The Cabbages of Doom

Every now and then, a piece of science is done that is truly ground-breaking and world changing. One such piece is:

Hutchison III CA et al. (2016) Design and synthesis of a minimal bacterial genome. Science 351(6280): aad6253-1. DOI: 10.1126/science.aad6253

Science has a summary here but it’s worth reading the whole paper. Syn 3.0 itself is pretty impressive, but what’s even more impressive is the approach taken to make it. In addition to using current knowledge of fundamental biological machinery, the Venter group used large-scale transposon mutagenesis and selection to identify additional genes that were either essential (i.e. no growth without them) or “quasi-essential”, where removal resulted in a major growth deficit.

They also had to overcome the problem of redundancy: even in a genome as reduced as the Mycoplasma species, there can sometimes be multiple genes that do the same thing. Removing one makes little difference but removing both is lethal - something hard to identify when knocking out single genes at a time. Whatever the Intelligent Design crowd would like to believe, biology is messy.

Of course, Syn 3.0 is just the start, as the goal was making a “minimal cell”:

“A minimal cell is usually defined as a cell in which all genes are essential. This definition is incomplete, because the genetic requirements for survival, and therefore the minimal genome size, depend on the environment in which the cell is grown. The work described here has been conducted in medium that supplies virtually all the small molecules required for life. A minimal genome determined under such permissive conditions should reveal a core set of environment-independent functions that are necessary and sufficient for life. Under less permissive conditions, we expect that additional genes will be required.”

Robust life will therefore need a lot more genes. It will be interesting to see how many are required for autotrophy - life that needs only inorganic chemicals and an energy source.

Even within the “minimal cell” concept, Syn 3.0 represents a somewhat arbitrary end-point. In identifying the “quasi-essential” genes, a judgement had to be made regarding what constitutes an acceptable growth rate*. Whittling down to 473 genes is impressive, but this number could no doubt be even smaller if slower growth rates were accepted. (Modern life is in competition with lots of other highly evolved organisms. Early life would have been able to get by with much lower growth rates, so this is not a “minimal cell” in that context.)

There is also a lot of exciting potential ahead for manually reducing the number of genes by true intelligent design. Fusing interacting gene products together, for example, might eliminate the need for so many genes contributing to core processes. (Looking for apparent protein fusion/fission events in evolution is a reasonably successful method for predicting protein-protein interactions.) With time, we might be able to “wind back the clock” and remove some of the unnecessary complexity that has probably crept into the system due to the underlying evolutionary process.

I also wonder how many of the current crop of genes of unknown function - a surprising 149 genes - can be replaced over time with genes of known function. (In other words, how many of them represent convergent evolution of functions we already know about but are not recognisable.) And how many of the rest are genome-/condition-specific?

Like all of the best science, this work opens the door to more questions than it answers! Some exciting times ahead, I think.

[*The important but oft-overlooked concept that any assessment of life is context- and environment-dependent exposes another flaw with Intelligent Design as a testable hypothesis: designed to do what? To assess how well-designed something is, one needs to know its purpose and/or the acceptable design traits. To hide from the fact that Intelligent Design is Creationism, supporters often make the argument that the identity of the designer (Creator) is not important - but without knowledge of the designer, how can one predict the motivation behind the design?]

The Sydney Society for Conservation Biology (SCB) have Michael McFadden, the Unit Supervisor of the Herpetofauna division at Taronga Zoo, for 2^nd May’s Conservation Cafe. That’s reptiles and amphibians to the rest of us:

This May, Sydney-SCB welcomes Michael McFadden, the Unit Supervisor of the Herpetofauna division at Taronga Zoo. Michael began working at Taronga Zoo in January 2003 and now oversees the maintenance and husbandry of the Zoo’s collection of reptiles and amphibians. He works closely with the Zoo’s conservation projects which include captive breeding and release programs for the highly endangered Southern and Northern Corroboree Frogs. The current focus of Michael’s work is developing techniques to improve captive breeding and rearing success in threatened Australian frogs and reintroduction biology.

