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Recently, I had an enjoyable chat with Graeme Hill on the subject of sleep. Also on the show was Karyn O'Keeffe, whose research interests are with the physiology of sleep (& the lack of it). My segment focused on the evolution of sleep and yes, I did quite a bit of reading in preparation!

Sleep is mediated by a chemical messenger, melatonin. The onset of darkness triggers the pineal gland to release melatonin, which alters the activity of the neurons in our brains, resulting in sleepiness. Exposure to light destroys melatonin, & so we wake. (Hence the concern about the use of tablets, smartphones etc late into the evening, because of the potential for this to upset the normal sleep-wake cycle.)

One of the things Graeme & I discussed was the evolution of sleep - when did this particular aspect of physiology & behaviour evolve? One of my favourite science writers, Carl Zimmer, wrote about this in 2014. He linked to a study suggesting that sleep may have evolved around 700 million years ago, on the basis of research into gene expression in a marine worm called Platynereis dumerilii.The larvae of these worms move up & down in the water column on a 24-hour cycle (a circadian rhythm), and while the 2-day-old larvae used in the study certainly don't yet have eyes, they do produce and respond to melatonin. Cells on the upper suface of these tiny larvae detect changes in light intensity, and with the onset of darkness, they turn on melatonin production. This stops the beating hairs (cilia) that allow the animals to swim towards the suface, and so they sink slowly down towards the depths. But not so deeply that the light-sensitive cells can't detect dawn's light, which destroys the melatonin and so the larvae swim upwards once again. (Apparently it's even possible to give them jetlag!)

"Well", said Graeme, "why do we sleep? It seems on the face of it a very risky business given the prevalence of nocturnal predators." 

And it's a good question. Why would sleep be selected for, given that you'd think it would make animals more vulnerable to predation? It must have some strong adaptive advantages, to outweigh that risk! Some of the possibilities are canvassed in this short piece in Scientific American, which notes that patterns of sleep and wakefulness vary enormously between species, and also within species depending on time of year - think of hibernation, for example. (Even that varies between species in terms of sleep duration: hummingbirds go into a form of torpor that may last less than a day each time.). The author, Christopher French, suggests that "sleep and related states provide periods of adaptive inactivity" - that is, that a lack of activity can also provide a selective advantage:

Most likely sleep evolved to ensure that species are not active when they are most vulnerable to predation and when their food supply is scarce.

He gives the example of a bat that sleeps around 20 hours a day, rousing to hunt insects that are active in the dusk. Searching for these insects during the day would be fruitless, but would also expose the bats to diurnal predators. But sleep must also be important in some way for the brain, as it's so markedly affected by a prolonged lack of sleep. (And now, I want to know how the melatonin thing works in species like this, that are active at night and sleep during the day. Apparently even nocturnal animals produce the most melatonin at night.)  

A few years back, researchers asked the question, "Is sleep essential?" (Cirelli & Tononi, 2008). (There's an excellent lay summary here - teachers would find it very useful.) I found the paper interesting because, in preparing to test their null hypothesis (that sleep is not essential), the authors first defined sleep:

Sleep is a reversible condition of reduced responsiveness usually associated with immobility.

Most work on sleep has been done in mammals & birds, but it seems that even the humble lab workfly, Drosophila, can be said to sleep: these little flies have periods when they become less responsive to stimuli; if they're forced to stay active, 'sleep pressure' increases; patterns of sleep & wakefulness change with age; hypnotic and stimulant drugs affect their activity; and gene expression in the brain changes with periods of sleep and wakefulness. 

Cirelli & Tononi's paper is open access & well worth reading. They feel that the available evidence doesn't support claims that bullfrogs, for example, do not sleep. Dolphins and other marine mammals, which are constantly moving, still appear to enter a form of sleep - in one hemisphere of the brain at a time - a statement supported by evidence of changes in brain wave activity.

