SciBlogs

Archive November 2009

moa evolution & new zealand’s geological past Alison Campbell Nov 30

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The Level 3 & Scholarship examiners often ask you to discuss the evolutionary history of a group of organisms (Hebe, cockroaches, cicadas etc) in relation to the geological history of New Zealand. Geological changes such as the widening of the Tasman Sea, and the uplift of mountain ranges including the Kaikoura ranges & the Southern Alps, can drive evolutionary change through the isolation of populations (the Founder effect, genetic drift) & changes in selection pressures.

A new paper just out  has done just this for the moa (Bunce et al., 2009), combining "mitochondrial phylogenetic information from 263 subfossil moa specimens from across NZ with morphological, ecological, and new geological data to create the first comprehensive phylogeny, taxonomy, and evolutionary timeframe for all of the species of an extinct order." This includes evidence that for much of the last 30 million years or so, the North & South islands were geographically isolated, which would have provided the basis for allopatric speciation of the fauna & flora on those 2 landmasses.

You may be reasonably familiar with the idea of adaptive radiation in relation to moa & other ratites, as it’s a common example of this pattern of evolution in senior biology textbooks in NZ. At the moment scientists think that ratites first evolved around 80 million years ago (mya) in Gondwanaland, diverging – as the supercontinent broke up – into groups that gave rise to the modern ostrich, emu, rhea, cassowary, kiwi, & the extinct elephant birds and moa. As a taxon, moa also show considerable adaptive radiation, although until recently it was difficult to tell just how many species there actually were. On the basis of morphological & aDNA data, Bunce & his colleagues suggest some changes from the till-now current taxonomy for moa, shown in the following figure (they reduce the number of species from 11 to 9, for example).moa systematics bunce et al.png

Fig.1 from Bunce et al. (2009): Systematics, dimensions and approximate distributions of moa in the three family, six genera, nine species taxonomy advocated in this study. doi/10.1073/pnas.0906660106

The data from ancient mitochondrial DNA also allowed the team to study the time-frame of moa evolution. Earlier studies have suggested that the moa radiation occurred about 15 mya, but Bunce et al.’s data indicate that the two main groups of moa (the Dinornithidae & Emeidae) happened just 5.27 mya - much more recently. (The 2009 paper discusses the reasons why their figure differs so significantly from the earlier one, which was also based on aDNA, & suggest this is related to how the data were calibrated.)

What was happening in NZ during that period, in ecological terms, that might have driven this divergence? One factor is the rapid orogeny (mountain-building) that we know was happening at around that time. This would have provided a range of new, untapped habitats for moa & other species to exploit – and new selection pressures as well. For example, as the Southern Alps rose up, they increasingly blocked the predominant westerly airflows, favouring the development of wet rainforests on the West Coast and a warmer, drier environment on the eastern side of the mountains, opening the way for niche specialisation and speciation. This could have been quite complex, as during glacial periods glaciers extended to the coast on the western side of the island & well down into the eastern low country, further subdividing habitats & providing additional barriers to gene flow.

In addition, from about 2 mya relatively short-lived land bridges linked the main land masses, allowing movement between the two islands. (This partly reflects the impact of glacials during the last ‘ice age’, at their peak lowering sea levels around NZ by at least 100m.)

moa evolution & changes in NZ geography.png

Fig.2 from Bunce et al. (2009) A spatial & temporal context for the evolution of moa. Molecular phylogeny and date estimates of the moa radiation… compared with the new paleogeographic model of Neogene New Zealand. doi/10.1073/pnas.0906660106 NB the authors caution that the timings of divergence for the various species are provisional – it would be useful to have data from many more moa specimens, to improve the accuracy of the calculations.

A great deal of new work has gone into developing those maps, particularly in the King Country, Taranaki, & central Hawkes Bay, plus data from exposed onshore marine sediments and oil exploration drill sites. During the Oligocene (> 25mya), the New Zealand land mass was reduced to a string of low, well-separated islands. Bunce et al. comment that, even when the northern landmass was re-emerging, it was still completely separated from the South Island by the Manawatu Strait (see maps above) until roughly 1.5-2 mya. Thus any land animals (& plants!) that couldn’t cross the strait were geographically isolated for that entire time. But – the moa genetic data don’t show any indication of divergence that far back, which means that the various lineages probably descended from ancestors on a single island. Fossil evidence fingers the South Island as the ancestral home, which means that moa couldn’t have colonised the North Island until less than 2 mya, only to be isolated again when Cook Strait first formed 450,000 years ago. (This interpretation is supported by data from other vertebrate remains.)

