I studied for my first degree at Bangor many years ago, though I have friends who still teach there now. I enjoyed my time there, and the facilities seemed adequate for the purposes of teaching. There is no doubt that larger and better funded universities are going to be able to offer a broader set of training experiments, final year projects and resources - but then larger universities also have a lot of other people competing for those resources. What I liked about Bangor was that it was small enough to get to know the lecturers quite well - the other main reason for choosing Bangor is the surrounds - beaches, islands, open water and mountains all on your doorstep.

If you are associated with the school of ocean sciences (they run a marine zoology course) there are some good resources, and Bangor is especialliy well known for it's marine biology and oceanography courses and has its own fully kitted research ship.

The university accommodation in Bangor, as in many of the other universities in the UK, is very similar and perfectly adequate. Some of the hall accommodation in Bangor, such as Bryn Dinas, offer unparalleled views over the Menai Straits, and others such as Elidir offer views over Snowdonia - but then it depends on your room position (and this will be allocated, not chosen). Accommodation for subsequent years varies greatly, from real holes to rather lovely houses. It's important to team up with other potential flatmates and find somewhere at the start of the second term of your first year if you plan to get the best choices.

Bangor is one of the cheaper areas in the country to live, with rents generally being a little lower than those in the bigger cities. Bangor is popular with international students (as well as mature students), and certainly always has a large number of South Asian, African, Japanese and SE Asian students (often for Agro-Forestry courses or accountancy) - I spent all of my time living and maing friends with overseas students, which I valued greatly. In many respects I always felt that Bangor was better known overseas than it is in the UK.

As for how your grades translate for their entry requirements, you will need to follow David's links above.

There was a computer game a few years back called Bio-Shock (http://en.wikipedia.org/wiki/BioShock), which took rather artistic licence with the concept of a 'plasmid', but none the less the concept of them providing some useful extra ability is broadly speaking true....in bacteria, not so for humans I'm afraid.

Creating plasmids is very much like a carpenter making their own tools for their work. Many scientists buy them, but I used to make my own - mainly because I actually worked within the discipline of plasmid biology - and yes, it can be very tricky! Cloning a gene into an already existing plasmid is not creating a plasmid (although it does become a different plasmid); whilst making a new plasmid seems easy on paper, as essentially you just need some DNA and a region that enables the replication of that DNA (there are numerous ways), if you try to get too inventive you can find that evolution by natural selection mangles and distorts your creation so that - as far as the plasmid is concerned - it replicates sustainably, but it's often barely fit for what you wanted to use it for.

MRSA, like many bacteria, can exist in a number of different phases of growth, and there is a phenomenon known as dormancy in bacteria. This is not a characteristic aspect of day to day growth, but is instead and alternative (and often temporary) period of non- or slow-growth. However, the terminology for this in bacteria are often confused and overlapping, and includes persistence, sensecence as well as dormancy.

These may mean different things in different bacteria, but they all roughly describe a period where the metabolic engines of the cells effectively shut down, thus the cells in many respects 'play dead'. The reason this is important is because antibiotics often act like spanners thrown into a machine - but if the machine is 'off', they don't cause any damage. Other antibiotics need the cell's own energy to be taken up by the cell, so likewise, if cells aren't active, this doesn't happen.

Persistence and slow-growth are particualar issues in diseases such as TB, but they've also been described in other infections, such as cystitis and some soft tissue infections. Most studies on this type of growth in MRSA have been performed in laboratories, and it's hard to say whether persistent colonisation, and stubborn infections are due to the baceria 'playing dead', or simply due to inappropriate treatment (or poor blood supply carrying immune system/antibiotics to the infection).

Ultimately a healthy immune system clears any infection (antibiotics can't do all the work), but in people with poor immune systems, we need to consider developing antibiotics that not only kill every growing cell, but also every non-growing cell too. There are a number academics and companies looking such approaches now, mainly led by TB, but also MRSA, e.g. http://www.helperby.com/.

Yes, sometimes bacteria merely need to move to another part of the body, and have an opportunity to invade a space where they're not normally found. Many 'would-be' bad bacteria are kept in check by the many other bacteria that surround them, each competing and finding their place within a particular part of the body.