They also discuss the effects of sleep loss - in rats, flies, cockroaches, and humans, prolonged sleep deprivation can ultimately be fatal. (This was the point at which Graeme told me about something called fatal familial insomnia, which sounds awful and is apparently one of the group of prion diseases, along with things like scrapie.) But well before that point, sleep deprivation affects performance, particularly in terms of cognitive performance. So, students take note! an all-nighter or two ahead of major exams is unlikely to work in your favour. 

Cirelli C, Tononi G (2008) Is Sleep Essential? PLoS Biol 6(8): e216.


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I've just come across a most excellent article by the Genetic Literacy Project. In it, Nicholas Staropoli notes that a proportion of the human genome actually has viral origins.

This might sound a bit strange - after all, we tend to think of viruses as our enemies (smallpox, measles, and the human papilloma virus come to mind). But, as Staropoli notes, there are a lot of what are called 'endogenous retroviruses' (ERVs) - or their remains - tucked away in our genome. (An ERV has the ability to write its own genes into the host's DNA.) And he links to a study that draws this conclusion: 

We conservatively estimate that viruses have driven close to 30% of all adaptive amino acid changes in the part of the human proteome conserved within mammals. Our results suggest that viruses are one of the most dominant drivers of evolutionary change across mammalian and human proteomes.

Carl Zimmer writes about one such example in his blog The Loom: it seems that a gene that's crucial in the development of the placenta (that intimate connection between a foetus and its mother) is viral in origin. In fact, one gene encoding the protein syncytin is found in primates - but carnivores have a quite different form of the gene, while rabbits have a different form again, and mice yet another!

This is a very complex evolutionary story indeed. And so you could do much worse than read the two articles, by Staropolis and Zimmer, in their entirety. 


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So, I own a pocket wolf.



Oh, OK, I own a little black mini-poodle. But, like all dogs, he has the same number of chromosomes as a wolf!

There've been several articles posted recently about the evolution of domestic dogs. While we've tended to think that domestication didn't begin until humans began to settle down & develop agriculture, DNA analysis suggests that wolves and humans may have begun a relationship up to 100,000 years ago. And a paper published in Science back in June presents evidence that there were two domestication events, one in Asia and once in either the Near East or Europe. There's a nice visualisation and explanation of the doggy family tree here.

A few weeks ago, I was discussing domestication with RadioLive's Graeme Hill, and one of the questions he asked was, why do we have so many different body forms in domestic dogs, and so little variation in form in cats? Was it because the dog genome is more 'plastic' & susceptible to change? My answer was that I suspected it had more to do with the length of the species' association with humans. Cats are sometimes described as 'semi-domesticated', and our shared history may go back just 10,000 years (with the possibility, again, of at least two separate domestication events). Whereas 100,000 years gives a lot of time for selective breeding by humans to produce all those different dog breeds.

Which takes us to bulldogs - the subject of a Scholarship Biology question in 2014. Bulldogs were originally bred to drive cattle, and had the strength and the ferocity (and presumably also a high pain threshold!) to subdue an animal by grabbing its muzzle and hanging on. They were subsequently used in bull-baiting, a cruel 'sport' that the UK banned in 1835.

Instead, the dogs were then bred for show. While their physical characteristics remained pretty much the same (short & squat, very muscular, the familiar very short face/muzzle with deeply folded skin) - by 1860 they had already begun to develop, as a result of selective breeding, their now-familiar gentle, non-aggressive temperament.

Unfortunately, selection for that very distinctive body form has brought with it a whole host of inherited disorders. You've probably met a bulldog with that snorfling, stertorous breathing - this respiratory problem is called brachycephalic syndrome, due to the very short face & nasal passage. Other heritable disorders include:

  • hip dysplasia (seen too in other breeds, such as labradors), where the hip joint can partially dislocate - this one is due to polygenic inheritance ie there are a number of different genes involved. 
  • a hole between the two ventricles of the heart. This is called ventricular septal defect (VSD), and an animal must inherit 2 copies of a recessive allele to express this disorder. It's autosomal, which means that male and female bulldogs are equaliy likely to express it.
  • cryptorchidism - one or both testes remains up in the body cavity instead of descending to the scrotum. This one is an autosomal dominant trait - only one copy of the allele is required. 
  • and - with all those wrinkles - dermatitis, also considered to be an autosomal dominant trait. The dermatitis often leads to bacterial infections. 