But there’s still a lot to learn! The authors conclude by saying that this "important new geological model of Neogene NZ emphasises our current lack of knowledge about the pre-Pliocene landscape, and raises important questions about the role of marine barriers and the biotic diversity of the north and south islands. The combined geological and genetic data suggests that the NZ Neogene terrestrial record is likely to have been marked by the significant loss of terrestrial endemics from a highly unusual environment, which is only just beginning to be characterised."

Bunce, M., Worthy, T., Phillips, M., Holdaway, R., Willerslev, E., Haile, J., Shapiro, B., Scofield, R., Drummond, A., Kamp, P., & Cooper, A. (2009). The evolutionary history of the extinct ratite moa and New Zealand Neogene paleogeography Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0906660106

 

facilitated communication? Alison Campbell Nov 27

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Like me, you may have seen this article in the Herald (or some other paper) on Wednesday this week. It tells the story of Rom Houben who, after suffering severe injuries in a car accident, was left in what doctors diagnosed as a ‘persistent vegetative state’ for 23 years. His mother, however, was insistent that her son was still both conscious & alert. Eventually, PET scans of his brain indicated that this appeared to be the case, & the article tells us that after 3 years of intensive therapy "the 46-year-old is now communicating with one finger and a special touchscreen on his wheelchair."

If only things were that simple…

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Before I go on, I have to say that the case described in this article represents one of my worst fears – being ‘trapped’ inside a body that’s no longer capable of any independent movement, & being unable to communicate that fact – a phenomenon described as ‘locked-in syndrome’. At least, if someone in this situation could even twitch some part of their body to indicate a conscious response, others would know that ‘you’ were in there. So why am I a bit ‘iffy’ about this story?

One reason is when you watch the video accompanying the story, it’s plain that Mr Houben isn’t actually independently using the keyboard – he’s assisted by a carer who believes that, after 3 years of working with him, she can detect tiny muscle contractions in his finger to identify which letters he wishes to select on the touch-pad. (This fact isn’t mentioned in the original  Herald article, although there is a slightly less credulous version here.) This is often described as ‘facilitated communication’ (a rather contentious field, as it turns out). I also noticed was that Mr Houben isn’t looking directly at the screen much of the time, & at times his eyes appear to be closed. Despite this, his assisted typing is both fast & fluent (which is surprising – I have extreme difficulty in finding the right key if typing one-fingered & viewing the keyboard obliquely).

This is not to suggest that the carer doesn’t genuinely believe that she is acting as an interpreter for Mr Houben. But it is to suggest that the media look at such stories with a more critical eye, instead of taking the whole thing at face value. There are certainly ways to examine what’s happening, includng the following possibility put forward by one of Orac’s readers in commenting on his post:

No one’s suggested the simplest way to test this use of facilitated communication.

I think all would have to agree that Houben must be able to see and read in order for this technique to work. So all that’s necessary are flashcards with short words on them. 4-5 letters each would do. A flashcard is shown to Houben but NOT the facilitator, and then Houben is asked to type that word. Any observer who stays in the room is similarly ignorant of the word, for double-blind purposes.

This way, the ‘facilitator’ doesn’t have to be blinded while typing or otherwise disadvantaged; it doesn’t matter that she can see the screen or has significant control over his hand. The test is just designed so that the questions have only one correct answer, and the facilitator does not know what that correct answer is.

