It’s always tricky raising a polarising issue, and occasionally especially so in an on-line forum with the potential for excessive trolling, but I (and evidently a lot of others worldwide) think it is definitely something on which needs to have an open discourse established, and I would hate for our wee country to miss out on the opportunity for growth and improvement – and informed comment.

The fact is; scientists are sexist.

Right, obligatory inflammatory by-line out of the way; now the research, and then the impassioned soap-boxing.

This study grew from the question of whether inherent sexism in science is the reason behind the gender disparity in employment; are women not applying for, or getting, science academic jobs because the employers are specifically sexist against them, or is it their own fault for not applying due to other reasons such as low pay/timing of family production/difficulty of training etc etc (“life choices” no less).

One hundred and twenty seven science faculty members, ‘academics’, were given a CV from either a male or female ‘student’.  The CV’s were exact copies, just with different, blatantly-gendered names attached.  The participants were asked to rate the student on employability/hireability, competence, the starting salary and the amount of mentoring they would offer the student.

The hypothetical student was applying for a laboratory manager position, before PhD study or postdoctoral employment.  This career period was chosen because it is at this point where women start dropping out of the pipeline, after being overrepresented in undergraduate studies.  The “formative predoctoral years” (how delightful!) affect how a student perceives a career in science, and if gender biased will effect opinions on self-worth with regards to scientific abilities and attractiveness of the career as a whole.

The study was carried out in a double-blind fashion, where the academic participants didn’t know that they were ultimately taking part in a gender bias study, and the experimenters didn’t know which results belonged to the female or male CVs until after the data was collected and analysed.  This hopefully avoids bias on behalf of the experimenters as well, in case they subconsciously wanted a biased result.  (Experimenter bias is actually an important confounding variable that people often forget about; is that embryo showing the staining pattern you want or do you really want to see that staining pattern you expect, so do?  Good article here about it).

In case you are thinking gender bias is only an issue in a particular area of science, physics in comparison to biology for example, the types of science academics surveyed were broad and represented biology, chemistry and physics professors, nationwide (USA).  And least you dismiss the study for coming from a ‘lesser’ institution, the research group is at Yale and the paper in PNAS.  The PI of the group is Jo Handelsman, a Professor of Molecular, Cellular, and Developmental Biology.  And finally, in case you think the academics were just throwing numbers around; they were all under the impression that they were rating the CV of a student who was intending to go to graduate school, had just applied for a laboratory manager position, and would indeed receive the feedback from that particular academic.  This feedback had consequences.

There are only two simple graphs, one table and one flow chart figure in the paper, and the data show that not only are female applicants rated lower on competence, hireability and mentoring than males, but that both female and male academics are guilty of the bias.  Also, starting salaries are offered lower from a female academic than a male, to a male student, and even lower from a female academic to a female student.  When faculty gender is collapsed (so ‘academics’ as a whole, rating potential job applicants) the results look thus for the rating scales, with a significance P-value of < 0.001:

And thus for the starting salary offer, with a significance P-value of < 0.01:

The supplementary information includes a detailed run-down of the scales and rating system used in the experiment and is a fascinating read, there is also included the cover story text that was given to the academics and a sample of the ‘CV’.  Here, if you feel like further reading.  I would also recommend reading Sean Carroll’s short and snappy blurb on the article, here, and Ilana Yurkiewicz’s commentary, here.  Also related; the 2011 snapshot of women in science in NZ by Shaun Hendy, here, and Peter Griffin’s replicated graphs of 2011 gender in science, here.  Brilliantly visual indications of a nation’s science-gender despair.

I’ve been following the thread throughout the internet and it is glaringly apparent that if you agree with the presence of gender bias in science; it’s weak, you feel bad, you need more data before you can be sure, or you are criticised as being a ‘nazi-feminist’.  If you disagree you are automatically labelled sexist – there is no middle ground, and no one is happy with the discourse itself or the result of any debate.  But if it is indeed subconscious, and knowing about the issue is enough to make a start at causing change, is that not enough in itself?  Is the beginning of change and planting the questioning seed not a worthy goal?