Poor bulldogs :( 

The actual exam question gave this background information & asked students to discuss two things: how humans may have manipulated the evolution of bulldogs from wolves; and how further selective breeding could be used to try to eliminate EACH of the named disorders AND evaluate how effective this might be. For students intending to sit these exams: remember that when you're answering these questions you need to provide both 'evidential' statements and justifications for them. And to do that, you'll need to integrate the resource materials provided in the exam paper with your own biological knowledge. 

The first part's pretty straightforward: you might consider, for example, why humans would want to select for non-aggressive wolves (eg for help in protecting a human or group of humans from other predators). Or what about the founder effect, which would come into play because of that small population of proto-dogs? The small sample of the wolf gene pool found in those first 'dogs' could mean that particular alleles were simply lost in the dog population, while others could become much more common.

You'd then want to address the sort of things a breeder would focus on to get from generalised doggy form to the highly specialised bulldog: insensitivity to pain; the short, powerful, upwards-facing jaw; the squat, heavily-muscled body. Don't forget the explanation: that the physical features would allow the dog to drive or subdue much larger animals, and that selection for those traits, if they had a genetic component, would see those particular alleles to increase in frequency in the bulldog gene pool.

And of course, once bull-baiting was banned, selection for gentleness/docility came into play. Because that called for further inbreeding in the existing bulldog population, it would likely result in a higher frequency of any existing harmful alleles as well.

The second part of the question tests understanding of students' knowledge of concepts around inheritance. In some cases it's probably possible to remove the deleterious alleles from the bulldog gene pool - but as a result the dogs would diverge from what's currently viewed as the breed standard. For example, selective breeding for a longer, less-wrinkled face could reduce the frequency of brachycephalic syndrome and dermatitis - but the resulting animals would be much less bulldog-like!

The same approach is less likely to be effective for hip dysplasia, however, due to the polygenic nature of this disorder, because it involves multiple genes rather than a single gene locus.

But selective breeding could help with VSD & cryptorchidism. For example, a dog that doesn't express VSD is either homozgyous dominant (with 2 copies of the normal allele) or heterozygous. So at the population level, breeding heterozygous individuals will on average produce 25% of pups with VSD, with the rest not expressing the disorder. Using a test-cross would allow you to breed only from parents homozygous for the normal allele, but it would take more time.  

And with cryptorchidism, you'd avoid breeding from males who had the disorder (which would have very poor fertility anyway, I'm guessing), and from females whose sons had undescended testes (because these females would be 'carriers' for the allele - while cryptorchidism is a dominant trait, you're only going to see it in males). 

Of course, you could also try out-breeding with other dog breeds - but then, the resultant pups may well not conform to the bulldog 'standard'. 

I must say, it does bother me that adhering to a breed standard - a human construct - can perpetuate known health problems in a breed such as this.

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Tunicates are more commonly known as 'sea squirts' - little blobby marine creatures that squirt water when you touch them (hence the name). We don't hear about them often, except perhaps when they make the news for all the wrong reasons. But from an evolutionary perspective they are fascinating little creatures - and it's largely due to their larvae.

As an aside: why do we call them tunicates? Because the body of the adult organism is enclosed in an outer sheath, aka a tunic. The majority of tunicate species belong to a group known as ascidians, which as adults live in shallow waters, attached to rocks or maritime structures (including boats). The remainder are planktonic & found out in the open ocean.

The larvae of many ascidians are free-swimming and, because of their body form, are often described as 'tadpole larvae'. (Some of the non-ascidian tunicates have adults with the same morphology.) These little animals have a number of features (shared with creatures such as the cephalochordate formerly known as Amphioxus) that link them with the chordates: a hollow dorsal nerve cord, a post-anal tail, a pharynx with slits in it (which feeds into the gut), and a living cartilaginous rod known as the notochord, against which the animal's muscles work. (The larvae, and the adults of some non-ascidian tunicates, are basically little swimming filtration units.)