For example, one type of bacteria that lives in the back of the nose, Staphylococcus aureus, can be quite a capable pathogen (disease causer), and has an arsenal of weapons it can use to cause infection, but many of these abilities are suppressed by the high salt content of the nose (amongst other things). Moving from that environment into, say, an open wound following injury or an operation can present it with an opportunity to attack, with less of the control elements there.

Whilst it can keep a low profile away from your innate immune system in the nose, once it enters the cavity of the body it is recognised by the powerful adaptive immune system and in most cases is cleared. Obviously problems arise when the immune system or blood circulation is poor, or the strain is spectacularly virulent.

Hi Esme,

It is not a given that all bacteria require glucose, in fact some would struggle with having too rich a glucose diet. Bacteria are simply after viable carbon-sources, and there are many carbon-molecules that can provide an energy source, and building materials for the cell to grow. Some may be other types of complex sugars, others you would barely regonise as a sugar. Different bacteria use different types of enzymes to break down cellular components; in some cases they can take the carbon-molecules that become available directly into their metabolic cycle, but others may need more 'chewing-up' by enzymes. In some cases bacteria can strip the sugar molecules that are part of protein complexes.

What is especially interesting about the sources of carbon different bacteria use is how bacterial communities can be inter-dependent upon each other. Such ecosystmes are sometimes called consortia, where one type of bacteria will break down rather complex carbon-sources, and take what they need, leaving smaller carbon-compounds that another set of bacteria can use, who take their fill, but also producing still further carbon-compunds that other bacteria can now access.

That being said, the surface of the skin is a very harsh environment for bacteria, which is why the bacteria you tend to find there are more specialised and colonising these areas, but as part of their evolution they've evolved mechanisms to extract the food they need from the sources available to them.

A kefir culture is a mixture or community of often quite a number of different microbes, predominantly well known species of the Lactobacilli, but often a few more exotic bacteria. Kefir cultures do have variation, depending on where and how they are prepared in the first place, but they do tend to be quite stable than monoculture starter cultures often used in yoghurt starter packs. Monocultures are susceptible to competition from competing bacteria species, and often because milk is usually pasteurised, robbing them of its normal (predominantly Lactobaccillus ssp.) flora, rogue bacterial species that subsequently contaminate the milk have an opportunity to proliferate.

The other thing that can aid stability is that over successive generations being re-started into the same environment, the culture evolves to make best use of this environment. This means that some species will become more predominant often at the cost of the loss of other species, until a stable community is established; however the relative abundance of individual different species of bacteria may vary depending on the age of the fermented product as acidity will tend to increase over time, which some species will like, and others less so.

However, without doing genetic analysis on the community over the course of your many years of using it, it is hard to say whether in fact it *IS* still the culture you started out with 25 years ago. Taste testing is one measure, but it is not a reliable measure as it is subject to alterations depending on accompanying foods, medications, age etc.

I've performed a number of 'home culturing experiments' over the years, so I would be of a mind to split the culture and continue to culture them independently (without cross contaminating them) to assess the extent to which they prefer goats milk as compared other types of milk. You might keep one only for goats milk, but take the other and try it on a range of other milks, before eventually re-introducing it to goats milk, and then compare it with the culture that only ever gets goats milk - preferably using the same source of goats milk for comparison. Can you taste a difference? From a microbiologists point of view, at the genetic level, there might well be some fluctuation in the culture composition.

However, if it tastes good, we can just be thankful for that.


This sounds like it is your research exercise to answer these questions. We do not do homework for students, at any level. We are happy to help with concepts that are not explained well in the literature, or genuine questions about the world around us. Research skills are an important part of your education, and I would suggest you make good use of Google / Google Scholar and PubMed to identify the information you require.

The only hint I will offer is that you need not limit yourself to 'elephants' per se, and perhaps develop an understanding of the circulo-respiratory system, before focussing specifically on pachyderms.

There are no hard and fast rules governing which initial bachelor's degree is required for specific postgraduate degrees. I've known people from broad biology background who have done PhDs in structural biology and zoologists who have gone on to study microbiology. Obviously it can be a competitive help if you have some background to your intended postgraduate degree topic, but as I say, there are generally no rules other that you have the requisite good grades in a scientific or medical background.

In the UK you would need to complete a postgraduate certificate in education (PGCE) and many universities offer such courses. I cannot comment on the requirements in the US education system if that is where you are based.

