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I've just read (via the NZ Skeptics page on FB) a fascinating article on Slate about the psychology of conspiracy theorists. In it, Will Saletan describes a series of studies from the past 20 years, that attempted to understand why a fair proportion of people seem to incline towards conspiracy theories (for example, a 2007 poll found that only 64% of adults in the US believed that the 9/11 attacks caught their government off-guard: most of the remainder believed that the powers-that-be either knew in advance or were actually actively involved). 

The experimental data Saletan discusses seem to show that the distrust (or at the very least, cynicism) that many participants demonstrated is based on how those participants perceived the character of others:

... it's a common weakness known as the fundamental attribution error - ascribing others' behaviour to personality traits and objectives, forgetting the importance of situational factors and chance. Suspicion, imagination, and fantasy are closely related. 

He goes on to say that

The more you see the world this way - full of malice and planning instead of circumstance and coincidence - the more likely you are to accept conspiracy theories of all kinds. Once you buy into the first theory, with its premises of coordination, efficacy, and secrecy, the next seems that much more plausible

and presents additional data to support that contention. (Orac has also written about this from time to time.)

I have to say, some of the anti-fluoride commenters we get on Making Sense of Fluoride certainly appear to fall into the fundamental attribution error. How else can one interpret the assumptions that fluoridation is the result of one big (global) conspiracy theory (linked, in the minds of at least some commenters, with a nebulous depopulation program), and that those discussing the science in favour of fluoridation are naturally being paid to do so.

And given that at least some groups who oppose water fluoridation (with statements such as "The problem is that the research and information is used to educate medical practitioners is completely false, they have literally been brainwashed when it comes to fluoride") also oppose vaccination (with talk of hoaxes), then I have to agree with Saletan that

Conspiracy believers are the ultimate motivated skeptics. Their curse is that they apply this selective scrutiny not to the left or right, but to the mainstream. They tell themselves that they're the ones who see the lies, and the rest of us are sheep. But believing that everybody's lying is just another kind of gullibility.

 

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if I lived in Hawkes Bay I'd be keen to attend this Royal Society public lecture, & I'll certainly be watching the video, which will be available after. It looks like being of interest & value to senior Biology teachers.

The ninth lecture in the 10X10 series
 

Why did the pigeon cross the road?

Dr Claire Postlethwaite


Napier | 7.30 Tuesday 19 November | Hawke's Bay Holt Planetarium | View Livestream

In this lecture, Dr Claire Postlethwaite  (University of Auckland) will talk about using mathematical models to understand animal behaviour, using examples from homing pigeons,  possums, bees and electric fish.

The lecture is being livestreamed courtesy of i-film NZ Science. You can watch the lecture live or watch it afterwards. You can also skip back and see earlier parts of the talk while it is livestreaming. 
Visit our website for full details of the 10X10 Lecture Series, including audio and video recordings of previous speakers in the series.
 
View Livestream

 

The lecture is free and open to the general public. 

Enquiries: 04 472 7421 or lectures@royalsociety.org.nz

 

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Every now & then the husband goes on a fossil-fossicking expedition, in order to add to his collection of things long dead & turned to stone. There are a number of good sites in the Waikato region, and one of them has yielded quite a few belemnite remains: specifically, the bullet-shaped fossilised internal shells of one group of cephalopods. Plus he's also found a few rather lovely ammonites, though nothing on the same scale as a giant specimen found near Kawhia Harbour in 1977. (Apparently the largest of all was found in Germany - its shell, if uncoiled, would be close to 11m long!).

The evolutionary history of cephalopods spans around 500 million years, and there's a good overview of this on the UCMP(Berkeley) evolution website. I hadn't visited this part of their site before, but was directed there by PZ Myers (who else?) & his use of this stunning image - too beautiful not to share :)

Beautiful, but deadly:

These little molluscs - members of the largest species grow to be about 15 cm long, head tip to tentacle tip - produce two different venoms. One, they use in hunting their usual prey1 of crabs and shrimps; the other is released when the animals are alarmed or agitated. While people certainly report blue-ringed octopus bites, it seems that the toxin may also be secreted directly into the water: the author of this website reports feeling localised neurological symptoms after putting his hand into a tank of seawater that had been used to transport a largish specimen. The venom contains the poison tetrodotoxin (TTH)2, also produced by a range of other organisms including a genus of newts, some harlequin frogs, snails, and worms from a number of different phyla. And, of course, the pufferfish, whose family name (Tetraodontidae) gives us the name of the toxin.

This poses an interesting question: why would members of so many different phyla evolve the same poison? It turns out that it's not actually the animals who make the TTH: the job's done by colonies of symbiotic bacteria living in their poison glands. Life really is more complex and more complicated than we can imagine.

1  Sometimes, the prey fights back: 

2 It's been suggested that TTH is the mysterious ingredient supposedly used in zombifying people - you'll find an interesting discussion of this idea here on HowStuffWorks.

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I must admit, I'd never really thought about this one (although I suspect littlies would find it amusing). However, it does appear that silence, in this case, is definitely not golden (and it's got a lot to do withe the mixture of gases produced during bacterial fermentation in the gut).