Do you think this is an issue in NZ?  Do you think it is an issue at your university? (See?  See that cringe you pulled just then?  The fact that you are scared to even contemplate it is indicative of fear that it does exist and you will be persecuted for saying anything about it).

The commentary is not all bad – there is mention of cases being brought to the attention of senior academics that were completely unaware of the habit and immediately corrected the behaviour.

Do you amend marks or impressions for a female student to take into account emotional responses and social interactions in the lab which otherwise would have no impact on ‘school work’, if the student had been male?  Have you dismissed the complaints of a student with regards a lecturer because ‘she was just an overreacting, emotional young girl’?  Will you ever be able to make such a call ever again without seriously examining your own behaviour?  Are you judging me right now for raising this issue, and being female?  What if a male had written this post?  Are you a female academic struggling to be held to the same standard as your male peers and overcompensating by being a harsher critic of other female scientists?

Is it time we started calling for job applications (and theses for marking…) without names or gender?  If you dismiss that idea out of hand, are you doing it because you think you need to know the gender of an applicant in order to make a hiring decision?  In which case – why?  Why on earth would you?!

—

I want to raise children and be a professor.  I want to have a successful scientific career and a happy, healthy family.  I want to raise my sons and daughters in a world where having a penis on your CV does not earn you more money or gain you more opportunity, or more mentoring or easier advancement.  I don’t want the issue to be an issue any more, especially in my own dear field.

There is no excuse not to examine your own actions and the actions of the academics around you.  If you see it, call it out.  Change is needed, and it will be good.  Don’t be afraid.  Let’s talk.

Clean Tenebrio cultures.  Photo: SM Morgan

Tenebrio molitor in its larval form is commonly called ‘mealworm’ due to it having a predilection for infesting cereal silos.  The larvae are also a favorite of pet shops, and are used to feed reptiles, fish and birds.  It is occasionally common to raise them with added juvenile hormone which keeps them in the larval form and induces much larger growth.  They are also used as fishing bait – the worm on the end of your hook.  And, apparently, when baked or fried the larvae are touted as a ‘healthy snack food’.  Delightful.
T. molitor is a holometabolous insect, which means it goes through complete body changes throughout its lifecycle.  Starting as an egg, a larvae (maggot) hatches and feeds, molting as it grows, until big enough to pupate.  The pupal form is mostly stationary while the body is reformed, and eventually hatches into the adult insect.  A lovely video of a developing and hatching pupa can be seen here.  The adult form of T. molitoris a beautiful Darkling beetle:

T. molitor adult.  Photo: SM Morgan
And the larval and pupal forms have some undeniable cute-factor going on:

T. molitor larva and pupa.  Photo: SM Morgan

T. molitor is used in science for, as a quick sampling; determining protein structures, testing pesticides, environmental stress research (effects of temperature, radiation and toxins on the beetle; and its response), and even investigation into the larvae as an alternative food source for humans.

And in a quick segue, because this is fascinating - that last paper was investigating the use of the mealworm as a ‘bioregenerative life support system’ – for long term space habitation.  Brilliant.  Astronauts need animal protein, and if the worms can live off plant wastes – so much the better.

However, perhaps most interesting (due to my own exposure via office-mates), the larvae produce a protein commonly called an ‘antifreeze’ which slows the formation of ice crystals, prevents damage from these sharp water-shards and ensures the insect can survive colder temperatures – in this case down to -13 degrees Celsius.  Antifreezes are typically called as such due to their ability to reduce the freezing temperature of a liquid, and can be salts, alcohols or proteins.  For this reason, the scientific field studying this particular topic prefers the full term ‘antifreeze proteins’, to avoid confusion.

The applications of such additives go further than your car engine in winter – two brands of ice cream in the US contain antifreeze protein to avoid that horrible icing situation which you find in the 6 month-old container you had forgotten about in the deep freeze.  Potential applications also include use in human organ/tissue transplant; if we could super-cool the organs without damaging the tissues by freezing, we could keep them in storage for longer, and potentially save more lives.  Also, if we could improve the freeze-tolerance of crop plants, the growth and harvest seasons could be extended, providing more food for a starving world.