Indeed, it's worth clarifying that just being resistant to an antibiotic, or indeed antibacterial wipe, does not necessary mean that the bacteria is any 'nastier' than one that is susceptible to such chemicals. Many people can pick up MRSA in and around hospitals (or when working with it) and remain as unharmed as they are when colonised by their own indigenous forms of Staphylococcus aureus. The problems arise when poorly people with weak immune systems get infections, or if you have a significant internal surgery that becomes contaminated. In these situations the resistance does become a problem to the management of the infection.

There should be no theoretical limit to the size of the plasmid being transformed, given that properly supercoiled plasmid molecules are reasonably compact structures.

Assuming that a 3kb and 50 kb plasmid have net neutrality effect upon introduction into a cell, it has more to do with the fact that the common unit of efficiency is based on a mass rather than number of moles. If you make sure you transform the same number of plasmid molecules, then you should see some consistency between the sizes (which is what I see when I work with my 50 kb+ plasmids - it just takes a bit more effort to prepare sufficient concentrations of supercoiled large plasmids!).

Heh, great analogy Combiz ;-)

I'm not entirely clear what it is you're asking, so I will provide three answers depending on what it is you might be getting at:

If the plasmids share genes that are required for survival, then this this will provide selective pressure to maintain / propagate the plasmid.

If the plasmid contains essential genes that are facsimile copies of similar genes on the bacteria, then there is a good chance that the plasmid will integrate via homologous recombination into the locus of such a shared gene on the chromosome; it may, at a later date, also loop itself back off the chromosome taking adjacent flanking genese from the chromosome with it.

If the plasmid carries an toxin-antitoxin module, then it is essential that the plasmid be maintained; by producing a long-lived toxin and short-lived anti-toxin, loss of the plasmid from the bacteria will result in the long-lived toxin killing the cell.

Not all recombinant plasmids will be capable of horizontal gene transfer (HGT), or being transferred. Certain DNA processing and mating-pair formation sets of genes are required.

Vertical gene transfer happens whenever a cell divides to give daughter cells, both with respects to the chromosomal DNA and to plasmids present within those cells (which may be divided up either by active partitioning into each daughter cell, or randomly if the copy number of the plasmid is sufficiently large).

HGT is the transfer of genetic material by a number of potential means, but an example of conjugative plasmids is fine, wherein transfer of plasmid DNA, and in rare circumstances even a goodly amount of chromosomal DNA, is transferred from one cell to another without there being a necessary vertical heritance between those cells. Thus it's not an act of sexual reproduction.

Vertical gene transfer happens in 100% of bacterial reproduction, whereas HGT may, in comparison, be a considerably rare event; perhaps as little as one in a million cells sharing an appropriate conjugative plasmid in a 16 hr period.

I would give it every chance to regenerate, Echinaster really do have impressive regenerative capabilities, so long as the central disc is not compromised. It's not uncommon for the regenerated limb to be slightly smaller in dimension to the original, though this depends how much nutrition is available to it. If the 'dissolving' of the limb appears to extend into the central disc, then it might be it is unrecoverable, so you might then give it a sea burial.


I have to say that this does rather sound like a homework question, because I have set similar questions for my tutees. The process you are referring to is 'plasmid partitioning', which can be either a 'passive' or 'active' process.

These key words should be good starting points for your research.

If you are asking purely from interest (and why not, because as a once plasmid biologist I find plasmids fascinating) then please do post again.


I would also add that it is always worth making informal contact with the principle investigator in any given academic job advert, and perhaps ask whether the job is 'earmarked' for someone, such as a finishing up PhD student in that lab. In my experience, both applying for such positions and being on interview panels for them, sometimes jobs are advertised that are clearly earmarked for a particular person, and they're being advertised externally due to the insufferable bureaucracy of human resources and employment law.

Hi Sofia,

Well, the market isn't exactly stunning over here at the moment either, but the usual routes I have taken in the past are:


It's worth noting that many academic science positions get filled internally and often aren't advertised, thus I would recommend identifying principle investigators at institutions where you'd like to work and enquire informally about work. There are many academic research centres in London, both within universities and at research institutes associated with medical research funding charities, e.g. MRC, so you will have to work your way through their various websites via Google. If you have a particular set of ideas that complement the theme of research in a particular lab, you might also consider assisting with an application for funding.

Kalí tíhi.

I've written a piece about the ecology of glacial cryoconites (http://www.mentalindigestion.net/?p=1361) that you may find of interest.

