carrots to mimic a spray-tan). But eating fat (whether saturated or unsaturated) in large enough amounts to noticeably affect your biochemistry is probably going to be very, very bad for you regardless. Biochemistry is in itself a complex thing, and may not establish causation.

Perhaps the most convincing cause-and-effect relationship with obesity in humans comes from genetics. It is true: our genetic makeup determines our body weight to some extent. Geneticists have shown, using large populations of people, that small variations in DNA sequence are associated with obesity. That is to say, people with a particular version of a DNA sequence are more inclined to be overweight than people who do not have that particular version. The stats are very convincing, and often the variations are within or near genes that could affect human bodyweight. But, like the dietary studies, this is still correlation. Surely, since we’re talking about genes here, and genes actually do stuff, correlation should equate to causation, right?

Not necessarily. DNA sequence variants near a gene called FTO are significantly associated with obesity. People with the risky version of the DNA sequence were on average 3 kg heavier than those with the non-risk version. So, scientists naturally assumed that FTO, being the nearest gene to the genetic variants, was responsible for the increased weight in humans with the risk version. They went so far as to suggest FTO is an ‘obesity gene’ in humans. The only fly in the crème brulee was, there was no correlation between the actual amount of FTO in humans and their body weight. Therefore genetic correlation didn’t entirely equate to causation, in the case of FTO.

But there may be an answer, after all. A highly significant new study in Nature (20 March 2014) shows that the genetic variants do not affect the function of the nearest gene, FTO, but rather, one that’s almost a million base pairs away – IRX3.

The piece of DNA that harbours the genetic variants communicates over this immense distance to the IRX3 gene, completely bypassing the nearest candidate, FTO. This communication happens by the creation of a large DNA loop that brings the piece of variant DNA, (known as an ‘enhancer’, because its role is to enhance gene expression), into contact with the IRX3 gene. And the snuggling up of the enhancer with the IRX3 gene really does seem to change IRX3’s function.

And when the scientists looked at how the IRX3 gene works in humans, they found that the amount of protein made by the IRX3 gene significantly correlates with obesity – more IRX3 usually means you are fatter.

The scientists then turned to mice to prove that it is the function of the IRX3 gene, rather than FTO, that is responsible for the weight changes observed in human populations. Mice lacking the IRX3 gene were 30% thinner than their littermates, and didn’t put on weight when fed the mouse equivalent of cheesecake.

Therefore IRX3 is now the best smoking gun candidate for an obesity gene, even though the genetic changes in humans are actually much closer to the FTO gene.

Only this large collection of functional evidence could convincingly place IRX3 as an important gene associated with human obesity. The collective evidence included mapping of human genetic variants, enhancer function and DNA looping analysis, and mouse models (complete with fat analysis).

It’s tempting to infer cause and effect from all sorts of human studies, including dietary studies. But this excellent genetic example is a good reminder to all that correlation is not causation, and we still have to figure out how things really work before we can assign causation.


Meeting your heroes. Genetics Otago Mar 12

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They* say that you shouldn’t meet your heroes. Yesterday I had the opportunity to meet one of mine, Professor Lord Robert Winston, as he came to visit Genetics Otago for the day. Prof. Winston, as well as being a pioneer in science communication, is also a key figure in genetics, being part of the team that invented the technique of pre-implantation genetic diagnosis.

Prof Winston came to talk to school kids, and he gave an inspiring address at Otago Boys’ to an audience of senior students from around Dunedin and Otago. He talked about the promise and dangers of science, and emphasised that scientific literacy is key to us extracting the good from science while avoiding the bad.

Prof Winston also talked to our postgraduate (and a few undergraduate students), about his career and his thoughts on current issues on science. Off-the-cuff he discussed science, science communication, gave career advice, and generally encouraged our students to achieve in their chosen career. It was an impressive performance, and judging from the reactions of our students, a well received one.


Professor Winston talking with Genetics Otago students

Prof Winston and I also had the chance to talk about our own science, and about science communication, which was incredibly useful and informative. I was left with the impression of a deeply thoughtful and caring man, with a real talent for both science and communication. His willingness to give up his time to talk to students and school kids, and his positive but honest message made his visit a pleasure.

I say meet your heroes; you might be left with a deeper respect for them.