As before, it’s free: RSVP on Eventbrite.

Courtesy of the Molecular Biology and Evolution Facebook page comes this awesome cover art:

According to the MBE Editor:

The author and artist info: The cover image depicts representative squamate species (lizards and snakes) playing poker, with the card and chip colors representing the sex-determining system most prevalent in each clade. The tabletop shows results from a comparative genomic analysis of squamate sex-determining mechanisms by Gamble et al in this issue. This study discovered that changes between sex-determining mechanisms in one clade, geckos, account for a half to two-thirds of the total transitions known in lizards and snakes. This remarkable frequency of transition is reflected in the illustration by the heightened activity at the gecko side of the table: the three gecko species in the foreground are cheating, implying that when it comes to sex determination, geckos do not play by the rules. The image was created by University of Minnesota biologist and artist Anna Minkina and pays homage to the Cassius M. Coolidge painting, “A Friend in Need”, part of the artist’s “Dogs Playing Poker” series.

h/t: James McInereny

Last year, I went down with tonsillitis on New Year’s Eve. The timing sucked a bit but I guess there are no good times for such things to happen. However, I was/am lucky: lucky because I live in an age where antibiotics are available and still work.

As a scientist, I often get frustrated about science funding. Firstly, there’s not enough of it (compared to other endeavours of less benefit to both society and the economy) but secondly, a lot of it goes to the wrong places, namely human diseases such as cancer. Don’t get me wrong: I’d love to see cancer cured. It’s just that there are bigger fish to fry, and global crises looming that would make diseases of old age such as cancer and Alzheimer’s a bit of a moot point.

An obvious need of greater funding is climate change, thrown into the spotlight again (as if it were needed) by the confirmation that 2014 was the the warmest year on record. Another is the development of new antibiotics.

Antibiotic resistance is a big problem and one that is currently only getting worse. We are heading for a “post antibiotic world”, which is a really scary thought. Indeed, some scientists have argued that antibiotic resistance is a bigger problem than climate change because we have the technology to combat climate change, we just lack the political will. We do not yet have the technical solution to the impending “antibiotic apocalypse”, hence the real need to throw money at research into solutions.

The annoying thing is that this is not a problem that has snuck up on us. In an editorial from 1997 entitled “Antibiotic Armageddon”, Calvin Kunin from The Ohio State University wrote:

“The advances of the antimicrobial era are being dissipated by the emergence and spread of resistant microorganisms, the inevitable consequence of intense use of antibiotics in humans over the past 50 years. The process is accelerating in the community as well as in hospitals and is a problem worldwide. The attrition of older drugs is sustained by the selective effects of new and more expensive drugs developed to overcome resistance. Novel compounds will no doubt be discovered, but their demise is inevitable. It is just a matter of time until resistant pyogenic organisms join the opportunistic microbes as major threats to humans.”

…

“[The] long-term outlook for control of antibiotic resistance is bleak. There are simply too many physicians prescribing antibiotics casually and too many people buying antibiotics without a prescription in developing countries. There is only a thin red line of infectious diseases practitioners who have dedicated themselves to rational therapy and control of hospital infections. The issues need to be presented forcefully to the medical community and the public. Third-party payers must get the message that these programs can save lives as well as money.”

Sadly, if these words were written today, I don’t think anyone would argue the point; not much has changed. And that’s without even mentioning the big problems caused by the long-running over-use of antibiotics is agriculture.