When you say 'in practice', does this mean that you actually plan to do this in a lab? If so, then I would imagine there are better sources for such technical information, such as literature related to the particular organism with which you wish to work.

If not, then a 'theoretical' knowledge will more than suffice.

Hi Emily,

It sounds like an interesting project, but it also sounds like one that you should be investigating yourself. We receive rather a lot of questions in this format and I can't understand why a teacher would have you ask a scientist these questions when you could learn so much more by actually researching the answers yourself.

Many of these questions can be answered with a few Google searches, but should any information be thrown up for which you really can't find an answer, please try us again.


This looks like a black variety of elephant hawkmoth caterpillar (Deilephelia elpenor): http://en.wikipedia.org/wiki/Deilephila_elpenor

August / Sept are the peak months for sightings of these.

There are quite a few anomalous eggs out there, in fact there's a website devoted to them, which I've had recourse to visit before:


They do describe a phenomenon (though rare) where an egg can form within an egg, ovum in ovo.

According to one Douglas Russell, curator of the Natural History Museum egg collection, ovum in ova most likely happens because “....the normal rhythmic muscular action,
or peristalsis, that moves a developing egg down the oviduct
malfunctions in some way.” (via

It looks rather like an emergent pupa, than an adult insect. A pupa is the type of transistional form you might see between the larval and adult forms of an insect. I'm afraid I don't know what this particular bug is (one way is to leave it be and see what it emerges as!), though it looks like it could be a beetle, it may even be a species of ladybird.

Perhaps one of the other biologists who has seen this insect in this form can give a definitive answer.

David, my position on probiotics (with some evidence) is pretty much reflected in the first half of this blog post of mine: http://www.mentalindigestion.net/?p=1476


Probiotics seem to be turning up in a variety of high-end pet foods, claiming to stimulate good digestions.

I remain to be unequivolcally convinced that probiotics added to foodstuffs are actually worthy of merit, though they have been shown to be of some value in treating some cases of infectious diarrhoea. This is not to say that they are harmful, or that the idea of supplementing dietary bacteria is a bad one, it's more the case that: a) it is often used as a marketting ploy to increase the commodity value of something, b) they're often poor quality, frequently actually 'dead' and ocassionally don't contain the bacteria they're supposed to, and c) adding one or two species to the natural mix of gut bacteria (which are comprised of hundreds of species) seems a little hit and miss.

In any case, to answer your question Enterococcus spp. (i.e. numerous Enterococcal species, including E. faecium) are naturally occuring (commensal) bacteria that exist in the guts of humans and other animals, at varying proportions. However, many such commensal bacteria can become opportunistic pathogens when an animal is immuno-compromised, or when the bacteria enter another part of the body than where they're normally found. In those situations they can cause disease.

The probiotics in this food should not represent an overt health risk, any more than the dog itself, which like any human member of the family, will be full of a great many other bacteria of different types. If your sister is undergoing out-patient chemo, ensuring good hygiene practises is always a general recommendation to prevent easy-preventable infections, as you would the very old and very young. With regards the dog food - treat as you would any food item: always remember to wash hands after preparing food, keep food bowls clean and washed (wash with a separate cloth if your are concerned, I generally do anyway), and all of us should be in the habit of washing our hands before before eating in any case.

Hope your sister gets well soon.

The image is a little small, so you have the advantage of having seen it up close, but I suspect that it is a white-lined sphinx moth (Hyles lineata). Their larvae are extremely variable, this being a black form with yellow or orange alternating stripes, but the confirmation is in the adult moth that emerges. By this account (http://artsandsciences.colorado.edu/mag … n-the-day/) the white-lined sphinx moth is quite common in Colorado Springs.

Hmm, your autofocus seems to have snapped to the decking floor, rather than the table top, which makes it a little hard to be sure of the details/size of these insects, but I would hazard a guess and suggest they may be Thrips (http://en.wikipedia.org/wiki/Thrips)

The phenomenon you're describing is process known as canalisation, where genetic variation can potentially be kept in check by a hypothetical mechanism called evolutionary capacitance, which maintains the outward appearance, or phenotype, of the organism, despite genetic variation.

Heat-shock proteins, such as hsp90, have been implicated in this role, but further evidence is yet to support the hypothesis of capacitance (though I quite like the hypothesis). Essentially, heat-shock proteins, as you will be aware, assist in the folding of numerous cellular proteins as well as signalling protein / transcription factors that control where, when and how numerous other genes are expressed.