Professor Lord Robert Winston was brought to New Zealand by Gravida: The National Centre for Growth and Development.Go check them out.

(*) No reference. Who knows who ‘they’ are, or why we should listen to them!

Why you should care about plasticity. Genetics Otago Feb 26

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Peter K. Dearden

In my last post I mentioned I was interested in how you get changes in the shape of an animal without a change in genetics. This process is, of course, important for animals like bees, but it is also important in our own biology. In recent years evidence has been building that suggests that our early life environment, pre-natally and perhaps even around conception, has a huge influence on our later life and health.

This idea mirrors the biology I study in bees, environmental influences affect the way genes work, leading to alternative forms, shaped or biology later in life.

The field gives this phenomenon a name; developmental plasticity. During the early life of an animal, it is thought that environmental influences, the maternal environment even post natal care, all can set biological parameters that can then lead to health or disease in later life. The data implies that your early environment may have a huge impact on your later health. If you are interested you could read (Hanson and Gluckman, 2008, Gluckman, Hanson and Mitchell, 2010) or if you want a more user-friendly version (Gluckman and Hanson  Mismatch : The Lifestyle Diseases Time-bomb).

Developmental biologists tend to avoid thinking about plasticity because, by holding the environment stable during development, they can better understand how genes influence growth and differentiation. These is a kind of mutual misunderstanding between human biologists and clinicians, who are interested in how the environment can be manipulated to improve health outcomes for people, and developmental geneticists, who want to know how genes build an organism.

A few years ago now, Prof Sir Peter Gluckman, asked me to join Gravida (or what was then, the National Research Centre for Growth and Development). This is a TEC funded Centre of Research Excellence looking at the affects of early life on health and productivity, how to identify individuals that will suffer health problems because of early life effects and how to intervene to improve human and animal health. We contribute our fundamental work on understanding how the environment interacts with the genome in bees, but work to translate that knowledge with clinicians, agricultural scientists, human biologists and more. It is an exciting collaboration, and one that has been fruitful, particularly in changing the way we approach our science.

The Centre of Research Excellence model is a great one for encouraging and supporting these collaborations, and using individual’s science in new and interesting ways. This morning I find myself writing this, while our big server crunches data from experiments that aim to discover if mechanisms for plasticity in sheep, are similar to those in bees. I can’t wait to find out!

Understanding how biology is shaped by environment is a huge challenge for science; but it turns out that it may be key to improving public health. The only way to turn that key is for collaboration across sciences that draws together multidisciplinary, enthusiatic and effective teams.

Why I study Bees. Genetics Otago Jan 13


Peter K. Dearden

I was recently asked why I work on honeybees, especially given my growing intolerance to bee stings. There are lots of easy answers to this questions, including how cool they are, how important they are, how remarkable their biology is etc etc, but when it comes down to it, there is a real answer. So just to see how strange scientist’s career pathways can be, I want to tell you how I came to be a bee biologist. To find out, we have to go back 540 million years…

If you are not a biologist, or even if you are, you might not have heard of the Cambrian explosion. This is a tragedy, because something remarkable happened, which echoes through evolutionary history. Geologists often divide up periods of geological history using key fossils as signatures of particular geological epochs. One of the biggest divisions is between the Precambrian, and the Cambrian. Most of our planet’s 4.5 billion year old history fits in the Precambrian, but around 560 million years ago, there is a sharp discontinuity, and the Cambrian starts. The discontinuity is that, in most places, there are no fossils in Precambrian rocks, but there are tons in the Cambrian. It is if in a blink of time, animals with hard shelly bits, which fossilise easily, evolved. This is the Cambrian explosion. Suddenly animal life seems to have gone from nothing to something that produced hard bits that turn up as fossils

In 1907 a geologist in the Canadian Rockies, Charles Dolittle Walcott, made a remarkable discovery; fossils of the soft bits of animals, which subsequently came to be known to date from near the Cambrian explosion. Suddenly we had the possibility of understanding what these first animals might be. Now the story of the Burgess shale fauna is too big for this blog, but go and look at the fossils at the Royal Ontario Museum website. We now know that this fauna is found in a few places in the world, and that there are animal fossils in the Precambrian, but they are weird.