The antifreeze protein in T. molitor has been investigated in the laboratory traditionally via recombinant means.  That is, the gene sequence for the protein is put into bacteria and the bacteria manufactures plenty of the protein of which you can then study.  However, bacteria perform different post-translational modifications on their proteins than insects do – they do not cut (where T. molitor does), differently fold and manipulate their gene products after they have been made so that the protein you extract from bacteria is different to that which you extract from the beetle itself, even if the protein was made from the exact same gene sequence.

It has been suggested that these bacterial modifications alter the activity of the antifreeze protein, so James McKellar, a Master of Science student under the supervision of Dr Craig Marshall here at Otago, is investigating these differences between the bacterial-produced T. molitor antifreeze protein and the protein extracted directly from the beetle larvae itself.  A process which involves instant death for many larvae via liquid nitrogen submersion.

The larvae are grown in porridge oats and while they can survive off metabolic water, an added piece of apple or carrot keeps them happy.  However, if left too long or without adequate ventilation, the extra moisture from the fruit can start keeping other things happy – like a delightful green mould.  Cleaning out the cultures involves tedious sifting of mouldy oats and built-up beetle waste, and picking out of beetles, pupa and larvae to place into clean, mould-free porridge.  The larvae however, hatch from eggs too small to see without aid, and as such when young are very small; so the process becomes similar to panning for gold.  The more help, the better.

Thus my playing about with a different insect for a short while.

Today saw some discussion in the press about a statement by Canterbury University’s Prof Jack Heinemann,  Prof Judy Carmen (Flinders University) and Prof Michael Antoniou (King’s College, London), around the risks of a new transgenic wheat variety being assessed for release by CSIRO in Australia. These statements released by the Safe Food Foundation, provide an opinion on the safety of this new wheat variety, and are interesting reading.

The new wheat variety aims to increase the amount of resistant starch, making this starch less easy to digest with apparent health benefits for the consumer. To make this variety, CSIRO has used a transgene that suppresses two plant genes, genes that make easy-to-digest starch. They have utilized a technique called RNA interference to do this. RNA interference is a modern technique whereby a small piece of double stranded RNA is made that is the same sequence as a gene you want to turn off. Now, RNA, the molecule that takes the sequence of DNA and is translated into protein, is normally single stranded. Double stranded RNA appears to be a warning signal for many organisms because they generate a response to it that causes all RNA of the same sequence to be degraded, and DNA with the same sequence to be silenced. Thus because genes are first transcribed into  RNA before making protein, double stranded RNA causes any gene with the same sequence to be turned off.  In this case, a small bit of DNA that, when transcribed, makes double stranded RNA of the same sequence of the two enzymes involved in making easy-to-digest starch, has been inserted in the plant genome. When active, these make double stranded RNA and thus turn off these genes, presumably making the starch produced by the plant more resistant to digestion.

Clever huh!

Now plants, and animals, also use small bits of double stranded RNA to regulate our own genes. The machinery that recognizes double stranded RNA is present in our cells, and used by them to do important things. A recent paper also shows that some of these small double stranded RNAs from plants can be found in Humans who have eaten those plants, and that they might cause some silencing of human genes. So it is possible that the bits of RNA that CSIRO has put into the plants to silence the making of digestable starch, might end up in people eating that plant. Now this normally would be no problem, because the process is sequence-specific, only genes with the same sequence as the plant gene being silenced in our own genome might be affected. Unlikely you might think? Think again. Organisms share a great deal of genetic information, and we do have a gene, called GBE, in our genome with similarity to the plant genes (SEI and SEII) being targeted. GBE encodes a protein that makes branched glycogen molecules. Glycogen is our way of storing carbohydrates, and GBE makes branched versions. Humans unable to make branched glycogen have a disease called Glycogen Storage Disease IV, that leads to damage in the liver, as pointed out by Prof. Judy Carmen.

So is it possible that this new variety of wheat, by making bits of RNA to silence the plant genes, might silence the human GBE gene in our livers leading to Glycogen Storage Disease IV? Possible, but, in my opinion, easy to avoid and unlikely

Let’s take this in bits….