The suggestion is that in times of stress, when the heat-shock proteins are sequestered by an increasing number of cellular proteins struggling to fold, those cell signalling proteins hsp90 normally maintains are free to adopt a range of altered behaviours. This can interfere with the development of the organism, resulting in morphological variants upon which natural selection can act.

More recently, it has more shown that mutations within hsp90 itself can generate new variation, rather than unleash pre-existing variation. I've written about this, and the experimental evidence for it, in an ResearchBlog (http://www.mentalindigestion.net/?p=1607), but basically the suggestion is that hsp90 also regulates the production of small RNA molecules Piwi-interacting RNA (piRNA), which are important in silencing various genetic elements, including transposons. Transposons are examples of mobile DNA that can snip themselves out of the chromosome and insert themselves elsewhere, sometimes mutating a gene in the process, and indeed, sometimes activating dormant genes in the process.

The researchers found that mutation of Hsp90 is directly coupled with an increase of activated transposons jumping around to other regions of DNA, and that the phenotypic mutations they saw in Hsp90-mutant fruitflies were due to mutations produced by these activated transposons.

I thought it was pretty interesting at the time, which is why I've written about it before. Various concepts in evolutionary biology such as canalisation, capacitance and contingency are all relatively new and highly experimental areas that are being investigated in molecular evolutionary studies. Exciting times.

Ah, this is a fairly common little bug, a type of shield bug (needless to say why they're referred to as that), with this particular one being a Forest Bug (Pentatoma rufipes) (http://www.britishbugs.org.uk/heteropte … fipes.html)

No, algae are not bacteria at all.

Algae (http://en.wikipedia.org/wiki/Algae) are classified as eukaryotes, which is ultimately the same domain of life that includes higher plants, fungi and animals (including us, of course). Bacteria are a domain unto themselves, and quite distinct. The only similarity between algae and bacteria is that they are single-celled organisms, at least when in planktonic form. Otherwise, they are actually quite different.

Where the confusion arises is in cyanobacteria (http://en.wikipedia.org/wiki/Cyanobacteria), which in the past were also known as 'blue-green algae'. As far as we're concerned, cyanobacteria are bacteria, all be it bacteria with the feature of being photosynthetic. They have no membrane bound organelles (typical features of eukaryotes), they have a single circular chromosome, a cell wall that contains peptidoglycan and prokaryotic sized ribosomes - all classic features of bacteria. They can form structured colonies in the form of filaments and sheets, not unlike algae, but then again there are numerous bacterial species that can also form super-structures comprising colonies of individual cells.

Yes, as Ajna says, air dried is best. Whilst clean water is fairly innocuous, I doubt the the water jar in your office is particularly clean. Any sugar carried over from stirring tea will help fuel a community of bacteria growing in the glass, and whilst I don't imagine there will be anything particularly nasty growing in there, it's best practise to avoid storing anything in warm, wet environments.

The original poster, Ellis, persisted and managed to get an identification via a senior invertebrate specialist at Natural England, who says that this is a Pallopterid, P. muliebris.


Pupa of Harmonia axyridis (Harlequin Ladybird).

The top two are certainly Ladybird larvae, my car is currently covered in them. Wonderful little things. I think this species is Harmonia axyridis (Harlequin Ladybird).

The bottom photo is a pupating Ladybird (metamorphosing between larval and adult form), so the same species as above.

I think it is some sort of Tephritid fly, perhaps some manner of Thistle Gall fly.

Ah, you succeeded in loading the photo. It is as I mentioned before you posted the photo:

"...Sphingids (a family of moths) can often be mistaken for Hummingbirds, or vice versa, and indeed one member of the family, the Hummingbird Hawk moth (Macroglossum stellatarum) is particularly impressive."

You do in fact have a Hummingbird Hawk-moth here, nice capture.

You don't seem to have posted the images, but some Sphingids (a family
of moths) can often be mistaken for Hummingbirds, or vice versa, and
indeed one member of the family, the
Hawk moth (Macroglossum stellatarum) is particularly impressive.

You don't seem to have posted the images, but some Sphingids (a family of moths) can often be mistaken for Hummingbirds, or vice versa, and indeed one member of the family, the Hummingbird Hawk moth (Macroglossum stellatarum) is particularly impressive.