In fact, because of their rather simple structure, tunicates have long been viewed as representing the likely common ancestor of both chordates (a group that includes us) and the slightly-more-complex cephalochordates like Amphioxus. However, a newly-published & fascinating article by Linda Holland (2016) looks at 

the highly derived body plans and life styles of the tunicate classes, their importance in the marine food web and their genomics [with an] emphasis ... on the impact of their especially rapid evolutionary rates on understanding how vertebrates evolved from their invertebrate ancestors.

It turns out that a genomic comparison, using nuclear genes from chordates, cephalochordates and tunicates, indicates that it's actually Amphioxus that sits at the base of this particular group. This in turn means that tunicates

have lost a lot of what the long extinct ancestral tunicate once possessed. 

This genomic work is fascinating on a number of levels. For example, the 'textbook wisdom' is only bacteria (ie Prokaryotes) have their genome organised into operons, where a single mRNA transcript contains several genes. But it turns out that tunicates, which have a rather small genome.

[have] a high percentage of genes in operons

something that Holland states they share with roundworms (nematodes) and some flatworms, which apparently also have "reduced genomes". In tunicates, it seems that among the genes that have been lost are some of the 'Hox' genes - genes that control the development and patterning of body form. 

I learned heaps of new things from this paper: tunicates are able to regenerate most of their bodies, for example (makes sense, I guess, as the sessile adult sea squirt can't exactly avoid being snacked on by predators). Apparently this is achieved by pluripotent stem cells in the animals' blood, though how it's done is still something of a mystery. And I had no idea at all that the animal's 'tunic'

contains cellulose, synthesized by a cellulose synthase that was evidently acquired in an ancestral tunicate by horizontal gene transfer from a bacterium. 

An animal that produces cellulose! Nature never ceases to surprise :)

L.Z.Holland (2016) Tunicates. Current Biology 26: 4 pR146–R152 DOI:

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Demodex mites are tiny little creatures that live in mammals' hair follicles. I first heard about them years ago, when I watched a documentary with my science class back at PN Girls' High. It was about animals that are parasitic on humans, and after the segment on eyelash mites, I don't know about the girls but I felt itchy for days!

For eyelash mites live where the name suggests, in the follicles of our eyelashes. (There are 2 species: Demodex folliculorum and D. brevis.) The common name gives an idea of just how small they are: adult length is 0.3 to 0.4 mm. They spend a lot of time inside the eyelash follicles, snacking on the sebum and dead cells (or maybe the bacteria) that accumulate there. But at night... at night, they come out and wander across our faces as we sleep, achieving a speed of 10cm/hr or more. Which doesn't sound much, but when you remember how small they are, that's quite an achievement. Presumably that's also when they mate, which they do where an eyelash follicle opens to the skin's surface. 

I was surprised to discover that these mites lack an anus. This sounds somewhat problematic, but the eyelash mites have survived, with their human hosts, for at least tens of thousands of years, so they obviously cope somehow. And when they die, their little bodies degrade and release their contents. On your face. Or in the follicles where they spent most of their lives.

Though demodex mites are tiny, there are an awful lot of them. There may be only one or two per hair follicle (they don't restrict themselves to the eyelashes), but an individual human has around 5,000,000 hairs on their body (Thoemmes et al., 2014), so that's an awful lot of available places for a mite to set up home in.

Thoemmes & her co-workers were interested in the genetic diversity of these mites. They predicted there'd be geographically-distinct lineages, because the tiny animals are very closely associated with their hosts and don't seem to be particularly mobile between hosts. However,

if Demodex lack strong geographic structure, it suggests the movement of mites among humans must occur very frequently (perhaps even with social greeting rituals) and across large geographic distances.

To test this hypothesis, the team examined adults (from a single North American population) visually, but also tested skin scrapings for the presence of mite DNA. The results showed that despite being able to see mites on only 23% of their sample population, 16S rDNA sequencing indicated that 100% of those sampled actually had mites present. The latter matched other research showing that 100% of dead bodies tested positive for the presence of Demodex.