Things are not without hope. Earlier this month, a Nature paper by Lin et al. reported the discovery of a novel class of antibiotic from a screen of 10,000 bacterial strains, following the development of novel method to grow hitherto uncultured bacteria:

“Antibiotic resistance is spreading faster than the introduction of new compounds into clinical practice, causing a public health crisis. Most antibiotics were produced by screening soil microorganisms, but this limited resource of cultivable bacteria was overmined by the 1960s. Synthetic approaches to produce antibiotics have been unable to replace this platform. Uncultured bacteria make up approximately 99% of all species in external environments, and are an untapped source of new antibiotics. We developed several methods to grow uncultured organisms by cultivation in situ or by using specific growth factors. Here we report a new antibiotic that we term teixobactin, discovered in a screen of uncultured bacteria. Teixobactin inhibits cell wall synthesis by binding to a highly conserved motif of lipid II (precursor of peptidoglycan) and lipid III (precursor of cell wall teichoic acid). We did not obtain any mutants of Staphylococcus aureus or Mycobacterium tuberculosis resistant to teixobactin. The properties of this compound suggest a path towards developing antibiotics that are likely to avoid development of resistance.”

Personally, I remain skeptical about claims that teixobactin is resistance-proof. It may not be easy but I am sure the bugs will stumble across a way to evade or destroy the toxin and evolve resistance. Nonetheless, the message is clear: there are new antibiotics out there to be found. This one was found in the backyard of one of the researchers! Bacteria have been killing each other for millions, maybe billions, of years and so the global diversity in nature is likely to be massive. We just need the ingenuity and funding to find them.

References

Farrar J & Woolhouse M (2014). Policy: An intergovernmental panel on antimicrobial resistance. Nature 509:555–557

Kunin CM (1997). Antibiotic Armageddon. Clinical Infectious Diseases 25:240–1

Lin LL et al. (2015). A new antibiotic kills pathogens without detectable resistance. Nature doi:10.1038/nature14098

Via the Youtube channel of a friend from (but no longer in!) Dublin, Jonathan Gordon, here are some awesome videos of octopus camouflage. (Yes, I know that “octopuses” or “octopodes” is more correct for the plural but “octopi” is more fun!) I’ve seen this kind of thing on documentaries before but never realised this kind of thing could happen when just “[diving] down to look at a shell”.

The screenshots give the game away, sadly, but even when you know it’s there, the camouflage is still so amazing that the octopus is hard to spot.

And if that’s too scary for you, here is another video from Jon featuring an über-cute baby octopus “walking on the beach”:

Yesterday’s excellent Australian Pathogen Bioinformatics Symposium 2014 (#APBS2014) reminded me that this post was a bit overdue: originally posted at the UNSW Science Wavelength blog on October 30, 2014. Following APBS2014, we are also looking into how we can identify which other pathogens might be using a similar strategy.

Read more at the Edwards Lab blog…

Kinases are one of the biggest and most important classes of enzymes (i.e. protein with catalytic activity) in biology. You can always recognise an enzyme because of the suffix “-ase”. What comes before the -ase then indicates the nature of the enzymatic activity.

The major classes of enzyme have names that give a good clue as to the general nature of this activity. Oxidoreductases, for example, catalyse oxidation-reduction (“redox”) reactions. Transferases transfer chemical groups from one molecule to another. Kinases are transferases: they transfer a phosphate group from one organic molecule (usually ATP, the cell’s primary energy carrier) to another (a protein, lipid or carbohydrate). And this is actually the origin of the kin- part of the name: from the Greek kinein “to move”.

For those wondering, there is also such as thing as a Phosphorylase but this does something subtly different; whereas a kinase transfers organic phosphate groups (i.e. phosphates attached to carbon-based biomolecules), a phosphorylase transfers inorganic phosphate groups (i.e. phosphate+hydrogen) to acceptor biomolecules.

But why -ase? This stems from the ending of diastase, the first enzyme ever discovered. According to Wikipedia:

“The name “diastase” comes from the Greek word διάστασις (diastasis) (a parting, a separation) because when beer mash is heated, the enzyme causes the starch in the barley seed to transform quickly into soluble sugars and hence the husk to separate from the rest of the seed.”

So there you have it. A kinase is an early example of an enzyme that moves something from one molecule to another, hence a name that literally means “an enzyme to move”.