I think this is in fact a Pellucid hoverfly (Volucella pellucens), one of the larger of the hoverfly species.

It is one of many species of Hoverfly (harmless nectar feeders and important for pollination; and all round awesome flyers) we have in this country, this one I believe is Volucella zonaria.

A recent article in Nature News, 'Researchers on a mission', highlights the broadening multidisciplinarity of marine biology (as is the case with many scientific disciplines), and is a good careers piece in general.

To be honest, it just like a regular Common Wasp (Vespula vulgaris), but there is some variabilty in the actual markings, which can make identification tricky. It would be useful to also have a head shot, as these can aid identification.

It could also be a Tree Wasp (Dolichovespula sylvestris), but again, without a head shot, hard to conclude.

Indeed, could well be a thrip - they're certainly common enough at the moment.

Good effort on the photograph, though still a little small. I suspect it is some sort of Rove beetle, which doesn't really narrow it down much, given that this family accounts for nearly a quarter of British beetles. My recent jaunts on my bike amidst the crop fields of the North of England have had me covered with these guys at various points.

Apologies. As we usually answer questions for school aged children, a complex question is often a dead giveaway that it is a teacher's question. What you surmise in the latter part of the above sounds a fairly plausible mechanism, assuming a basic evolutionary process of mutation -> feedback -> revision.

What you're asking about are some of the finer points of 'tetrapod evolution' and evolution of the nervous system, which are terms that will provide some useful search hits. However, you question is a rather big one and could probably fill quite a bit of space. For my own part I am neither a neuroscientist, nor any specialist in tetrapod evolution; though there are others on this network who can shed more light. In my own opinion, your question could be resolved by addressing the underlying mechanism of neuronal development per se, tempered by the consideration that such mechanisms will be enacted over an evolutionary timescale.

In a recent review on the subject of fin to limb evolution a proportion of the discussion devoted to the genetic basis for limb development - which is based on a conserved bauplan (top level anatomical instructions, namely the hox genes) shared between all vertebrates, but which is obviously further refined for the purposes of the tetrapod bauplan.

Jennifer A. Clack (2009) The Fin to Limb Transition: New Data, Interpretations, and Hypotheses from Paleontology and Developmental Biology. Annual Review of Earth and Planetary Sciences. Vol. 37: 163-179. DOI:10.1146/annurev.earth.36.031207.124146 (I can provide you with this paper if you so wish).

What we understand from hox genes is that anatomical changes from fin to limb do not necessarily require the degree of genetic re-writing that some might imagine. "In vertebrates, limbs or fins start off as paired swellings in the ventral body wall that will become pectoral and pelvic appendages, called limb (or fin) buds. ... In tetrapods, as the limb grows outward, these genes continue to be expressed, whereas in zebra fish their expression soon ceases, and the bud does not extend distally." Duplication and inversion of gene clusters controlleded by hox genes have suggested some of the mechanisms by which development of the limb is co-opeted from existing plans for the development of the fin.

The review highlights that improvements that aided air-breathing while the animals were still aquatic (the support and elevation of the upper body above the water-line) were the driving factors for limb development, rather than locomotion. However, such developments often open up unforseen (as evolution has no 'aim', of course) advantages, in this case locomotion, leading to strenthening of the bones, larger surface area for the attachment of muscle ligaments, and (one imagines) the coevolutionary refinement of the necessary controling motor neurons. In such a scenario we can imagine that the limb structures may have run ahead of the motor controls that subsequently developed for their use in locomotion.

Given that all vertebrates have a centralised nervous system, they are all working on a similar basic nervous bauplan that mirrors the more obvious gross anatomical framework, all of which (at least developmentally) are controlled by hox genes. Thus we can imagine that changes in one are likely to be reflected by the other, with such anatomical changes still being innervated by the same essential nerve groups (or off-shoots of these nerve groups), but further refined by increased motor control in the brain (subject to new uses for such appendages).

In terms of understanding the specific biomechanics of motor neuron development from fin to limb, this would require a more complete understanding of the skeletal mechanics and limb growth and function of earlier tetrapods, which is something (the review states) that is still being studied.

However, without going to the lengths of comparing fish motor neurons with tetrapod motor neurons to understand how it is that such neurons develop, we can look closer to home. Even between chimanzees and humans there is a significant difference in the density of neuronal grey matter controlling motor function (which, incidentally, I have satired elsewhere), thus our own cognitive development seems to have evolved hand in hand with the fine tuning of our motor neuron control; this division between chimps and humans is discussed in more detail in post by Neurophilosophy.