Figure 2 from Thoemmes et al. (2014): Maximum likelihood (ML) phylogeny of mites based on 18S rDNA sequences.

While the results of their phylogenetic analysis of the mite DNA are based on samples from only 29 people, they're interesting nonetheless. It appears from that analysis that the 2 species, D.folliculorum & D.brevis, probably colonised humans at different times. Because D.brevis' DNA indicates that their nearest living relatives are mites living on dogs, then the researchers suggest that we acquired this species from our doggy friends, perhaps as recently as 11,000 years ago but possibly as many as 40,000 years ago. There does appear to be some regional variation (based on a comparison of the US data with earlier sequencing results from Chinese populations), but there's also quite a bit of variation within populations, due perhaps to individual humans picking up different mites on different occasions as individual humans came into close physical contact.

And after reading all this & watching a few videos, I feel itchy again!

Thoemmes MS, Fergus DJ, Urban J, Trautwein M, Dunn RR (2014) Ubiquity and Diversity of Human-Associated Demodex Mites. PLoS ONE 9(8): e106265. doi:10.1371/journal.pone.0106265

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Once upon a time, I wrote about traumatic insemination in bedbugs. (Those of my friends who are still traumatised by learning about the reproductive habits of various slug species may not wish to follow that link.) Now, two papers just published in Nature Communications describe the results of sequencing & examining the genome of the common bedbug, Cimex lectularius

Bedbugs have probably been with us since humans first lived in caves, where the bugs jumped (possibly literally) from bats to Homo. They're now a widespread human ectoparasite (found on every continent apart from Antarctica) and have developed resistance to the pesticides once used to control their populations. In introducing their paper on their analysis of the C.lectularius genome, Rosenfeld & his colleagues (2016) comment that

There is a limited molecular understanding of the biology of the bed bug before, during and after feeding on human blood, which is essential to their life cycle since bed bugs are temporary ectoparasites, whereby they access their hosts for blood feeding and then seek the refuge of the indoor environment for digestion, waste production and mating.

To increase our understanding of the bugs' life cycle, Rosenfeld's team looked not only at the genome sequence but at changes in gene expression, finding the most pronounced changes occurred after the insect had sucked its fill of human blood. They also found that these changes in expression 

included genes from the Wolbachia endosymbiont, which shows a simultaneous and coordinated host/commensal response to haematophagous activity. 

In other words, gene expression in both host and parasite changes in a synchronous way after the bug has fed. (Just as an aside, Wolbachia is a bacterium that has a significant impact on the reproductive lives of its host.) In the bugs the change could be described as huge: "20% of all stage-regulated genes" showed differential changes in expression after a blood meal.

As you'd expect, the bugs have a number of genes with anticoagulant activity - after all, having blood coagulate in their needle-like mouthparts while feeding would really gum things up - plus other genes associated with blood-feeding. The research team also identified a number of mutations that confer resistance to pesticides such as pyrethroids & cyclodienes, plus others that may underlie metabolic changes that speed up detoxification. Genes that have an impact on the thickness of the bugs' cuticle also have an impact on resistance (also noted by Benoit et al. 2016). 

In the second paper, Benoit and his colleagues (2016) also analysed the common bedbug genome to produce

a comprehensive representation of genes that are linked to traumatic insemination, a reduced chemosensory repertoire of genes related to obligate hematophagy, host–symbiont interactions, and several mechanisms of insecticide resistance.

Traumatic insemination involves male bugs stabbing their sexual partners pretty much anywhere on their bodies with a sharp, pointy, penis. It's a habit that can lead to the females picking up a range of pathogens, and unsurprisingly natural selection has driven the evolution of a range of adaptations minimising the physical harm and risk of infection. 

Because the bugs are obligate blood-feeders (haematophagous), their chemosensory system has evolved to allow them to find their particular hosts (ie us). The team observed that the genes involved in this system differed between C.lectularius & the related species that feeds on bat blood, as the 2 species have specialised on different hosts. They identified a total of 102 genes involved in chemosensory pathways, well down on the number found in related bugs (hemipterans) that feed on a range of plant species. (On the other hand, they have a much-expanded repertoire of salivary enzymes, compared to the plant-sucking bugs.)