The key is sequence similarity. The human gene GBE has similarity to the plant genes SEI and SEII, but this is limited and not across the whole sequence. The similarity is probably in the active site of the enzyme, which is presumably doing a similar job. The important thing is not protein similarity though, but DNA sequence similarity, which is low. To avoid the problem, however, all you need to do is make the bits of RNA you are expressing in the plant, from regions of the plant genes that ARE NOT similar to the Human gene. Simple. Has this been done? Who knows? CSIRO have not released to the public the sequences that have been used to silence the plant genes (I assume the regulators have seen them).

Certainly if I were doing this, I would target a region of RNA at the end of the gene, which doesn’t encode protein, and evolves fast. This region, named the 3′ untranslated region, is not similar between plants and mammals, and is the natural target of the double stranded RNA system, so likely to be a safe and effective method of silencing.

Prof. Heinemann also suggests that the manner in which the double stranded RNA is made in the plant could produce molecules with unexpected targets, again causing problems in humans. This seems less likely. It is relatively easy, with modern sequencing techniques, and good control of transgenesis, to make sure that these unexpected molecules do not occur, or occur in such low amounts that they are unlikely to have an effect.

So while Prof Heinemann and friends do raise important points I think it unlikely that this crop will cause the disease.  It is important to say, however, that CSIRO needs to be sure that they aren’t using sequences found in humans, and need to disclose that. Part of the problem here is the secrecy around intellectual property. I cannot judge if they have or have not used the sequences similar to humans because they haven’t told me. They would be bloody stupid if they had used those sequences!  As an aside, it is also odd that, even though Prof. Heinemann is correct in his statement that the plant and human genes are similar, he uses a sequence from another plant, not wheat, in his analysis.

But the way this issue has been raised seems unhelpful. By producing a press release as the decisions on this crop are made, rather than engaging with the decision-making process, two things have been lost. One is credibility. By not engaging with the decision-making process, but then releasing a scientifically backed query about the plants, you make it look like your aim is to disrupt, rather than inform. The second thing lost is the opportunity to improve the plants being produced. No company wants to sell a new strain of plants that would cause a human disease, or even target a human gene unexpectedly. If CSIRO haven’t thought about, and mitigated against, the issues raised, then they may have done if they had been informed earlier. Now there is mistrust and anger, neither of which helps the general public get the high quality, safe products they deserve.

So two problems here; secrecy because of intellectual property, and lobbying, not engagement. We need light not heat!

Actually it’s freezing here in Otago, so heat would be good too….

Isn’t the really interesting thing here the idea that plants might make double stranded RNA to specifically target genes in herbivores. When you eat a carrot, is it directly suppressing some of your genes? And if so what, and why? Isn’t Science cool?

You might have seen the press coverage of the release of the ‘Encode’ data which significantly increases our understanding of the functions of the Human genome. I have spent some time trying to explain it to the public, usually through using very unhelpful metaphors.

I thought, just in case people were still confused ( or more confused), that I’d write something about it.

The Encode consortium takes in more than 400 geneticists from across the world who have just published 30 papers, in various leading journals, about the functional bits of the human genome. This all springs from the publication of the human genome sequence in 2002. That sequence was an enormous achievement, allowing us to see what the genome codes for. What that sequence couldn’t tell us, however, was how the genome works. The Encode consortium has put one foot on the ladder to determining that.

The genome is very complicated, but less complicated than its regulation. Genes are not always turned ‘on’, indeed different genes are ‘on’ in different cells and tissues, and make those cells and tissues different from one another. Embryogenesis can be thought of as a vast programme of events, that, in a coordinated fashion, turns on the correct genes at the correct time and place, and turns off genes that shouldn’t be on in that cell type. With 20,000 odd genes in your genome, all of which are expressed at multiple times in your life and in multiple tissues, you can see that controlling when a gene is on or off is not only very complex and difficult, but key to understanding many Human conditions, including cancer.

This is the problem the Encode consortium has aimed to address. Using many different techniques they have begun to identify the ‘control elements’ that regulate the activity of a gene. Just to make life difficult, it turns out that their are multiple layers and types of such control elements,all acting to ensure your genes behave nicely. The published papers include ones on transcription factor binding sites, non-coding RNA, DNA methylation, chromatin modifications and more and more (Nature has a great site if you want to explore the papers)

This breakthrough is built on three things.