Your question raises in my mind a similar question of the evolution of speech and language. The evolution of speech can be studied independently of the evolution of language, and indeed the two processes are distinct to a point; but to what degree, or at what point, did language start playing a role in the development of nervous control of the speech apparatus (diaphram/larynx/tongue/lips), or was the apparatus pretty much ready and waiting for language to come along?

(posted in Evolution)

I'm sorry, but this sounds like a homework question, and we don't do students' homework for them.

I'm assuming this isn't homework as I can't imagine a biology teacher using the example you cite. So firstly, the gene for baldness (APCDD1) is certainly not a mere 15 bp, it is some 100x longer.

Genes are generally in the order of hundreds to thousands of base-pairs. I think you are getting confused between swapping DNA sequences (a kin to your example) and define coding regions / genes.

In your example, you have just effectively mutated a short sequence of DNA, which isn't the same as swapping the order of genes; your example would likely be deleterious to whatever gene you did this within.

With regards to what I think you're asking, in some circumstances you can change the position of whole genes within the genome (and this depends heavily on what the gene is, what the organism is, how those genes are regulated, whether they are genetically linked with other genes etc). Suffice to say, you can do it in bacteria, so long as you also move the control element for the gene as well, and consider the above caveats); thus at one level you could say the DNA sequences had been swapped.

There are natural process of recombination that occur during sexual reproduction in higher organisms, however even here it the alleles (the variations of any give gene) that are swapped between parental DNA, but crucially they still occupy the same locus (position) on the DNA, thus the actual order of genes themselves doesn't change. Chromosomal rearrangements can and do happen within populations, however it id difficult to predict the outcome of such phenomena, or indeed whether they will be viable.

This website should answer any questions you have regarding birth control pills.

Michael, I believe suggestions are being made to your previous request:

http://www.askabiologist.org.uk/answers … hp?id=4602

It is true, and it is indeed possibe, though rare.

The BBC has a good write-up of it here.

A statement of numbers that descrive the majority of mutations as being negative is just incorrect. I would also echo Joe's point regarding what exactly a 'beneficial' mutation is? It seems that to be regarded as 'beneficial' it has to meet some criteria of 'improvement', which is very much a subjective position within the eye of the beholder. As evolution is not 'self-aware', nor has an 'aim', who is to say that a mutation that could (subjectively) be regarded as 'negative' wouldn't, given a change in environment, become positive?

One (of several) recent mechanisms within evolutionary biology flagged up in recent studies is the ideas of 'Contingency'. This is where a middling mutation, likely a neutral mutation with no observable phneotype, acts as the linchpin to a further mutation at some point in the future, a mutation which wouldn't in fact happen without this earlier mutation. Thus the later mutation is 'contingent' upon the earlier. Such contingent mutations potentiate (make possible) a route less travelled, opening up new potential adaptations which wouldn't otherwise have been possible.

So whilst many people interpret neutral mutations as having no determinative influence on evolution, there is inceasing evidence to suggest that many factors act to build upon such mutations.

Indeed other mechanisms may seek to suppress the effect of mutations, thus permitting a gradual increase in genetic variation without any apparent effect on the phenotype (appearance) of the organism; this idea (sometimes called canalisation, or capacitance) means that species can remain apparently unchanged for millions of years. The hypothesis (which has some grounding in evidence) is based around the actions of heat shock proteins, which typically assist in the folding of other proteins; in this situation it is the manner in which they control the correct folding of other proteins whose function is to dictate how the instructions of DNA are actually interpreted. At some point, perhaps under stressful environmental conditions, the control over these proteins is slackened, initiating a process wherein the accumulated mutations can be released, thus seeming to result in a rapid radiation of phenotypic traits, some of which may result in individuals with properties suitable to adapt to the new environment. Of course, as with many things in evolutionary biology, there's still a lot of work to be done.

Both these mechanisms are just two of many that both describe how seeming 'leaps' in evolution, and increased 'rates' of evolution can occur, amidst the usual regular grind of spontaneous mutation, genetic drift and natural selection, and provide an argument against those who try back of the envelope statistcs to state that there is insufficient mutation/variation for evolution to have happened. I scoff at the very notion.