The bedbugs' specialisation on human blood as their sole food source did have some potential pitfalls, as apparently vertebrate blood lacks some of the micronutrients that arthropods require. And that's where Wolbachia comes back into the story: 

such specialization also drives obligate associations with symbionts, including Wolbachia, that generate critical micronutrients that are deficient in vertebrate blood (Benoit et al., 2016).

Wolbachia does this by providing its host with 

a cocktail of specific B vitamins that are critical for reproduction and development

The research team also found genes encoding proteins (aquaporins) that allow the bugs to rapidly shed the excess water imbibed in a blood meal, and concluded that differential expression of aquaporin genes (and others) allow the bugs to survive periods of starvation and dehydration in between hosts.

In their conclusion, Benoit et al. comment that the wealth of information uncovered by these genomic studies may allow us to move towards an answer to a pressing question: 

What triggered the current bed bug resurgence?

To which harassed travellers would probably add, and how can we bring them back under control?

J.B.Benoit, Z.N.Adelman, K.Reinhardt, A.Dolan, M.Poelchau, E.C.Jennings, E.M.Szuter, R.W.Hagan, H,Gujar, J.N.Shukla, F,Zhu, M.Mohan, D.R.Nelson, A.J.Rosendale, C.Derst, V.Resnik, S.Wernig, P.Menegazzi, C.Wegener, N.Peschel et al. (2016) Unique features of a global human ectoparasite identified through sequencing of the bed bug genome. Nature Communications 7 Article number 10165 doi:10.1038/ncomms10165

J.A.Rosenfeld,D.Reeves, M.R.Brugler, A.Narechania, S.Simon, R.Durrett ,J.Foox, K.Shianna, M.C.Schatz, J.Gandara, E.Afshinnekoo, E.T.Lam, A.R.Hastie, S.Chan, H.Cao, M. Saghbini, A.Kentsis, P.J.Planet, V.Kholodovych, M.Tessler et al. (2016) Genome assembly and geospatial phylogenomics of the bed bug Cimex lectularius.  Nature Communications 7 Article number: 10164 doi:10.1038/ncomms10164

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By now many of you have probably seen images of green-glowing zebrafish, or pigs whose snout & trotters glow in the dark. In both cases the animals are genetically modified and are expressing a fluorescent protein originally sourced from a jellyfish. (The body form of a jellyfish is a medusa, while that of sea anemones & their freshwater relative, Hydra, is called a polyp.) There are a range of these proteins, which collectively belong to a group called the Green Fluorescent Proteins (what else?), and while a wide range of jellyfish produce them1 there are only occasional reports of glowing polyps.

However, in a paper just published in the open-access journal PLoS ONE, Andrey Prudkovsky & his colleagues describe finding tiny (~1.5 mm) fluorescent polyps living in the Red Sea. More specifically, growing in colonies on the shells of small gastropods, a relationship described as epibiotic. The snails are active at night on the sandy seabed, and the researchers noted that the little gastropods buried themselves in the sand when a torch shone on them. They also noticed that the snails, as they moved about in the moonlight, were covered with tiny pinpoints of green light.

Where fluorescence has been described in other polyps, it's mostly been in the 'stalks' of the little animals, but in all the polyps Prudkovsky's team studied, the intense green glow came from a region known as the hypostome - the region around the animal's mouth & encircled by its tentacles. Because both the intensity and the site at which the proteins are expressed is so unusual, the researchers suggest that this could be a useful taxonomic characteristic, given that it's hard to tell one colonial polyp species from another.

They also speculate on the adaptive significance of a polyp having a green glow around its mouth, suggesting that 

[f]luorescence in the hypostome of Cytaeis sp. has probable ecological significance as prey are likely to be attracted to the tentacles and mouth of the polyps

although I do feel that until there's actual observational evidence of this happening, it's a little like an evolutionary just-so story. But isn't the combination of little snails and glowing polyps rather beautiful?