If you want to know some of the story, go and read “Wonderful life” By Stephen Jay Gould, but realise that the interpretation of the meaning of the fossils is disputed by others (see for example here). It looks as if this first animal fauna not only had examples of the Phyla of animals living today, but also some very strange looking animals that look like nothing on earth (g and look at that one, its awesome).

When I was an honours student at Victoria University, ‘Wonderful life’ was set as a reading, and the equally wonderful Dr Geoff Rickards set an essay question asking us poor students to answer the question if normal evolutionary processes could explain the sudden appearance of the Burgess shale animals.

My idea was that they could, but that the different shapes of the burgess shale animals came about because they had a very plastic developmental system, which allowed for lots of morphological diversity without much genetic change. Hence this diversity could have evolved very quickly, because of flexible developmental programmes. Not a terribly original idea, but one that got me thinking about how you make an animal, and how much genetic change you need to make that animal a different shape.

Now we know more. We know that some of the weirder Cambrian animals are intermediate forms between living groups, and it has been proposed that the history of these animals may be quite a lot older that their fossils suggest. Perhaps these animals didn’t evolve quite so rapidly. But my question remained, how much genetic change do you need to have morphological change?So I went and studied how morphology is made in an animal, and how those mechanisms that make morphology differ between animals; always circling, but not answering, the question.

Then, when looking for new research directions on returning to New Zealand, I realised that the way to answer to this question was staring at me in the face. There are animals that produce morphological change WITHOUT ANY genetic change. Most of these are insects, and the phenomenon is known as a polyphenism. The coolest polyphenisms are in bees and wasps, and the easiest to study is in the honeybee.

Honeybee females are either workers or queens. That doesn’t really get across how different workers and queens are. They differ in shape, morphology, size, behaviour, brain function, ovary activity. They are different. But that difference isn’t genetic, it is due to what larval bees are fed. Larvae fed royal jelly become queens, those not, become workers. The environment can radically change the morphology of these animals, without any genetic change.

We have been studying this phenomenon for a few years now, with the support of the Marsden fund and Gravida, and have recently published our first paper describing what Royal Jelly does to the honeybee genome (don’t download it yet, BMC have mangled the figure legends and I am waiting for them to fix them).

So that’s why I work on bees. Because of the Burgess shale fauna, and Stephen Jay Gould, and Geoff Rickards and because frankly, bees are really cool (and important).

Is your educational achievement determined by your genes? Genetics Otago Jan 01


Peter K. Dearden

I am loath to write this post, not only because it is New Year’s Day and I am in Melbourne, but also because the subject matter touches some raw nerves. The problem is I have been increasingly angry at the way genetics is beginning to be used to inform policy in education. Not so much here in New Zealand, but in the UK there are worrying signs that genetics is being used as an argument to de-invest in education. Given that NZ often follows the UK, I wanted to point out a few problems with what has been reported (for example here, here and here).

The facts are that measures of ‘intelligence’ have been shown to be highly heritable. This is a difficult statement to make because it sums up a great deal of research which is all flawed in some respect. The first problem is one of measurement, intelligence is measured as a ‘g-factor’, a measure of general ability, which is based on a number of tests, but is often thought similar to IQ. Any measurement of intelligence is flawed, as testing will only address some of the attributes that might count as ‘intelligence’. That such tests are flawed, and need to be treated with extreme scepticism is demonstrated most clearly by the ‘Flynn effect’, a general increase in IQ scores since 1930 first identified by Prof Jim Flynn, one of New Zealand’s National Treasures.

Such tests, however, measure something, and the inheritance of that something can be studied. Most of the studies to address this question have been made using twins. Twins are a wonderful way to study genetics in humans because of the different degrees that monozygotic (identical) twins and dizygotic (fraternal or sororal) twins share their genomes. Monozygotic twins share 100% of their genomes, dizygotic on average 50%. By comparing the number of monozygotic twin pairs in which a particular trait is present in both twins (concordance) with dizygotic twins you can get a measure of the heritability of that trait.
Unfortunately heritability isn’t a simple measure of the genetic contribution to a trait. The differences in phenotype between individuals in a population are due to a combination of genes, environment and gene-environment interactions. Heritability is a measure of just the genetic contribution to a trait, but this is very difficult to disentangle from the environment. This is because the environment can affect the heritability. This sounds odd, but lets take a simple example. Measures of the heritability of smoking have been made (for example see here ) that show that initiation of smoking is heritable. There are genes that, presumably, predispose you to smoking. But if you live in a world with no access to cigarettes etc, then that heritability must drop to 0. Smoking is heritable but ONLY in a specific environment.