PS And now I see that Darcy (over at Scepticon) has beaten me to it… Dr Steve Novella (who as a neurologist certainly knows more about the issue than I do!) has also provided a very thorough review of this particular case.

evolutionary image… fail Alison Campbell Nov 26

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Such a cute t-shirt logo (I want one!) but it has the FAIL in so many ways when it comes to evolution…

evolution of the cat.jpg

off to entertain at cafe scientifique Alison Campbell Nov 24

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Well, the mad rush to confirm degree completions is finally over (6.32pm & counting…) & I’m off to meet Marcus at the pub for the last Cafe Scientifique of the year. The topic: strange science. It’s open for the audience to bring up any topics they want to discuss, but we have the odd (& I use the word advisedly!) idea of our own :-) Including the problems of queuing on buses, baguette-carrying birds & the Large Hadron Collider (ask Marcus!) , Chickenosaurus rex or, rejigging chickens & getting dinosaurs, & of course fellatio in fruit bats :-) An entertaining time should be had by all!

regulating supplements Alison Campbell Nov 23

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Last Friday the Science Media Centre’s media alert included the following:

Dietary supplements such as multivitamin tablets and energy drinks are an increasingly common part of our lives, but should they be?

Concerns have been sparked recently by the availability of ultra-high caffeine energy drinks, the proliferation of people taking (often large) doses of vitamins/minerals every day, and an industry which appears to have very little legislation to guide its behaviour.

I will confess to having drunk caffeine ‘energy’ drinks in the past (despite their – to me, anyway – awful taste) when I’ve been particularly tired & had to keep working. Not because they contained energy – caffeine has a stimulant effect on the nervous system, so the only energy content would be in the sugar added to the drink, & anyway I went for the sugar-free kind! But I stopped when I found that my blood pressure had gone way too high & that my teeth ‘buzzed’ after I’d drunk one. And that was on the basis of one per day & not every day… Certainly caffeine can have negative physiological effects. (I was intrigued to discover that coffee & other caffeinated drinks aren’t recommended for anyone with a tendency to faecal incontinence, for example.) So I’ll be interested to see the briefing notes tomorrow.

But I also wonder how the idea of regulating vitamins & other ‘dietary supplements’ (I’d go as far as to include complementary & alternative medicines (CAM) in this grouping) will go down with the wider community. Certainly the last time the idea was raised, the outcry from various interest groups led to the whole thing being quietly dropped. Which I thought was quite interesting – you’d think there’d be a lot of support for something which would ensure that the pills & potions that fall under the ‘supplement’/CAM umbrella would contain what they are claimed to contain, and in standardised amounts. This would after all be beneficial to the consumer – there are significant safety issues associated with non-standardisation of these supplements, and also with contamination by non-declared heavy metals (or even prescription drugs). So why the fuss?

It’s certainly a discussion we need to have, & hopefully one that will be better addressed by the media than has been the case in the past.

whence the nucleus? Alison Campbell Nov 22

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One of the deepest divisions among living things is the split between prokaryote and eukaryote cells. In eukaryote cells, the chromosomes are enveloped in a layer of phospholipids – these cells have a ‘true’ nucleus surrounded by a nuclear membrane, something that’s absent from prokaryotes. And there are other differences: eukaryotes either have, or have had, mitochondria (tiny organelles where aerobic respiration occurs) and plants & algae also have chloroplasts, & there’s a lot of other cellular infrastructure besides. Now, we teach students about the origins of mitochondria & chloroplasts (most likely by the process of endosymbiosis, first put forward as an explanation by Lynn Margulis), but what about that nucleus?

There have been various hypotheses put forward to explain the origin of the eukaryote nucleus. One is that the chromosomes of the ‘pre-eukaryote’ were somehow surrounded by a section of the cell membrane. Certainly some prokaryotes have extensive infoldings of the cell membrane, but if this hypothesis was correct it should mean that the nuclear membrane is a single continuous sheet of phospholipid bilayer, & it’s not.

As well as ‘how’, scientists have also tried to answer the ‘why’ question – just why do eukaryotes surround their chromosomes in a membrane. The usual answer – the one I was taught – is that this protects the nuclear contents; against what, we weren’t told. If a nucleus is so useful, why did this structure never evolve in bacteria? Reading Nick Lane’s Life Ascending pointed me in the direction of another possible answer, first proposed in 2006 by Koonin & Martin.

Introns are non-coding sequences. apparently the molecular corpses of jumping genes, found within eukaryote genes. ‘Active’ jumping genes are able to cut themselves out of a sequence of DNA using what could be described as molecular scissors, & reinsert a copy of themselves somewhere else. Introns have lost this ability to cut themselves out of a gene, but the cell must do so in order to remove these non-coding sequences prior to the process of translation & production of a functional protein. It seems that eukaryote cells do this using the same molecular scissors as jumping genes, modifying messenger RNA sequences by ‘splicing’ out the introns. However, this process takes time (Martin & Koonin, 2006).