It was looking inevitable and this week two high profile Nature articles on “STAP” (stimulus-triggered acquisition of pluripotency) stem cells were finally retracted in Nature:

Several critical errors have been found in our Article and Letter (http://dx.doi.org/10.1038/nature12969), which led to an in-depth investigation by the RIKEN Institute. The RIKEN investigation committee has categorized some of the errors as misconduct (see Supplementary Data 1 and Supplementary Data 2). Additional errors identified by the authors that are not discussed in RIKEN’s report are listed below.

...

We apologize for the mistakes included in the Article and Letter. These multiple errors impair the credibility of the study as a whole and we are unable to say without doubt whether the STAP-SC phenomenon is real. Ongoing studies are investigating this phenomenon afresh, but given the extensive nature of the errors currently found, we consider it appropriate to retract both papers.

Nature cover the retractions in an editorial, “STAP retracted”, which runs with the tagline,

“Two retractions highlight long-standing issues of trust and sloppiness that must be addressed.”

You can get a sense of those issues from the retraction statement and the editorial, which concludes:

“we and the referees could not have detected the problems that fatally undermined the papers. The referees’ rigorous reports quite rightly took on trust what was presented in the papers.”

They also highlight “sloppiness” in science, manifest as a “growth in the number of corrections reported in journals in recent years”. (Something not helped, in my opinion, by high profile journals such as Science and Nature burying so much of the important methods in Supplementary Data, which is rarely reviewed or edited as critically as material in the main text body.)

You can read more about those issues in the editorial and elsewhere, such as the Faculty of 1000 blog. The STAP papers, their initial irreproducibility and eventual retraction highlight potential failings of the current scientific system, which places far too much emphasis on output quantity and impact rather than (true) quality and integrity.

However, they also highlight the tremendous success of the scientific system.

The fact is, the experiments were repeated, the failure to reproduce results was documented, suspicions were raised and investigations made. Science works because, ultimately, you cannot fake it. Whatever data you make up, whatever results you misinterpret, whatever sloppiness leads to “conclusions [that] seem misleadingly robust”, the truth will out eventually. You cannot hoodwink nature.

And that is why science remains far and away the best (probably only) method we have for establishing the truth about reality. The system maybe flawed, it may waste money and it may lead poor unsuspecting suckers chasing wild geese, but eventually it will self-correct. So, whilst I would never put my trust in individual scientists (unless they have earnt it) or results, and I remain skeptical of every new claim, I still emphatically trust science itself.

I was sad to read a post on the Evolution Directory (Evoldir) by my PhD supervisor, John Brookfield, that Professor Bryan Clarke died last month. Bryan founded the Genetics Department (later Institute and now Centre for Genetics and Genomics) at the University of Nottingham , where I did both my undergrad degree and PhD. He and retired when I was still an undergrad but, as Emeritus Professor, he was still heavily involved in the department for the rest of my time there.

Although I did not know Bryan well, he always had time for students and was an inspirational character - and that was before the Frozen Ark project was launched. I was particularly impressed by the way that he managed to combine ground-breaking basic science with regular visits to Pacific island paradise!

With permission, I have repeated John’s post below:

It is with great sadness that we have to report to the evolution community the death of Professor Bryan Clarke FRS on Thursday, the 27th February 2014.

Bryan Clarke was a leader in our understanding of the process of evolution for more than four decades. He made fundamental contributions, both empirical and theoretical, particularly in elucidating the forces that maintain genetic variation in populations, and in throwing light on the process of speciation.

Bryan was born on the 24th June 1932, and, following service in the Royal Air Force, was educated at Magdalen College Oxford, from where he received both his BA in 1956 and DPhil in 1961. From 1959 to 1971 he worked at the University of Edinburgh, starting as Assistant Lecturer and rising to a Readership. In 1971 he was the Foundation Professor at the new Department of Genetics at the University of Nottingham, and remained until 1997, when he became Professor Emeritus.