To remove the environmental influence in twin studies, researchers have compared twins raised together with twins raised apart; a way of removing the ‘shared environment effect’. If twins raised apart show high concordance, then that similarity must be genetics, not environment. The problem is that these are people, and twins raised apart are rare, and often the agencies that control adoption will try and match the environments of a pair of adopted-out twins. These studies, therefore are flawed. This doesn’t mean they are useless, but it important to know the difficulties with them before we use them to inform policy.
In more recent years (for example here) modern genetic techniques that circumvent some of the problems with twin studies have been sued to show that ‘g’ is highly heritable. Such studies have their own suite of problems, but I think we can accept that ‘g’, a measure of something related to intelligence, is highly heritable.

So what does that mean for education? It seems likely that this means that some differences in educational attainment is related to genetic factors. Does that mean that there is little point in investing in education because achievement is heritable? The answer is most certainly not.

Again we have to worry about the subtle interplay between genes and environment. The heritability of a trait is affected by the environment. No amount of ‘good genes’ is going to improve your educational achievement if you have no access to education. While those with ‘good genes’ might do better than those with ‘bad genes’ in such a situation, it is the environment (education) that is key to the outcome. If you think about it, the genetic differences in educational achievement will become MORE apparent the more similar the environment (educational quality) becomes. Surely then the argument must be that the education must be of the highest quality for EVERY student to ensure that everyone gets the chance to demonstrate their ‘good genes’. Part of this ‘highest quality’ may be the use of genetics to help identify aptitudes, or best modes of learning, for students, but genetics is no argument for a reduction in investment in education.

Policy should be informed by science. But we as scientists need to make sure that that science is properly interpreted before it is used. In this case, all I can see here is genetics being used as an argument to support the continuance of a ruling elite (For example, see this speech by the current mayor of London). Education is too important for ALL of society to be lavished only on those thought to be ‘genetically superior’.

Working out what makes us human. Genetics Otago Dec 20


Peter K. Dearden.

One key question in biology is what makes us different as a species. Humans have a remarkable set of adaptations that distinguish us from even our closest living relatives. We walk upright, we have larger brains, we use language, and we are consummate tool-makers and users. From the point of view of an alien, perhaps, these differences may be subtle, but they are key to our spread around this planet, and the ability, for better or worse, to modify our environment. These differences must be encoded somewhere in our genes. Something about the way our DNA works, or is organised, must underpin these differences in our biology. Such differences are key targets for scientists seeking to understand the biology of our species.

Before we sequenced the human genome, we thought that we probably had hundreds of thousands of genes in our genome, as compared to the 13,000 odd in flies and worms. Sequencing our genome  indicated that actually we have around 20,000, and that that number is pretty much the same in all mammals. Sequencing the genomes of the Gorilla  and the Chimpanzee showed that our genomes are very similar to theirs. Comparing the DNA sequence of genes in our genome with those in other primates indicates that we do not have a huge pile of ‘extra’ genes that make us humans, or help us run our huge brains. Indeed it is very hard to identify any genes that are only in our genome, and not in any other species. We do have variants of genes, however, our version of a gene may differ slightly from the version in other primates. Of course this is true within our species, different people often have different versions of the same gene.

We are beginning to understand, however, that the differences between species may not be due to differences within genes, but in the way genes are turned on or off; the regulation of genes. While the best-known examples are in insects (for example see here ) changes in gene regulation, with no change in the genes themselves, may underlie much species difference.

Recently the knowledge about our closest relatives has been dramatically improved. Advances in DNA sequencing allowed us to sequence the genome of a Neanderthal despite them being extinct and only their bone fragments remaining. Even more excitingly, such sequencing has even identified new as previously unknown human species, including the mysterious Denisovans. Now a much more complete version of the Neanderthal genome has been produced, by a group in Germany. By sequencing the DNA from a toe bone, this group has show that the bone is from a Neanderthal, and increased the amount of sequence data from this species. The authors of this paper report all kinds of interesting things, but towards the end of the paper, they start to talk about the genetic differences between us and Neanderthals. It’s thrilling!