In general, prokaryotes don’t have introns. A piece of prokaryote mRNA will be translated into a protein almost as fast as the mRNA is itself being produced, because DNA, mRNA, and everything else needed to manufacture proteins are all in very close proximity within the cell. It’s suggested that eukaryotes acquired introns very early on, picking them up from their new endosymbionts, the mitochondria. Supporting this hypothesis, the presumed bacterial ancestors of mitochondria do have a particular type of intron; and Martin & Koonin note that the evolutionary relationships of the proteins associated with the nuclear membrane also suggest that this membrane formed in cells that already contained mitochondria.

The presence of introns would have presented significant problems for the early eukaryote cells. Because RNA splicing is relatively slow, if mRNA was translated into proteins as soon as the mRNA was produced, many of those proteins would be faulty because they’d be produced by translating the ‘wrong’ intron information as well as the ‘right’ information encoded in the functional part of the gene (the exons). Any cell with structural features that provided at least some separation of transcription & translation would thus be at a selective advantage, because they wouldn’t be wasting energy in producing faulty proteins . Martin & Koonin are suggesting that the nuclear membrane evolved in response to this selection pressure, providing a mechanism to separate the two processes – production of mRNA & production of proteins – to give sufficient time for the introns to be splieced out before the assembly of a protein could begin. It’s a fascinating hypothesis, although only time (& lots of research) will tell us if it’s a good model for the origin of the eukaryote nucleus.

(NB introns aren’t always spliced out in the same way every time a gene is expressed. This underlies the fact that, while the human genome contains around 25,000 genes, our cells can contain 60,000+ diffierent proteins!)

W,Martin & E.V.Koonin (2006) Introns and the origin of nucleus-cytosol compartmentalisation. Nature 440: 41-45. doi:10.1038/nature04531

PS below is a good explanation of how & why introns are spliced out (there is a large range of excellent science videos at the site this came from):

 

argh! the dreaded mercury! Alison Campbell Nov 21

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One of my commenters asked the following question, & while I answered it quickly in that thread, I thought it might be useful for her (& maybe others) if I found a few references to support what I said.

One of my friends has this as their current status on Facebook, and I wondered if you had some facts at your fingertips which I could steal to reply (as I’m sure it’s not scientifically sound):

"the swine flu itself has killed about 2-3,000 people total. The regular flue kills 40,000+ per year. The vaccine contains 2 dangerous compounds, one is thimerosol. It is made 50% of mercury. It binds to receptors in your brain, and can cause brain damage. The other is squalene. It accidentally tricks your immune system into killing your own cells. So people, what do we think?"

Just as an aside, I’d say your friend is using information from an anti-vaccination site, since I’ve seen the same wording elsewhere (in the comments thread at this link). You could maybe ask her to provide hard evidence in support of those statements… But anyway -  it’s true to say that (so far) H1N1 influenza hasn’t killed as many people as the ‘normal’ seasonal flu. Worryingly, however, those it kills tend to be young, while it’s more likely to be the elderly who are affected by the seasonal variety. In addition, the northern hemisphere is going into its second winter with H1N1 circulating in the population, & there are signifcant concerns that the virus will be more virulent second time around. Hence the mass vaccination campaing currently underway in the US.

Thimerosal. Aaahh, thimerosal. Thimerosal is a mercury compound, which used to be widely used as a preservative in vaccines. However, it was phased out of childhood vaccines early this century, although it’s still found in some adult vaccines – including H1N1, although this vaccine is also available without thimerosal. One of the reasons for that phasing-out was the widespread (but erroneous) belief in some quarters that thimerosal was the cause of an ‘autism epidemic’ – yet there has been no decline in the rate of autism diagnoses since then, which would tend to indicate that there’s no causal link. Thimerosal – also known as ethyl mercury – is present in very low doses in vaccines – in the case of the H1N1 vaccine, at a concentration of 0.01%. This is the same as 1 in 10,000, & since thimerosal is roughly 50% mercury by weight, a 1-in-10,000 concentration contains around 25 micrograms of mercury per 0.5mL. Unlike methyl mercury, ethyl mercury doesn’t bioaccumulate & is excreted from the body. There is no evidence of any link between thimerosal/ethyl mercury and any form of brain damage/disorder (including autism): Orac has written very extensively on this.

