Thanks for the explanation of reverse transcriptase and retrotransposon, after 10 pages of reading on this thread I finally learned something.
Keep up the good work WLC, way to think outside of the box.
Thanks for the explanation of reverse transcriptase and retrotransposon, after 10 pages of reading on this thread I finally learned something.
Keep up the good work WLC, way to think outside of the box.
...We can't just assume that any old bit if viral code will have the desired effect. (In fact quite how a bit of viral code has the effect of supplying a resistance to the bee is not explained either.) So we also have to assign a probablity to the transposed viral code being a useful piece (and never mind the mechanics of just it works). Whatever that probability is now has to be multiplied by 10,000 (the probability of insertion happening at the right place).
That, I would guess, would bring us into the same sorts of realms as good old mutation by background radiation - one in lots and lots and lots cubed lots of times.
This rather makes a mockery of WLC's analysis of his 1 in 10 hives experiment. His is a very far from impartial 'analysis' of a very badly conducted 'experiment' on a very inadequate sample. It is, lets recall, a 'theory' supplied by several posters over the course of a week or so - WLC being unable to explain it himself.
To take another easy pot: if bees were able to gain resistance every 10 matings in 'challenged' circumstances, it follows that viral problems would be fixed before they had even arisen!
I'm all for thinking outside the box, but this box has more holes than swiss cheese.
Let us also remember that much of our own DNA and that of virtually all animals was originally viral code. It's one of the mechanisms of evolution.
That's not the same thing at all as incorporating it as a way of gaining resistance to the doner virus.
We gain resistance to viruses through the workings of our own immune system, by exposure mostly. But resistence is also passed down through colostrum - the first part of mother's milk. This is necessary because viruses constantly mutate - you need an up to date 'patch' as it were.
Any virus incorporated into our own code in the manner WLC suggests would be out of date within a generation or two.
Its worth reading this piece at wiki - particularly the part relating to animal husbandry. http://en.wikipedia.org/wiki/Colostrum
I wouldn't say we took it. But it got in there.
In bacteria, viruses insert themselves into the code (remember a virus is not a living thing, essentially only a section of RNA) and then may live on as part of the bacteria and its offspring indefinitely. At some point in the future, even many generations later, it can reemerge.
My breeding program takes advantage of the natural winnowing, natural exposure, and traditional breeding up of resulting performing stock.
Funny thing, back when the treatment-free thing was in its infancy, you'd hear things like 'you can't breed wolf resistant sheep.' But you can. Nobody does, but you can. You may get sheep with long legs that run fast, or that are well camouflaged, or that eat wolves, or who knows what. Once you have them though, you're going to have to work on breeding back in the traits for wool and meat production. All things considered, bees have ended up being much easier than that.
Introns help make diversity but viral code added to animal cells is different than plant and with meta-genetics and the importance of mythelation in both expression and deactivation of areas of introns because they are unfit... well its a great area of science but thinking you can split a viral infected hive and in your lifetime create a new gene from viral code is a joke the idea it will be a helpful gene is sad. dna has many repair mechanisms. the best we can hope for in our lifetime is micro-evolution as in changing the ratio or combination of genes for a better (or synergistic) effect to combat viruses and parasites.
granted in plants it may be different
This is a great field but what you learned in school is rather useless in five years and from several of the above statements I'd say careful listening to one person or book... though I dont remember even in school being told viral dna(?) could create a intron that would make a new gene for a protein that would benifit the host... wow
behavior, so it is hard to imagine that it was at most a guess
and a hope only 17 years ago when Kefuss began to
experiment with the idea. His respected doctoral mentor,
Ruttner, opined that bees could not be bred against mites,
saying, “Sheep can’t be bred against wolves.”
From 1999 to 2005, Ralph
Buchler tested 13 lines of bees from different areas in Europe on the island of Unije in Croatia for resistance to
Varroa without treatment. Kefuss’ bees from Toulouse were the last to die out. “Ruttner told me that it turns out
that sheep can be bred against wolves.”
Sheep were pretty wolf resistant from the start. Their main defence was probably their exquisite climbing ability. There's a wonderful example of the extraordinary climbing of - in this case - goats, here:
Well there you go. If I could just come up with these things before everybody else does, maybe I could get my name on something beside my own website! :scratch::lpf:
In reference to the article that is the basis for this thread, my reading suggests that the Varroa mites had suppressed reproduction in the Gotland colonies and these same mites were tested in other control colonies and their reproductive success was notably improved to a statistically significant degree. This answers a criticism I have seen in other venues (and possibly this thread, I don't remember) that the "obvious" explanation for the reduced reproductive success was essentially entirely on the basis of the selection of a less fecund mite population.