The authors determine that we have 96 differences, within only 87 protein-coding genes, from Neanderthals. Outside genes, they catalogue around 3000 differences that might change the regulation of genes. We can only hope that somewhere within this catalogue are the genetic determinants of human-ness.

But wait, how different are Neanderthals to us? They made tools, they may have had language, they walked upright, they buried their dead, and we had sex with them. Should we perhaps we be looking for changes that we share with Neanderthals that aren’t in more distant relatives?

More importantly, how can we ever know which of those changes in the genome make us us? We could never do an experiment that would put a human version of a gene or regulatory sequence in a Neanderthal, because they are extinct. Nor would we modify a human genome to put in a Neanderthal sequence, because of the obvious ethical issues. If we cannot test what these differences in our genome do, how can we ever know which bits of our genome encode our unique biology, and which encode the unique biology of our relatives?

AgResearch, Invermay and Genetics Genetics Otago Nov 26


Peter K. Dearden

The opinions below are my own, and not necessarily those of the University of Otago, my employer.

You may be aware that AgResearch has decided to move its genetics/genomics team from Invermay near Dunedin, to Lincoln. This move has excited a great deal of attention in the Otago press, and some consternation around here. Genetics Otago  has been drawn into this as a centre of research excellence and hub for genetics and genomics that AgResearch is linked into, that they will lose the benefit of if they move. This has led to some unfortunate exchanges in the media, so I thought I would write something from my point of view.

AgResearch has had a long-term and excellent genetic/ genomics group at Invermay. Many of that group are members of Genetics Otago. Genetics Otago has over 200 members across the University of Otago, AgResearch, AbacusBio, and others (both companies and individuals) across Otago. AgResearch is a small, but important, part of that collaboration. Indeed AgResearch members have always been members of our administrative group, and we greatly value that input. It is also worth pointing out that we are a very broad organisation. Genetics is a tool for understanding biology, and we have people who use genetics in a great number of fields (see our website), including members in Law and Bioethics who study the impact of genetic technology and findings on society. Genetics Otago is wholly funded by the University of Otago.

In recent weeks I have been disappointed by the way we, and the University of Otago, have been portrayed, in the continuing argument about AgResearch leaving.

There are three points that I think have been unfair.

1) Only Massey and Lincoln Universities have the capability of training new agricultural scientists.

This is more than a little unfair. We, in Genetics at least, have spent a great deal of time ensuring that Agricultural and Horticultural genetics is taught in all our lectures and labs, and indeed have invited members of CRIs to teach in our papers. Indeed one outstanding geneticist from AgResearch teaches a large block of lectures on quantitative genetics.We do this because a) the scientist involved is an outstanding world-leader in this field, b) we think that this is a key skill that our young geneticists must learn to fill gaps in NZ industry and c) it gives us the opportunity to introduce our students to AgResearch, a potential employer and key research agency in NZ. Alongside this, many of our lecturing staff have links into agricultural research, and, in the spirit of research-led teaching, ensure this aspect is taught in our programmes. Outside genetics, many of our teaching programmes encompass topics of importance to agriculture. Otago’s teaching aims to produce excellent, flexible and broadly capable members of the workforce. Many of our students go on in Agricultural sciences as a result of these traits.

2) AgResearch’s links to Genetics at Otago are only a ‘few people thick’.

This is not quite true. While there may be few funded grants with AgResearch currently, the relationship between Otago and Invermay is much deeper. Many of our members have funded or unfunded collaborations with AgResearch, some (including myself) use Agresearch’s facilities for their research. Even more importantly, through joint seminars and symposia, we discuss research and technology with our AgResearch colleagues, develop new ideas together, share equipment and chemicals, and generally act as a diverse, vibrant, sharing community. This community will continue without AgResearch, but AgResearch will lose those connections if they move.

3) The University of Otago is not collaborative.