The Darwinian theory of evolution by natural selection identifies genetic differences in populations - polymorphisms, as the key to evolutionary change. It is of fundamental interest whether polymorphisms are affected by natural selection, or solely by genetic drift. Bryan’s research focussed on polymorphisms in snails, including members of the genus Cepaea, the shells of which vary greatly in colour and in their banding patterns. While some had naively suggested that this variation might have no effect on the organisms’ fitness, earlier experiments and observations, from Cain and Sheppard in particular, had demonstrated that these variants were indeed subject to natural selection. But, if there is selection operating on this genetic variation, why does the population not come to consist of only a single, best-adapted, type? The answer is that selection can, in some circumstances, maintain variation rather than destroying it. One mechanism for the maintenance of genetic variation is heterozygote advantage, which explains, for example, the high frequency of the allele causing sickle cell anaemia. Bryan knew that the patterns of inheritance of the polymorphisms in Cepaea could not be explained by heterozygote advantage. Rather, he was able to demonstrate that these are maintained by a different mechanism, frequency-dependent selection, in which the fitness of genetic types increases if their frequencies in the population diminish, thereby creating a stable equilibrium in which multiple genetic types are maintained. His studies of frequency-dependent selection were able to demonstrate the near-ubiquity of this phenomenon when visible polymorphisms are studied in wild populations, and also showed the selective agents which brought this about. The frequencies of polymorphic variants in snails can vary greatly in space, without any obvious environmental correlates. An important and influential step in the understanding of such “area effects” came from Bryan’s models of morph-ratio clines in his 1966 American Naturalist paper.

Studies of visible polymorphisms were augmented, from the 1960s, by the study of polymorphisms in the amino acid sequences in proteins, investigated initially through electrophoretic detection of differences in the electric change on enzyme molecules. As with the visual polymorphisms in Cepaea, some assumed that the changes were invisible to natural selection. Bryan Clarke advocated the view that a large proportion of the changes were indeed subject to natural selection and demonstrated experimental support for this view, particularly for variants in the enzyme alcohol dehydrogenase in Drosophila melanogaster. The study of selection acting on polymorphic differences in amino acid sequences is a direct way to obtain evidence about whether the long-term evolution of the amino acid sequences of proteins is shaped by natural selection. Some believe that protein evolution is almost completely dominated by random forces in which the successful variants were so not because of the advantages they gave to their bearers, but as a result of genetic drift. Bryan Clarke was one of the main advocates of the view that a large part of the evolutionary changes in the amino acid sequences of proteins were indeed driven by Darwinian natural selection, a view that results from large-scale DNA sequencing are confirming in many species.

Bryan Clarke also played a large part in developing our understanding of the process through which species form. He carried out a long-term study of species of the land snail Partula on the South Pacific island of Moorea and neighbouring islands. He appreciated that, in the early stages of speciation, matings between members of populations undergoing speciation do not stop instantly- some hybridisation persists. Species stay distinct notwithstanding there being some gene flow between them. Thus, selectively important genetic differences between species, such as those determining form, colour and behaviour, are maintained as distinct and recognisable features, while the low levels of gene flow resulting from hybridisation allow genetic differences which are not selectively important to randomise themselves between the hybridising forms. These phenomena have been documented in Partula, where less important differences have been shown to be shared between species which live in the same geographic location. The ability to study these early events results from the choice of the Partula species, where speciation has been “caught in the act”. Increasingly, similar phenomena are now being documented in patterns of DNA sequence diversity in other species studied at these early stages.

Through these diverse achievements at the cutting-edge of understanding of the process of evolutionary change, Bryan Clarke was a great mentor and role-model for younger scientists in evolutionary genetics, and supervised more than thirty research students, at least six of whom are now professors. He was a co-founder of the very successful Population Genetics Group, a meeting for population geneticists from the UK and Europe that has been running for almost fifty years.

He was co-founder and trustee of the charity “The Frozen Ark”, which preserves, in the form of DNA and cell lines, the genetic material of endangered animals, to allow future scientific study.