That's not it.
The original 'Bond' studies claimed that the bees had adapted rather than the mites. However, they still can't provide specific evidence for the mechanism.
My own view is that they haven't demonstrated 'co-evolution' between mites and bees.
However, Maori et al. (2007) provided specific examples of co-evolution between IAPV and Honeybees. They found IAPV fragments in the Honeybee genome (providing resistance), and Honeybee sequences in IAPV!
It does seem obvious to me that where bees are targetting large mite families and leaving smaller ones alone, the result will be the emergence of mite strains that have smaller families. The 'coevolution' is the result of bees effectively breeding less fecund mites.
If, as you say, the mites were tested in other colonies and found to tend to return to larger families, that would tend to confirm the hypothessis that the first (VHS) bees were responsible. (An extract would be handy)
The mechanism responsible would be the VHS bees' tendency to uncap and destroy larger mite families, but to leave small families alone. There appears to be evidence (see below) that the bees even leave alone and recap small mite families - at least I think that is what is being inferred - the writing isn't explicit.
That's how I make sense of it.
In this case I think its safe to say (against WLC's view) that co-evolution is what is being observed. We should note that this 'evolution' can switch back rapidly - there's nothing fixed about it.
BTW: We need to acknowledge the multi-layered nature of the term 'mechanism'. 'Mechanisms' are known to be tricky things to talk about. I've speculated about a 'mechanism' above, and it seems like a plausible explanation to me for how VSH 'works'. But it doesn't say anything about the lower level 'mechanism' responsible for the bees' behaviour in the first place. This is known to be genetic - because it is heritable - but the exact gene locations responsible are undiscovered as yet. So WLC, who is interested in the molecular level - is quite right in saying 'the mechanism' is unknown - at that level. It is also right to to say that part of the second-level mechanism - of how bees detect varroa in closed cells in the first place - is unclear. (The best guess as far as I know is by odour.)
Saying 'the mechanism is unknown' is true therefore in some respects, but not in others. And we must be careful not to elide - to infer unknowns from one area are unknowns in others - where things are better, even if imperfectly, understood.
Its worth bearing in mind too, none of this need concern beekeepers at all. As long as you follow the method of propagating from best - boosted if necessary by more intense breeding measures - all will be well. You don't need to know any more than how to apply to bees the dictum 'put best to best'.
Bees with the trait were initially bred by the USDA Honey Bee Breeding, Genetics and Physiology Laboratory in Baton Rouge, LA from colonies in which mite populations grew only slowly.
The factor causing slow mite population growth was found to be heritable. The rate of mite population growth was found to be correlated with the reproductive rates of mites, resulting in naming the factor “suppressed mite reproduction” (SMR). It was subsequently discovered that the factor is founded on hygienic activity of adult bees, so SMR was renamed VSH.
VSH activity results in (1) an abnormally low proportion of mites that produce offspring within the population that remains in capped brood and (2) reduction of the brood infestation rate by greater than 70%. The specifics of how hygienic bees detect mite infested brood currently are unknown.
Extension.org: Selecting for Varroa Sensitive Reproduction
Select on mite infertility
The most reliable method is to select for a high infertility rate in the mite population (Fig. 2). We are not certain how it happens, but somehow VSH increases mite infertility. Generally, 15-25% of mites in non-resistant colonies do not lay eggs. Infertility increases to 80-100% in colonies with pure VSH queens. Mite populations eventually decline in these colonies because so few mites lay eggs.
Removal of mite-infested brood is probably triggered by unusual odors that penetrate the cell cap to the outside where hygienic bees patrol the comb surface. We have observed that VSH bees respond vigorously to highly infested brood (e.g. 15–25 mites per 100 capped cells) that is transferred into the colony (Fig. 4). They uncap and remove many mite-infested pupae quickly. They respond with much less intensity to brood with low infestation rates (1–5 mites per 100 capped cells), probably because the chemical signals that trigger removal are less concentrated and harder to detect.
Another characteristic of VSH bees is a reduced fertility of mites, when compared to non-VSH bees. In a colony, mite fertility is reduced several weeks after introduction of VSH queens into non-selected colonies.