Fig 3.  Hydroid polyps of Cytaeis sp. from the Saudi Arabian Red Sea, scale bar 2 mm; (A) fluorescence of living polyps on the shell of the gastropod Nassarius margaritifer; (B) polyps on the shell of a N. margaritifer specimen, scale bar 2 mm; (C) close-up of polyps, scale bar 0.5 mm.

Fig 3 From Prudkovsky et al., 2016: Hydroid polyps of Cytaeis sp. from the Saudi Arabian Red Sea, scale bar 2mm; (A) fluorescence of living polyps on the shell of the gastropod Nassarius margaritifer; (B) polyps on the shell of a N.margaritifer specimen, scale bar 2mm; (C) close-up of polyps, scale bar 0.5mm. doi:10.1371/journal.pone.0146861.g003

1 And also in comb jellies, marine arthropods, and cephalopods cephalochordates (thanks to herr doktor bimler for picking up the evidence of my brainfade).

Prudkovsky AA, Ivanenko VN, Nikitin MA, Lukyanov KA, Belousova A, Reimer JD, et al. (2016) Green Fluorescence of Cytaeis Hydroids Living in Association with Nassarius Gastropods in the Red Sea. PLoS ONE 11(2): e0146861. doi:10.1371/journal.pone.0146861

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Well, probably not1, in the sense that most would place on the term 'tummy bug' (where a close proximity to the toilet is a Good Thing), but it turns out that he did have some rather interesting intestinal bacteria.

Ötzi is perhaps better known as the 'Iceman', who died around 5,300 years ago in the Otztai Alps of the Italian Tyrol. (He's the subject of a fascinating web page & I have to say, I'd love to visit the museum, maybe when we next visit family in Europe.) His body, clothing, and equipment are exceptionally well-preserved & are yielding a great deal of information on life in Neolithic Europe - including, as described in the latest issue of Science, the nature of his microbiome. (You'll find the full paper here, but there's also an open-access summary here. I do have a gripe about the use of the term 'tummy bug' in the latter, though!)

In their just-published paper, Maixner's research team reports on their finding of a strain of Helicobacter pylori in Ötzi's stomach contents (he'd apparently eaten a full meal not long before he died). I've written about H.pylori before: while it's been found to be associated with development of gastritis, stomach ulcers, & sometimes cancer in a small proportion of those carrying it2, there's also evidence that it has a protective effect against other disorders, including acid reflux and oesophageal cancer. And it's been with us for a long time:

Predominant intrafamilial transmission of H. pylori and the long-term association with humans has resulted in a phylogeographic distribution pattern of H. pylori that is shared with its host. This observation suggests that the pathogen not only accompanied modern humans out of Africa, but that it has also been associated with its host for at least 100,000 years. Thus, the bacterium has been used as a marker for tracing complex demographic events in human prehistory.

Most modern Europeans carry one particular strain of this bacterium, which is believed to have originated via recombination of two earlier strains. However, the origins of these strains have been uncertain, & the researchers hoped that Ötzi's gut microbes might throw some light on this. The Iceman himself was born and lived in Southern Europe, and DNA comparisons link him to early European farmers. However, the strain of H.pylori found in his gut is most closely related to a haplotype now found in central and southern Asia, and not to those of Europe and Africa.

The detection of an hpAsia2 strain in the Iceman’s stomach is rather surprising because despite intensive sampling, only three hpAsia2 strains have ever been detected in modern Europeans. Stomachs of modern Europeans are predominantly colonized by recombinant hpEurope strains.

Maixner suggests that the Iceman's ancestors must have brought this Asian strain of H.pylori with them when they migrated to Europe. Well after Ötzi died, later immigrants from Africa brought their own strain of the bacterium, and subsequent recombination produced the modern European strain of this microbe. This is evidence for rapid evolution of H.pylori in Europe as waves of human migrants moved into and across the continent.

The researchers also noted that Ötzi's version of the bacterium represents a strain that's associated with stomach inflammation in modern humans - and that protein biomarkers expressed in his gut indicate that he had an inflammatory response to the infection. This may or may not have manifested in actual disease - his stomach lining was not sufficiently well-preserved to let them draw any conclusions on this.