I guess we have a bit of a reputation for being old fashioned, focusing on excellence, and perhaps not playing nicely with, or ignoring, more applied aspect of science. This reputation, in genetics at least, couldn’t be further from the truth. Our collaborations and connections with AgResearch, in particular, are old. The AgResearch Molecular Biology Unit, the forerunner of the excellent genetics research at the Invermay Campus, sprang out of, and was hosted for many years by, the University of Otago Biochemistry Department. Indeed the office where I write this too-long blog was their old meeting room. I turned down a job with AgResearch some years ago in this very room. In the lab next door the Inverdale and Boorula mutations, now used to manipulate sheep fertility nationwide, were isolated, and studied. Some years ago, the lab moved out to Invermay, with support from the University in the form of the Centre for Reproduction and Genomics, jointly funded by AgResearch and Otago, and Genetics Otago. Under that banner, the first draft of the sheep genome, the basis for AgResearch’s successful sheep genotyping technologies was sequenced. That sequencing was done on an Otago-bought machine, with support from Otago staff. The final version of the sheep genome is just about to be submitted for publication, and includes the names of a number of University of Otago researchers, as well as their AgResearch counterparts. The collaborative relationship between Otago and Agresearch has been a long and successful one. Collaborations will continue if AgResearch leaves, but they will change, and they will be less effective.

AgResearch has set forward clear reasons as to why they wish to move genetics/genomics out of Invermay. They have also been building up their capability in this area at their other sites. More geneticists are good, but they will, in my opinion, lose capacity and connectivity, by moving away from the genetics hub based here in Dunedin.

We will still be a collaborative group, and will welcome collaboration with AgResearch, or indeed, any partner. There is no need to denigrate what we do to support AgResearch’s business plans.

Finding future treatments for Cancer Genetics Otago Sep 25

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Dr Elizabeth Duncan

Cancer.  It is a small word, but one that has a big meaning for a lot of people.  Most of us know someone who has had cancer, or are cancer survivors.

As a geneticist I can sometimes have a dispassionate view of the world around me, but last night as Jessica Wapner read an excerpt from her book “The Philadelphia Chromosome” I almost cried.  Jessica began her talk with a poignant tale of a man named Gary Eichner.  Gary was diagnosed with chronic myeloid leukemia (CML) at the age of 43.  CML causes the bone marrow to make too many white blood cells.  If Gary had been diagnosed 20 years ago he would have had a poor prognosis, almost no chance of surviving 5 years.  Now, thanks to a drug called Gleevec (and its derivatives), Gary has a 95% chance of surviving 5 years and a 90% chance of surviving 10 years.

This drug revolutionized our approach to cancer medicine. For the first time scientists were able to discover the genetic cause of a cancer and design a drug to specifically target that cause.  One of the cells in Gary’s bone marrow had made an error while replicating.  This error caused a little piece of chromosome 9 to swap with a piece of chromosome 22 making a new protein.  This new protein (called BCR-ABL) was telling the white blood cells to divide, a process that is stopped by Gleevec.

The genetic cause of this cancer was first discovered in 1959, but we didn’t really understand it until the 1990’s.  A lot has changed since then.  We now have the sequence of the human genome and genome sequencing is now cheaper and faster than ever. We can now look for the root-causes of particular cancers, find what changes have occurred in the DNA of a cancer.  Professor Ian Morison, a clinical haematologist at the University of Otago, has used the new genome sequencing technologies to find a chromosomal abnormality in a local family that causes this family to be more susceptible to a particular kind of blood cancer.  In clinics in the USA and Europe genetic tests are being used routinely for some kinds of cancer.  This information is then used to determine the best course of treatment.

The talk by Jessica and by Professor Ian Morison, hosted by Genetics Otago at Toitu (Otago Settlers Museum), highlighted the immense power of new genetic technologies for finding the root cause of cancers and other genetic diseases.  Knowing the genetic changes that cause particular cancers will not only allow doctors to give patients the most effective treatment but will also provide targets to find novel drugs.

The talk by Jessica Wapner and Professor Ian Morrison was part of the inaugural Genetics Week, hosted by Genetics Otago

Fork Futures Genetics Otago Aug 06

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Peter K. Dearden

It is hard to avoid the news that last night, a beef burger grown in the lab was consumed by a number of people. The idea was that meat, grown in dishes in the lab, could replace meat grown in animals; last night was a demonstration of the principle.