The VSH bees shown in Fig. 7 have about 30% reproductive mites (a normal family capable of producing a mature daughter). About 55% are infertile or non-laying mites (blue slice), and there are mites that die without producing offspring (red slice). There are also mites that produce a family, but their daughters do not mature before the bee emerges (yellow slice). These are fertile because they laid some eggs, but they are also considered non-reproductive because they will not produce even 1 mature daughter.
Sometimes, uncapped cells are recapped. VSH bees will exhibit this recapping more then non-hygienic bees, as seen in the following data (Villa et al 2010)
•Recapped cells (%)
•VSH: 38 ± 0.3 a
•Hybrid: 19 ± 0.8 ab
•Control: 17 ± 0.3 b
It is possible that uncapping and recapping interferes with mite reproduction.
Was it like your 'I made ten splits and one didn't show symptoms, so that one has become resistant.'?
Could you provide extracts of the descriptions of their tests?
The name is WLC.
It wasn't 10 splits, it was 8. We won't know if anything 'jumped' for a while.
Maori, Tanne, and Sela used Southern, Northern, and Western blot analysis, DNA sequencing, and Primer walking, to prove both co-evolution and virus resistance. You really should at least read the abstract. If you want to read the paper, you'll need institutional access. No, I won't send it to you for free.
In addition, both they and U.S. scientistis demonstrated that the IAPV fragment could be fed to bees as dsRNA to make them resistant to IAPV via RNAi.
Their work is rock solid.
The only place I can really see cooevolution in the Locke paper is the title.
Its soooo easy to express an opinion; its much harder to substantiate it. But you have to to be convincing. Unless you're winning the argument with better positions than mine you're - or just by showing how mine is flawed - you're losing it. Swim or sink.
Show us _why_ you think my position - and the authors' - is wrong.
If you want to know how Maori and the Beeologics team did it, I can only recommend that you get hold of the papers yourself.
While we might be able to do the 'jumping gene' detection and preliminary RNA based evidence for resistance, we can't do the key proof.
We can't feed jumping genes back to bees.
Anyway, I'd settle for the detection alone. It's more than enough to find something at that site in the Honeybee. No one else is looking.
Hygienic behavior was described as a possible mechanism in the Avignon hive, but not in the Gotland hive.
So, hygienic behavior is a 'possible' but not a 'definite' at Avignon.
That still leaves us with a need for a 'deeper understanding' of what is occurring at Avignon and Gotland.
I still don't see any proof for coevolution.
Just the usual conclusion: it needs more study.
WLC you're not responding to proper criticisms of your positions, nor addressing direct questions that have been put to you. (I could list them, and they probably come to 20 or 30 by now) You've barely acknowledged any of the points made by others.
This is very telling. It is natural for us to understand that trying to meet these challenges would reveal yet more weaknesses. It speaks of deep bluffing. Its also very un-academic and unscientific. You are not engaged in a discussion with us, aiming to elucidate the facts of your case. You're avoiding difficulties and simply re-stating your beliefs.
That alone wouldn't matter - although its tiresome - and greatly irritating to those whose conversations you're obstructing. But it gets worse.
You are recommending to beekeepers, under cover of scientifically dominstrated fact, an untested GM method of raising resistant bees. The method flies in the face of tested breeding husbandry - anyone following it could expect rapid stock collapse.
It may be a legitimate and valid system - if you're into GM - but -even if if works, and that appears to be unknown, its utterly unsuited to practical bee raising.
Do you understand many people have a great attachment to their stock? Many are dependent on their stock for part of their livelihood, some for their entire livelihood?
Anyway, I'd settle for the detection alone. It's more than enough to find something at that site in the Honeybee. No one else is looking.[/queen]
More than enough for what? To be able to reinforce your message to beekeepers - 'breed from 'challenged' bees and your problems will be over?
The bees and mites at Avignon and Gotland have clearly changed in response to the pressure put upon the bees by the mites. The bee-mite pairing has 'bred' bees capable of living together. The result is a bee-mite pairing that can survive and thrive. Each has changed in response to the other. And that is called 'co-evolution.'
As to the need for further study: WLC there is pretty much always a 'need for a deeper understanding'. And it is normal practice in any academic/scientific paper to supply directions for further research in the conclusion. It doesn't indicate a confession of failure of any sort in the study being presented.
Do you not know this? In what field are your 'advanced degrees'?
I tend to answer questions selectively. You know, I avoid questions like, "Do you still kick your dog?"
Biology and Administration.
It's OK for me to test hypotheses.
I'm saying that bees are naturally transgenic. They can become resistant instantly and naturally.