Honours and awards for Professor Clarke reflected his outstanding role in modern evolutionary genetics. He was elected a Fellow of the Royal Society in 1982, became an International Member of the American Philosophical Society in 2003, and a Foreign Honorary Member of the American Academy of Arts and Sciences in 2004. Medals and awards include the Linnean Medal for Zoology in 2003, the Darwin-Wallace Medal of the Linnean Society in 2008, and the Royal Society’s Darwin Medal in 2010.

Bryan leaves his wife Ann, his son Peter and daughter Alex.

Picture from Bryan Clark's obituary in The Telegraph.

I’m deep in grant- and lecture-writing at the moment (hence the lack of posts) but the QS World University rankings are out for 2013/2014 and UNSW is ranked 50^th in Biological Sciences. Obviously, I haven’t been there long enough to have contributed to this but still good news and worth a mention! Overall, UNSW was ranked 52^nd.

Pretty good result for the University of Southampton at 86 too. (U. Sydney is 38^th but you can’t have everything! :op)

After 24 hours, not a lot…

I am not entirely sure whether MOOCs (Massive Open Online Courses) have any tangible benefits to the participants (or the hosting institution beyond publicity). Nevertheless, there is no denying that they represent excellent value for money (being free!) and are a great opportunity to learn some really interesting things.

If oceans are your thing and you have a bit of spare time in February and March then check out the Exploring our Oceans MOOC being run by Oceanography at the University of Southampton:

In this six week interactive course, you will see how the ocean depths are no longer out of reach and how they are connected to our everyday lives. We will engage you in our most recent expedition findings and share our knowledge on the least touched areas of our oceans.

Together we’ll look at the animals that swim in these dark waters, the creatures that live on the seabed and the makeup of the underwater environment they live in.

Visit the Exploring our Oceans MOOC page for more details - or to sign up!

When one pictures fossil hunters, one normally imagines someone carefully chipping and brushing away at some exposed rock. The picture that springs to mind is rarely someone sitting on a box of explosives. With Professor Mike Archer at UNSW, however, that’s exactly what you get.

I first found out about Mike’s extraordinary approach to fossil hunting at the UNSW family BBQ a couple of weeks ago. As described in the Australian Wildlife notes on Riversleigh, a world heritage fossil site in north-western Queensland: (my emphasis)

As water dissolves the rock, bones and teeth can be seen protruding from the rock. Releasing them from the rock is not so easy. Quarrying techniques must be used, including the occasional use of light explosives. Many of the areas are so inaccessible that the larger rocks have to be broken up with sledge hammers, bagged and labeled and lifted out by helicopter.

Once they finally reach the laboratory, the fossils are freed by dissolving away the surrounding limestone with dilute acetic acid. After treatment with preservatives, the fossils are then ready for study by scientists.

This approach has reaped rewards, including the recently reported giant toothed platypus fossil.

Another example of dramatic palaeontology doing the rounds is the amazing set of dinosaur footprints in a Bolivian quarry, which presumably were unmasked by something similarly explosive.

Opponents of evolution often point erroneously at the gappy nature of the fossil record, conveniently ignoring that not only do past organisms need to have been subject to the relatively rare conditions that result in fossilisation but then that bit of rock needs to be exposed again and then someone needs to find it before it’s destroyed! Given of all this, I think that the fossil record is actually remarkably complete! (Not to mention, of course, that even as more and more fossils get added, the fossil record is entirely consistent with evolution and extremely inconsistent with a recent global flood or Young Earth Creationism.)

Today we went to the Australian Museum in Sydney. The main reason for the visit was to join and get tickets for the Tyrannosaurs: Meet the family exhibit but, even with a very lazy Sunday morning, we had a bit of time to wander round some of the exhibits and so paid the Australian fauna section a visit. I’d already been back in February when I was over for my job interview but you always spot new and interesting things in a museum like this. Today’s interesting fact…

Unfortunately, the museum had little more information than that but thankfully the internet is more forthcoming on faecal facts. (The picture above is from (where else?) Wikipedia.) It appears that the function of the exciting excreta is to stop the stools from rolling away, as they are used for marking territory etc. The secret to the shaping of the poo is the moisture content, apparently. So there you go. My other interesting wombat fact is that their pouches open backwards relative to other marsupials, which stops them from filling up with dirt when burrowing.