Firstly; The Human genome sequence and the variation we are finding in human genomes as we sequence them.

Secondly; new and novel techniques, often pioneered by the modENCODE consortium, who have being doing the same work in model organisms like fruit flies and worms.

Thirdly, and I think most importantly, a group of scientists, working across disciplines and national borders to address this massive problem.

I firmly believe that this approach is the future of modern biology, crowd-sourcing knowledge and expertise to help your own work, but also to ensure your work is contributing to the biggest problems that biology can provide. I long for the day my more traditional colleagues wake up to the fact that the paradigm of modern biology is changing, and open collaboration is the key.

Enough ranting. Mark the 6th of September 2012 as a big day in Genetics. My congratulations to ENCODERs around the world.

- for those of you who want a metaphor, it’s like the human genome is like a piano, and ENCODE has just found a book of music. Or, the human genome is like a Christmas pudding and the genes are the raisins…  Nope…

The media has been all of a flurry this last week over a paper by Mattison et al out of Maryland, reporting on the lifespan extension effects of caloric restriction in Rhesus monkeys – or more specifically, the lack of lifespan extension after caloric restriction in Rhesus monkeys.

The paper created such a stir because in the majority of model organisms, the restriction of access to food, without inducing malnutrition, is sufficient to cause a significant lengthening of life. To further complicate matters, a similar study reported earlier in 2009, by a different research group, found the monkeys did exhibit an extension of lifespan as a result of caloric restriction. And of course, the media loves the sensationalist view of something either making humans live forever – or denying them that opportunity.

Caloric restriction is the term given to the practice of limiting the ingested number of calories via diet to below that of which would be consumed freely, or ad libitum (access to as much food as you want, whenever you want). The research field, specifically investigating the extension of lifespan as a result of altered nutrition, and the mechanisms behind the control of it, has actually made a move more recently towards calling the phenomenon Dietary Restriction, to reflect a change in the knowledge. It is possible to induce this extension of lifespan effect by composing the diet of different macronutrients (so different levels of protein and carbohydrate) while maintaining the same calorie value, thus the calories themselves are seemingly not that important.

Traditionally the field has focused on the laboratory staples: nematode worms, fruit flies and house mice. The extrapolation of the research to more complex organisms, and primates in particular, is an exciting step forward. In this case, however, it might prove to be a tad premature.

This particular study used two groups of monkeys; old-onset monkeys, with whom the CR protocol was implemented later in life, at around 16 – 23 years of age, and young-onset monkeys for whom diet was restricted from an early age, unspecified and not included in the supplementary information. The only indication of the starting ages of this group is “young-onset (includes juvenile, adolescent and adult)”, and presumably younger than 16 – 23 years. The study was begun in 1987, obviously before any of the current knowledge was amassed, or modern techniques established to regulate dietary macronutrients. In terms of a longevity study in a long-lived organism, however – this shows remarkable foresight. The young-onset group of monkeys contains some still alive today, coming on 30 years of age, with the older-onset group having died out by ~40 years of age.  These monkeys are older than I, and have been involved in lifespan research science for longer as well.

The numbers of animals in each category is fairly small, but with regards using primates as a research model, the expense for so many years must be extremely prohibitive. There were 22 young males eating normal food and 20 eating a restricted diet. 24 young females on normal food and 20 on restricted diet. In the older-onset group there were only 10 males eating normal food and 10 on a restricted diet, and 8 females on normal food and only 7 on restricted diet.

The analysis of the data (and some fancy statistics) to date shows males to be living longer than females, but within the sex groups there is no significant difference in lifespan – it doesn’t appear to matter what the monkeys are eating, they’re living for the same length of time. The study also investigated fasting serum triglycerides, cholesterol, and fasting serum glucose (Have a closer read of the paper if these measurements interest you).

The main point of contention, as I see it, is the disparity with the results of the WNPRC study, based in Wisconsin. This study showed in preliminary results (due to the entire cohort not being dead yet, and again some fancy statistics) that in Rhesus monkeys fed a 30% calorie restricted diet from adulthood onwards (7-14 years, and in this case falling into the current studies ‘young-onset’ group) survival was improved over that of control animals.