I've presented it as 'evidence' for why treatment-free beekeeping can work.
I've also made the case for why Maori's work is still the strongest evidence to date for coevolution between bees and pathogens.
Now, if someone could do something similar for bees, varroa, and other pests/patohgens vis-a-vis treatment-free beekeeping, then we'd have a complete coevolution package.
The 'Bond' bees of Avignon and Gotland are well documented study hives. However, the evidence for coevolution is always presented as 'conditional' statements in the studies done.
They think that it's coevolution, but they're still studying it.
Barbara Locke has her work cut out for her.
Hygienic bees, in my opinion, are artificially selected stock bred by different programs/operations.
So, even though I bought VSH bees and didn't use standard treatment practices, I have no delusions that my bees represent a 'natural population' of bees.
So, I hope that you understand my own 'informed' assessment of the state of coevolution research in bees.
The Bond bees and hygienic bees aren't the best existing evidence for it.
Maori et al. still have the best evidence of coevolution between Honeybees and a pathogen to date.
You do know that they've found a bunch of transposable elements in the genomic survey of Varroa destructor? Right?
I hope that you can see that I'm advocating for a line of inquiry.
Since you have a ba (minimum) in Biology you must know what I mean?
Unless the probabilities can be shortened from (my) current estimates dramatically [understatement alert], the effect of following your recommendations will be to negate (actually reverse) the well tested methods of finding health through selection for strongest - since you advocate propagating out of weakness (vulnerability to the target virus).
This, as I've pointed out to you, will have the effect of rapidly undermining apiary health. Do you wish to challenge that statement? Or does that fall the wrong side of your response-selection process for some reason?
Furthermore there is already a fulsome account of why treatment-free beekeeping works. I'm not saying its complete, but the understanding of raising beneficial and required alleles in a population a la natural selection via artificial selection supplies what is widely accepted to be an adequate explanation.
This understanding is supported a large and growing body of evidence, and has ample scientific underpinning.
You reserve the term 'evolution' for such changes that are reflected in additions to the genome.
Lock, myself and others allow that the term 'evolution' can be used to describe the processes by which shifts in population genetics occur.
We allow that the raising of alleles within a population supplying resistance to varroa due to natural selection are examples of an evoltionary process. Similarly changes in (mite) fecundity might be explained by nothing more than the concentration in the mite population of alleles coding for low fertility. We describe that as evolution - referring primarily to the _process_ .
You deny that. You want to see a stronger degree of permanance to any changes before you'll allow the description 'evolution'.
Have I got that right? We're arguing at cross purposes, due to differences in what we regard as proper use of the key term?
Do you mean home-made GM?
Or do you mean natural/semi natural (beekeeper aided) transgenesis? In which case we must return to:
a) the long odds question,
and (not 'or', _and_)
b) the difficulties inherent in selecting for health while selecting from diseased stock!
I hope you're beginning to understand the nature of the constraints of evidence and the difficulties in application of your ideas.
It means that I know how to formulate and test hypotheses.
Responding to some of what folks write simply goes too far afield from the main thrust of my argument or the thread.
I've previously tested these bees for insertions at the site of interest and have detected many, and sequenced a few. They're already there. I've used and studied transposable elements before, and have even developed methodologies to get them to insert into sites preferentially.
Why use bees with an overt DWV infection to look for DWV insertions and even resistance? Viruses can overwhelm the bees molecularl immunity (RNAi) to such an extent, that transposable elements are no longer suppressed (my interpretation of the Johnson, 2009, paper). They start jumping. Transposable elements are known to 'jump' when sperm and eggs are being formed.
So, if you want to select for DWV resistant bees, you need to have plenty of DWV, and then you need to make new queens. You can find that evidence by taking Maori's and Hunter's approach (general structural gene insertions, or you can can use my approach (site specific). For beekeepers, it's just another Artificial selection method, but it has a solid theoretical foundation.
You don't need to be treatment-free for the above methodology to work. Sorry.
The coevolution hypothesis in the Locke paper is supported by conjectural evidence. But, they're still looking. I've endeavored to show you what evidence actually looks like.
I was describing finding jumping genes in bees, varroa and viruses that prove both recombination and resistance (coevolution).
The problem with proving coevolution in hygienice bees is that they still can't identify the genes involved. In fact, they can't even get candidate genes for hygienic traits from different studies to match. They don't have any solid evidence, yet.
Mike, since you clearly don't understand what you're reading in a scientific paper, I'll keep my own counsel on what I should be doing. :)