You can find out more at a page at “Today I found out about”: Wombat Poop is Cubic and Other Fascinating Wombat Facts. It’s a sadly ad- and pop-up-riddled page but does end with the great “bonus fact”:

Wombats are protected under Australian law, presumably mostly due to being awesome.

The old adage that “you are what you eat” is not really true unless you are thinking at an atomic level. Even here, a lot of stuff passes straight through you or is absorbed only to be filtered out again because it is toxic and/or you have too much of it. The exception, perhaps, is bacteria.

Bacteria get a bit of a rough ride from most humans, largely because most of the bacteria that we have been historically aware of - and interested in - have been harmful to our health. Apart from saving humanity from the Martians, what have bacteria ever done for us? Well, lots to be honest and we certainly wouldn’t be here without them. Not just that but we would be without them.

As highlighted in this week’s BBC Discovery podcast, one of the most important realisations of the past few years has been the importance of what we call the “human microbiome”, i.e. the total microbial (e.g. bacterial) complement of the human ecosystem - and an ecosystem is exactly what you and I are. The idea of a human navigating his or her way through the world as an individual animal - occasionally under attack by parasites - is an idea that is pretty firmly fixed in our sense of self but it is really a falsehood.

The “friendly bacteria” of yakult etc. have popularised the notion that not all bugs are out to get us and that some of them are actually our allies but I still think that most people are probably unaware of the role they play and just how crucial they are to our health (and, when things go wrong, ill health). In many ways, an individual person is more bacterial than human. Not in terms of biomass, it is true, (for bacteria are small) but in sheer numbers the microbes have it: 10 trillion cells may sound like a lot but there are approximately 100 trillion bacteria in the average human. A lot of fuss has (rightly) been made of the Human Genome Project but a human only has around 21,000 protein-coding genes plus a whole bunch of non-coding ones making a total somewhere in the order of 100,000 different genes (no one knows for sure yet). The diversity of bacterial genes in your body is harder still to measure but is estimated to be 100 times this number at around 10 million. (An individual bacterium has far fewer genes that a human cell but there are many different species/strains of bacteria living within you.)

These bugs are important too and play critical roles in priming your immune system, defending you from other unfriendly bacteria and, perhaps most importantly, helping you to digest your food. Indeed, the biggest concentration of bacteria is in the intestine and the population here is heavily influenced by diet - part of the reason that a major shift in diet can cause some upsets down there. Furthermore, evidence now links a healthy gut population with a healthy person, and poor diets have been implicated as possible contributors to poor health beyond simple nutritional deficits. As a consequence, fecal transplants are now being touted as possible cures for all sorts of gastric conditions.

So next time you find it hard to motivate yourself to have a varied, balanced diet, spare a thought for your microbiome!

[Picture from matt over matter, where you can read even more about the human microbiome.]

I opened my email this morning to the news that Fred Sanger had died. This was not entirely surprising, given that he was 95, but still sad. Although I have never met him, I think it is fair to say that I am one of many scientists whose careers have been shaped and influenced by the work of this great scientist.

I still remember sitting in lectures as an undergraduate and discovering how “Sanger” sequencing worked - like many of the ideas that change the world, it was gloriously simple and yet spectacularly clever. And, I think it is fair to say, it changed the face of biology forever.

Indeed, that was back in 1977, and Sanger sequencing is still used all over the world today, even in the face of stiff competition from “Next Generation” methods. It was the sequencing method (albeit in a much tweaked and automated version) that got us the Human Genome and one of the world’s leading sequencing centres - the Wellcome Trust Sanger Institute at Hinxton, outside Cambridge - still bears his name.