You can buy squalene commercially – in this form it’s derived from sharks & people apparently take it as a dietary supplement. (I wonder if they realise the damage they could be doing to themselves? Oh dear!). It’s also produced in your body as a part of normal metabolic processes (including synthesis of cholesterol), it’s found in olive oil, & it’s present in some vaccines as an adjuvant – something which enhances the vaccine’s ability to stimulate an immune response (some antigens used in vaccines don’t elicit a sufficiently strong immune response without an adjuvant also being present).  Those opposing the use of squalene claim that it stimulates the production of anti-squalene antibodies, which will then go on to attack & destroy squalene wherever it’s found in the body, causing all sorts of nasty illnesses including ’Gulf War syndrome’ - a claim which (again) is not borne out by well-designed & performed scientific studies.

The trouble with claims like those I’ve looked at there is that there’s a risk that people will be put off vaccinating their children (or themselves) as a result of this scare-mongering. And this is bad for the population at large. Not everyone reacts strongly to a given vaccine – I’ve never produced any lasting high levels of antibodies to rubella, for example, despite getting vaccinated before attempting to get pregnant. Children who are too young to be vaccinated rely on the herd immunity generated by having a high rate of vaccination in the population at large, as do those who are immuno-compromised for some reason (those undergoing chemotherapy, for example, or recipients of organ transplants).

So, Renee, I hope you can persuade your friend to reconsider her stance on this one!

what’s in the water? Alison Campbell Nov 20

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Procrastinating like crazy, I’ve just come across an interesting post over on Science-Based Medicine. It’s about the hazards associated with water births (sometimes promoted as a ‘natural’ way to deliver a baby…). I’ve wondered before about the sense of delivering a baby under water (the ‘diving’ reflex only kicks in in cold water & no mum-to-be is going to sit around in a chilly tub) but I hadn’t really thought before about the microbiological side of things. Faecal contamination (eg via meconium) + body-temperature water – not a good combination…

speciation in darwin’s finches Alison Campbell Nov 19

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This afternoon the daughter sat Level 3 Biology (she seemed to quite like the paper). She said that one of the questions was about Darwin’s finches, based on some of the work of Peter & Rosemary Grant, who’ve been studying finches on the Galapagos Islands since 1973. During that time they’ve trapped, measured, banded & re-trapped every finch on the island of Daphne Major, collecting longitudinal data on the birds in perhaps the longest-running study of its kind. Among other things, the Grants were able to document how the finch populations changed in selection to the selection pressures imposed by a severe drought.: evolution in action. Nonetheless, a stock creationist remark concerning the Galapagos finches claims that this is not an example of evolution because the birds ‘are still finches and the changes cycle with changing environmental conditions.’ 

This really is a ridiculous statement: given the timespan involved, you can’t really expect more than gradual, incremental changes in population characteristics – changes that are not directional, or purposeful, & which may be reversed if selection pressures alter. Which makes a new, just-published paper by the Grants all the more exciting – it seems that they may be witnessing an example of allopatric speciation

When the Grants arrived, Daphne Major was home to two species of finch: the medium ground finch Geospiza fortis and the cactus finch Geospiza scandens. (A third species, G.magnirostris, began breeding there in 1983.) By 1981 the Grants had banded more than 90% of the birds on the island, which meant that when a new individual arrived from one of the other Galapagos islands, they were able to recognise it. The immigrant was an unusually large male ground finch with a distinctive song; genetic analyses suggested that it probably originated from the G.fortis population on the island of Santa Cruz – and also that it was a hybrid, with alleles from both fortis and scandens genomes. This bird went on to mate with another, rare, hybrid individual. The Grants note that they ‘have followed the survival and reproduction of this individual and all of its known descendants [the immigrant lineage]… for seven generations spanning 28 years.’ (The ‘immigrants’ were characterised by their larger size – including larger beaks, different song, & the presence of a unique genetic marker.)