 

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It's much harder for a sperm to swim, than it is for a sperm whale. Why? This excellent TEDed video explains: 

I think I'll use it next year, during the 'reproduction' section of my first-year biology paper :)

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Last year's Schol Bio paper contained (as is usual) some interesting and challenging questions. One of them was about earwax. More specifically, the earwax phenotypes 'dry' and 'wet', and what their distribution can tell us about patterns of human evolution. (Note to those sitting these examinations: most questions have a reasonable amount of resource material provided and this one was no exception. Remember to use this information in your answers! Ignoring it, or - just as bad - copying bits rather than incorporating the material properly - is not a sign of a good response.)

I was particularly interested in this question because we used to look at the distribution of various phenotypes, wet & dry earwax among them. The examiner provided information about the nature of the genetic information underpinning the two phenotypes, along with data about the global distribution of people with wet & dry wax in their ear canals, including a very helpful map. The following graphic is not that map, but is very similar - showing allele frequencies rather than the phenotype distributions used in the exam - & accompanies an excellent blog post on the Discover magazine site. The 'A' and 'G' represent the 2 alleles involved in determining the relative dampness of your earwax: 

Earwax is wet unless an individual has Adenine (A) at a particular site instead of Guanine (G), in which case the wax becomes the dry form. People who inherit the version of the gene that has A from both parents have dry earwax. People who inherit two of the G versions, or one G and one A, have wet earwax.

The actual question asked candidates to

use biological knowledge, together with information from the resource material, to discuss:

  • the origins and inheritance patterns of dry earwax
  • the evolutionary factors that may have resulted in the present-day distribution of both types of earwax.

And as always, a successful candidate would address all parts of a question. Nor would they assume that the examiner 'knows' what they know - you do need to spell out your understanding. 

So, for the first bullet point: we're dealing with a substitution mutation, where a change in a single base (from G to A) has led to a single amino acid change in the final protein. That secretory protein's function is altered so that the wax that's produced is now 'dry'. The mutation must have occurred in a gamete-producing cell, or at the least during meiosis, & subsequently entered the human population's gene pool. We know it's a recessive mutation as someone must be homozygous for the allele to express wet wax, while heterozygotes have dry earwax. And you could also add that it's not a sex-linked mutation, because (as the resource material notes) the gene involved in wax secretion is found on chromosome 16.

The second part of the question requires you to relate the information on the distribution of 'dry' & 'wet' wax phenotypes to your knowledge of patterns of human dispersal (in this case, the 'out-of-Africa' model). The fact that there's no 'A' allele in African populations suggests that this mutation must have arisen after our species started to spread out of Africa. Furthermore, it could well have appeared once a small founder population had arrived in China, with subsequent genetic drift removing the dominant (G) allele from that founder group - this would explain the very high frequency of the A allele (up to 100%) in that region. You could also argue the possibility of positive selection pressure on this version of the secretory protein (an idea critiqued by the author of the Discover blog post).

However, the A allele is also found at fairly high frequencies in other Asian countries - the most likely explanation here is that subsequent migration and interbreeding has introduced it to those populations (with 54% of Indians and 69% of Japanese now expressing the 'dry' phenotype). Until fairly recently there was only minimal migration from China into Russia & Europe, which accounts for the very low frequency of the recessive allele in those populations.

What about the Americas? Our current understanding is that humans migrated into North America from Asia via a land bridge across the Bering Strait, during a glacial period. (There's an interesting discussion around this here, including some work done using a molecular clock based on mutations in the common human pathogen Helicobacter pylori to estimate migration paths & times.) In dealing with this part of the question, I can think of a couple of options: that the lower frequency of the A allele in native American peoples reflects a founder event where the allele was at lower frequency to begin with, & subsequent genetic drift; or that the A allele frequency originally reflected that in Asian populations, but was diluted by a significant drop in population size following European settlement & some later interbreeding with the settlers. Simiilarly, the low A frequency in non-native Americans simply reflects their relatively recent arrival from Europe.

Who'd have thought that the story of earwax could be so fascinating?

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The daughter & her friends play Assassin's Creed from time to time. This little arachnid would fit right in:

Photo: Jeremy Miller

For this is an assassin spider, one of a number of species (in the superfamily Palpiamanoidea) that prey on other spiders.

The assassin spiders have a long history: a combination of fossil & DNA evidence suggests that they go to before the supercontinent Gondwana began to break up under the slow but irresistable influence of plate tectonics. While there's one fossil found in what's now the northern hemisphere, all living species are found south of the equator, in Madagascar, South Africa, and Australia.

These strange little creatures are only a couple of millimetres long, but have a set of adaptations that allow them to strike their prey from a (reasonably!) safe distance. Their fang-tipped jaws are enormous - in the image above, the jaws holding the spider's meal are about the length of the animal's abdomen. The long 'neck' is an extension of the cephalothorax - the first of the 2 major sections of a spider's body (the other is the abdomen, or opisthoma). The combination of neck & jaws means an assassin spider can impale another spider before the latter is within range to strike back. That's after they've found their prospective dinner by following lines of thread it's left behind, using their very long forelegs (which may also be used to lure the prey closer.

Which is probably quite enough for those of you who aren't fond of spiders, not even itsy little 2mm-long spiders. But for those who want to find out more, try this video:

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