The centre has a press release about the “remarkable man”, which has been written by greater wordsmiths than I:

“Fred Sanger, who died on Tuesday 19 November 2013, aged 95, was the quiet giant of genomics, the father of an area of science that we will explore for decades to come.

His achievements rank alongside those of Francis Crick, James Watson and Rosalind Franklin in discovering the structure of DNA. We are proud that he graciously agreed to allow our Institute to be named after him.

In research marked by two Nobel Prizes, he developed methods that allow us to determine the order of the building blocks of DNA and of proteins. This technique allowed the languages of life to be read.

Because of Fred’s work we have been able to interpret those languages and to use that knowledge for good.”

There is more, including quotes and links out to other resources about his work, at the site.

I remember thinking in those lectures back in Nottingham how I wished that one day I might have an idea as good as Sanger sequencing. I doubt that I ever will; instead, I will just have to settle for trying to do the best I can with all of the amazing sequence data that now exists as a result.

One of the things that first struck us when we arrived in Sydney were the amazing purple trees that could be seen around the place. Although not native to Australia, Jacaranda trees can be found all over Sydney and really stand out with their amazing purple blossom. Sometimes, when the wind blows hard, it looks like purple snow falling to earth.

I don’t really have much to say about them other than I think that they are awesome!

[Top and Bottom, Jacaranda standing out at the Botanical Gardens; Right, Jacaranda outside Sydney Town Hall.]

Reported in last week’s Science News article, The War Against Weeds Down Under, Australian farmers have been getting creative with non-chemical warfare against the weeds that blight their island continent.

Increasingly, weeds are becoming resistant to herbicides and switching to a new herbicide often just results in new resistance after a few years. On top of this, there is generally a progression into nastier chemicals - and more of them - as favoured herbicides lose effectiveness, which is clearly not good for sustainability or the environment.

Australia has particular problems of pest plants with multiple herbicide resistance - one of the worst is a species introduced for sheep feed, Ryegrass - and have been pioneering new versions of more old-school solutions: physical warfare. One of the simplest is just burning the weeds after harvest to destroy their seeds. This is pretty effective - for Ryegrass, at least - but has some disadvantages including loss of nutrients from burning.

An alternative with particular promise is going sheerly physical and grinding weed seeds out of existence. As published in Soil Science last year, Australian farmers and scientists have converted mining equipment called a “cage mill” or “impact crusher” into the “Harrington Seed Destructor”, which is able to destroy a reported 95% of Ryegrass weed seeds. As well as being more effective than burning, all the nutrients from the destroyed chaff is put back into the soil, presumably reducing the need for fertiliser into the bargain.

“Nothing will survive in there…”

Picture from: Walsh MJ, Harrington RB & Powles SB (2012). Harrington Seed Destructor: A New Nonchemical Weed Control Tool for Global Grain Crops. Crop Science 52(3): 1343-1347.

Another advantage of physical destruction over chemical attack is that it seems more difficult for the weeds to fight back. Thanks to the awesome power of Natural Selection, it is probably only a matter of time before resistance evolves to any given herbicide. Whether they could evolve to have seeds small/tough enough to survive the Harrington Seed Destructor is less clear, especially without compromising their competitive advantage. Either way, it’s useful to have another weapon in the arsenal, even if it is a bit pricey at the moment at $A250k. It’s also good to see that future weed management could potentially be effective and environmentally friendly. Hopefully, other countries will follow suit.

Today, I was catching up with some old podcasts. One was the Naked Genetics podcast from last January, which featured a book that I had never heard of but sounded rather cute. It’s called Little Changes and was written by Dr Tiffany Taylor from the University of Reading as a way to introduce evolution (by Natural Selection) to under 11s - and their teachers. I’ve not got it - I don’t have any under 11s - but the preview on Amazon looks fun and the illustrations look sweet too.

I won’t reproduce any sample text here as it is all copyrighted but you can “look inside” on Amazon if you are interested. Apart from someone who (ambitiously) got it for their three year old, the customer reviews are good too.