1  Which is a real pity, as I was so going to steal my friend Grant's suggested phrase, "the Tyrolean trots", for my title :( 

 It's "found in approximately half the world’s human population, but fewer than 10% of carriers develop disease that manifests as stomach ulcers or gastric carcinoma" (Maixner, Krause-Kyora, Turaev, Hoopmann et al., 2016)

F.Maixner, B.Krause-Kyora, D.Turaev, A.Herbig, M.R.Hoopmann, J.L.Hallows, U.Kusebauch, E.Vigi, P.Malfertheiner, F.Megraud, N.O'Sullivan, G.Cipollini, V.Coia, M.Samadelli, L.Engstrand, B.Linz, R.L.Moritz, R.Grimm, J.Krause, A.Nebel, Y.Moodley, T.Rattei, & A.Zink (2016) The 5300-year-old Helicobacter pylori genome of the Iceman. Science 351 (6269):162-165 . DOI: 10.1126/science.aad2545

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In one of my classes we talk a bit about cloning, in the context of discussing various biotech techniques and their applications. Sometimes someone asks if I'd clone my dog (or my husband!) after they'd died, & my response is always to say 'no'. Not because I don't love them both (husband much more than dog, he'll be glad to hear!), but because I know that whatever I got, it wouldn't be the original being. 

So when this story popped up in my newsfeed, I thought to myself that it would make a useful starting point for class discussion - after all, 'Dead dog lives on after British couple pays to clone him back to life' does have a certain morbid appeal to it. But my own answer would still be 'no'. For several reasons (none of which are mentioned in the original news story).

First up, the dog isn't going to be an exact genetic replica of the original. This is because the technique that was used involves implanting the nucleus of one of the dead dog's cells into a donor egg that's had its own nucleus removed: the nuclear DNA will be that of the original dog, but the mitochondrial DNA - in the egg, and in all subsequent cells - will come from the egg donor. This is because mtDNA is passed on almost exclusively down from mothers to children. And since mitochondria play a role in other cellular functions besides production of ATP, then this potentially affect the phenotype of the new organism.

In addition, the dog developed as a foetus inside a host mother: the intrauterine environment would not, could not, have been the same as that in which the original dog developed. Because these different environments can have different effects on how the information coded in DNA is expressed (a phenomenon known as epigenetics), it's again quite possible that aspects of the new dog's phenotype could be changed in subtle and unpredictable ways. 

And a third consideration is this: the fail rate of cloning is far greater than its success. According to this page on the University of Utah website

Cloning animals through somatic cell nuclear transfer is simply inefficient. The success rate ranges from 0.1 percent to 3 percent, which means that for every 1000 tries, only one to 30 clones are made. Or you can look at it as 970 to 999 failures in 1000 tries.

That's a lot of donor eggs (the collection of which involves a certain amount of risk), and a lot of host mothers, to get a single dog - a dog that will not, cannot, be exactly the same as the original. Biologically, ethically - personally I would not go there. I'd rather mourn, remember with love, and move on.


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Well, this sucks, & that's putting it mildly. From Kevin Folta's blog, Illumination:

Dr Folta has been under constant attack in recent months since it emerged that Monsanto had donated  $US25,000 to fund a science outreach program he was running. Not his research, but an outreach program. He was accused of a conflict of interest by those opposed to genetic modification (one of the topics covered in the program) & ended up returning the money. However that didn't stop the attacks or the calls for his university to fire him. And so now there's this: the possibility I touched on when I first wrote about this issue has become reality.


And yet it's somehow OK, & not at all hypocritical (/snark) for anti-GMO speakers to demand tens of thousands of dollars in speaking fees to promote their message, or to pay similarly large amounts for research into eg organic farming. 

On Code for Life, Grant Jacobs has a very thoughtful piece on GMO legislation. And that's what we need from both sides of this question: careful rational thought, not anger.


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  • Alison Campbell: Hi Sharon - you're probably best to check with the read more
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