So what is different? Why are the studies showing different results? The paper is actually very good at addressing such questions, and has a very objective yet nicely argumentative tone. ‘These are the issues, look at this data compared to this data’ with no sweeping generalisations and making it a delight to read.

Firstly, the diets fed to the animals were different between studies. The current study used a natural ingredient-based diet, where the Wisconsin study used a purified, specified ingredient base, with added minerals and vitamins. The second biggest difference I find important is that the monkeys in the control group in the current study were not truly fed ad libitum, they were to some small degree restricted in their diet, though less so than the experimental restriction group. While this distinction prevented obesity in the current study, the group as a control was better in the Wisconsin study, where the monkeys could regulate their own intake and eat as much as they wanted.

The third difference which I find particularly notable is the origin of the monkeys in the studies. The current study included monkeys from both India and China, while the Wisconsin study had strictly Indian monkeys. This means the genetic diversity of the current studies group is greater than that of the Wisconsin study, and with such a great genetic influence on lifespan (becoming more apparent through more recent research), this is further muddying the waters of the lifespan results.

So my final impression? This is far less exciting than the articles in The Guardian, Discover Magazine, Nature, Science, WSJ and the rest, lead me to believe. I also think there are further confounding variables which go ignored in such a large-organism study. Did they monkeys have sufficient playtime/monkey-contact/sunlight? Did they suffer from monkey depression or anxiety? Do they suffer from the loss of traditional monkey society? Were the participants mated? The act of mating and the effort of full reproduction has drastic affects on lifespan. If so, were they allowed to stay with their mate/offspring? Was there forced or encouraged activity? Because you can restrict diet, but if one group is exercising more than the other, results would be affected regardless. What was the parental and prenatal situation like, and was it controlled between individuals? Did all the participants have ‘happy’ childhoods and normal early development? Especially in such an intelligent animal, I think such effectors on quality of life are relevant to quantity of life.

Don’t even get me started on such potential studies in humans.

Last week Genetics Otago wrapped up the University of Otago Lecture Winter Lecture Series with a lecture from A/P John Knight who spoke on the marketing aspects of food which has been genetically modified. John’s research looks at the response of overseas markets to genetic modification in New Zealand, and his research suggests that the impact of growing GM crops on our ‘clean, green’ image, would be less than we think it would be.

John can be a polarising figure, and his research has produced surprising results, but the key point here is that it IS research.  John publishes his research, it is peer reviewed, and behind it is solid data.

Whilst many people may not agree with what John is saying, it is interesting to note that before his talks on Wednesday and Thursday last week, GE Free NZ issued a press release stating that John’s work is outdated, with demands that the University of Otago put caveats on John’s work .

So what is the truth here? The fact is, John has taken the initiative and he’s asked the questions and investigated an aspect of Genetic Modification that I think many New Zealanders want to know about. One issue raised at the Royal Commission on Genetic Modification is the impact on our overseas image; John has done some research to address that. You might think his methods are wrong, or that he asked the wrong questions, but at least he has asked the questions, and openly presented the data with the methods used to obtain it; giving us the opportunity to interpret what he says, and make our own mind up.

Research doesn’t always provide us with an answer to the question we want, but what it does do is provide data that can be used to make an informed decision. Surely this is what we need in contentious issues such as Genetic Modification which is obviously an issue that excites strong feelings. In a contained, controlled, research context it is a vital tool to help us understand and improve our world.

Should we be growing transgenic crops? Is Genetic Modification the way forward? The answers to those questions are for YOU to decide. But rather than pre-empting research in a negative fashion, let’s welcome and encourage open discussion where data, and research, is valued, rather than undermining it because it doesn’t agree with your point of view. Yes, there are good reasons NOT to grow transgenic crops in NZ, and good reasons to do so. But let’s allow data, with an understanding of how it was generated, to inform the process so we come to solutions that are informed and sensible.

We do no damage to our international reputation by not growing GM crops, but our reputation will truly be damaged if our stand is based on fear and loathing, rather than informed decision making.

I love books.  I’m just that kind of person.  I also love genetics, convenient then (or deliberate, depending your world view) that I am, or will soon be, a professional research geneticist.  Earlier this month a research group split between Baltimore and Boston published a brief paper detailing their method for storing large amounts of data in DNA form – specifically, a book encoded in DNA.