The Galapagos Islands are periodically affected by severe droughts, which have a significant effect on the various finch populations. (The L3 exam focused on the impact of a drought in the mid-1970s.) One such drought, in 2004, saw the ‘immigrant lineage’ reduced to just two birds, a brother & sister. They bred with each other, & the Grants’ detailed genetic data show that from that point on the ‘immigrant lineage’ was reproductively isolated from the resident G.fortis population. They suggest that this isolation is due to two main factors: morphology, & song. The song is learned, & so an element of imprinting is involved. This is significant: the Grants observed only 13 instances of hybridisation between fortisscandens over 21 years, & comment that this ‘generally results from the learning of the song of another species during the early sensitive peirod of song learning’ (as is also the case for indigobirds). Morphological differences centre on the beak, which is noticeably larger in the ’immigrant’ lineage.

This morphological difference already existed: the original immigrant probably came from Santa Cruz, where fortis individuals are bigger than those on Daphne Major. In other words, this difference arose allopatrically. However, once on Daphne Major the difference between the different groups was exaggerated by a drought in 2004, which saw a decline in the size of resident fortis birds (including beak size). And it was maintained by breeding within the ‘immigrant’ & resident lineages, mediated by those learned differences in song & by mate selection on the basis of beak size.

Are the differences enough to say that we are looking at a new species? To the Grants, the answer is, qyuite possibly -  they view the inbreeding, ‘immigrant’ group ‘as an incipient species because it has been reproductively isolated from sympatric G.fortis for three generations and possibly longer.’ Of course, whether this reproductive isolation will be maintained remains to be seen. Watch this space :-)

See also Allan MacNeill’s very thorough commentary at The Evolution List .

P.R.Grant & B.R.Grant (2009) The secondary contact phase of allopatric speciation in Darwin’s finches. Proceedings of the National Academy of Sciences early edition, p 1-8. www.pnas.org/cgi/doi/10.1073/pnas.0911761106

hummingbirds & the high cost of s*x Alison Campbell Nov 18

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One of the nice things about reading books by great science writers is that I just know I’m going to learn lots. I’ve just got back into Nick Lane’s latest book Life Ascending (it’s been my lunchtime reading at work & recently other things have intruded…). Lane has a lovely lyrical way of writing that I really enjoy, & I thought I’d share a couple of paragraphs with you. They’re from the chapter titled Sex: the greatest lottery on Earth. in which he’s discussing how & why sexual reproduction evolved. At the heart of this excerpt is the idea that the biological costs of sex are quite hard to measure, but can be very high. The example here is hummingbirds – the go-betweens for sex in many species of tropical plant.

Rooted to the spot, plants are the most implausible of sexual organisms, yet the overwhelming majority of them are exactly that; only dandelions, along with a handful of other species, cock a snook at sex. The rest find a way, the most spectacular being the exquisite beauty of flowering plants, which swept through the world some 80 million years ago, turning the dull green forests into the magical painted glades we know today. Although they first evolved in the late Jurassic, perhaps 160 million years ago, their global takeover was long delayed, and ultimately tied to the rise of insect pollinators like bees. Flowers are pure cost to a plant. They must attract pollinators with their flamboyant colours and shapes, produce sweet nectar to make such visits worthwhile (nectar is a quarter sugar by weight), and distribute themselves with finesse – not too close (or inbreeding makes sex pointless). Having settled on a pollinator of choice, the flower and pollinator evolve in tandem, each imposing costs and benefits on the other. And no cost is more extreme than that paid by a tiny hummingbird for the static sex life of plants.

The hummingbird must be tiny, for no larger bird could hover motionless over the deep throat of a flower, its wings beating at 50 beats a second. The combination of tiny size and colossal metabolic rate needed to hover at all means that hummingbirds must refuel almost incessantly. They extract more than half their own weight in nectar every day, visiting hundreds of flowers. If forced to stop feeding for long (more than a couple of hours), they fall unconscious into a coma-like torpor: their heart rate and breathing plunge to a fraction of that in normal sleep, while their core temperature goes into free fall. They have been seduced by the enchanted potions of plants into a life of bondage, moving relentlessly from flower to flower, distributing pollen, or collapsing into a coma and quite possibly dying.

With costs like that, the benefits of sex have got to be significant. That, and the evolution of this complex practice, occupy the rest of the chapter. I am so enjoying this book :-)

N.Lane (2009) Life Ascending: the ten great inventions of evolution. Norton.

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