The beef burger in question was grown from muscle stem cells in plastic dishes, the cells collected and squished together to make a meat-like substance. Consumers of the burger made statements such as “lacked flavor” and “needed some fat”, not exactly a glowing endorsement, but perhaps no worse than most folk’s opinion of the ‘mechanically recovered meat’ often lurking in such burgers.

The cost of this burger has been reported as 250,000 Euros ($425,000 NZ dollars), proving conclusively that growing meat in animals is still cheaper and more efficient.  As an aside, most cell culture experiments use animal serum to help grow the cells, meaning this approach is not animal-free. But is this more than just a publicity stunt; are there implications for New Zealand?

New Zealand is outstanding, to quote my friend Prof Hugh Blair, in exporting sunlight and fresh water. Our primary production systems are geared towards taking water and sunlight, turning that into plant biomass, then converting that into animals, whose products we sell. If we could use solar power to grow cells in culture, could we cut out the middle men, grass and animals, to produce some of those animal products? Is the future of New Zealand farming in cell culture, with the animals going away?

Well, the cost of meat production in vats needs to come down, but it will. The cost of farming is likely to go up, as the costs of fertilisers goes up, environmental mitigation becomes more of a problem and land and water becomes more expensive. Someday they will meet, and vat-meat will be cheaper and more efficient to produce. We must remember that our current role in the world is generally, to make food, and with an increasing world population we need to make more, more efficiently.

So should New Zealand take this route? We have always been world leaders in agriculture research. Our economy is built on our ability to efficiently farm. Is it time for us to be researching this alternative approach? Surely it could make more efficient use of our sunlight and water, perhaps with much less environmental impact.

It’s a question for us all to think about, but currently I don’t think we have a choice. Without sustained investment in the science that will be required to develop this technology we will not be able to implement it. This is not an unexpected scientific development, both science and science fiction has been signalling developments like this for some time. Given NZ’s outstanding history in agricultural research, why are we not at the forefront of this new wave in food production?

Lethal doses and Bees Genetics Otago Jul 30

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Peter K. Dearden

More bad news for bees this week. Honeybees around the world are struggling in the face of disease and insecticide threats. In New Zealand we have Varroa mite, that increases costs for beekeepers, destroys unmanaged beehives and vectors viruses, making them more virulent. Overseas, Colony Collapse Disorder and pesticide-threats are adding to the woes Varroa brings, meaning bee numbers appear to be declining.

The loss of pollination capacity due to the loss of bees should be a big issue for all of us. In New Zealand, honeybees are estimated to support 35% of our primary sector, contributing $5.1 billion in export revenues (Laas, F., Foster, B. & Newstrom-Lloyd, L. Report to the Select Committee on Pollinator Security in New Zealand. (2011)).  Beyond this, the pollination of the beans and fruit trees in your garden and parks, is dependent to some extent on bees. New Zealand would be poorer, both environmentally and economically, without bees.

A paper published this week adds to the problem. It finds that bees that consume pollen with high fungicide levels have an increased probability of high rates of infection of Nosema ceranae (Pettis et al, PLOS One 8:7 e70182). Nosema is a unicellular parasite (microsoporidian) of honeybees, and have been linked to Colony Collapse Disorder. High rates of Nosema are detrimental to bee and hive health. The finding that fungicide dose affects Nosema infection is surprising, because fungicides should be perfectly safe for bees. The doses here are not high, but they seem enough to disrupt hive health, perhaps producing honeybee declines.

The bad news is that all but one of the fungicides found to have an association with Nosema are used in New Zealand. We also have Nosema.

Let’s be clear here; this is not a black and white issue. Agrichemicals are key parts of our production systems, and are not, in the main, used indiscriminately.  Now there is a balancing act: ensuring bee health while maintaining efficient production. This is not going to be an easy equilibrium to maintain.

Perhaps more pressing is the need to investigate more sensibly the affect of agrichemicals on bees. Determining the lethal dose (the dose at which a bee dies) of a chemical, does not determine if sub-lethal does have effects on the behaviour or health of the whole hive. Bees are incredible animals because of their hive behaviour, their division of labour and their sociality. This also makes them sensitive in ways that non-social insects are not. We need to know more about the impacts of agrichemicals, used validly to improve our primary production output, on the remarkable super-organisms that are bees.

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