The research was designed as an effort towards solving the “Big Data” problem.  BD is the term affectionately given to the problem facing a society which, when the ability has presented itself, wants to save everything.   (Those file copies of assignments you did at uni 7 years ago which you still have saved on your hard drive, for example).  For big businesses like Google, the problem is vastly exacerbated.  Having access to smaller and smaller means of data storage makes saving bigger and bigger amounts of data possible.  (Let’s not debate the self perpetuating cycle, for the moment).

The researchers, from the departments of Genetics and Biomedical Engineering, worked with the proposal of using DNA as a format of large-scale data storage.  DNA is, as you learnt at high school, the means through which living organisms store the data required for building and maintaining a body through its lifetime.  This information is encoded in four nucleotide bases; adenine, thymine, cytosine and guanine, which pair up A-T, C-G to form a ladder or helix shape, which in turn can be packaged up to fit inside the nucleus of a single cell.  If you are unsure of just how small a single cell is (or how completely mind-blowing our universe), I suggest you have a look at this delightful interactive info graphic.

As a proof of concept, the researchers converted a book, a draft of something, containing 53.5k words, 11 .jpg images and 1 Java script program (I would love to know what it was; why was that information not more notable?!) into a 5.27 megabit bit stream of binary code.  This string of 0s (A or C) and 1s (G or T) was then synthesised into a DNA strand in 159 nucleotide-long blocks.  These blocks contained 96 nucleotides of book data, a barcode to give the ‘address’ or location of the piece (19 nucleotides), and a tag sequence of 22 nucleotides at either end for amplification and sequencing of the DNA.

The DNA strands were synthesised using what is basically a very, very small inkjet printer, on a glass slide, or ‘microchip’.  Once the book was printed as such, the researchers reversed the process to prove their ability to do so.  The ‘library’ was amplified using PCR and sequenced using Illumina HiSeq, which is just a brand name for a machine capable of reading the sequence of bases contained within a DNA strand and displaying it in a readable format.  Each wee piece of the book was read 3000 times, a common process in DNA sequencing, to ensure the code is correct and the reading trustworthy.  In this particular case, the entire book was retrieved from the DNA with an error rate of 10 bit errors out of 5.27 million (so 10 tiny errors in 5.27 million digits of binary code).

The use of DNA as a data storage mechanism is favorable due to its ability to pack such large amounts of information into a small scale, and to last for, potentially – millennia, but also to store that data in a 3D state – you could have a cup full of information for example, instead of a single sheet.  As the technology for synthesising and reading DNA becomes more exact, simpler and cheaper, this option of data storage becomes more and more attractive.

This experiment has actually been attempted before.  In 1988, small messages in DNA were demonstrated, as a science-art collaboration, the fascinating journal article of which is actually worth a read.  The scale and specificity of the current study however, are unique, and the complete storage of a book, is delightful.  It was this aspect of the study which fueled the media attention, and misled some readers: “Other applications of the technology they are overlooking… 1st off, the ability to upload or inject a file of data directly into a subject. Secondly, being able to extract our DNA and literally break down every experience into reading material. Imagine learning to play a violin with a simple injection of DNA or find out that you already know how because it has been recorded into your DNA and passed down for generations!”.  Perhaps misunderstanding the function and reality of DNA…

However, it also induced a pithy comment from Mashable writer, Peter Pachal, when discussing the immortal language of DNA and future generations retaining the ability to read it (ignoring the fact that the language etcconverted is still modern, and subject to change), that this is a premise “that assumes artificial intelligence doesn’t exterminate or replace human society, of course”.  At which point one would assume the ‘Big Data’ problem, is no longer a pressing issue.

Upon arrival the meeting was  in many respects already in full swing. The Brain Researchers were deep in thought, the Cancer Biologists and Drug Discovery scientists engrossed in conversation. What a wonderful atmosphere – and right here in Otago!

In just a few hours the Honourable Steven Joyce is expected to open the meeting officially, and from then on… Headlong into the Science! Stay tuned as the adventures unfold at Queenstown Research Week!