We used different sets of microsatellite markers to deter- mine individual genotypes (Table 1) and a Chelex proto- col to extract DNA (Walsh et al. 1991). The microsatel- lite target sequences were amplified by multiplex poly- merase chain reactions (PCR) with fluorescently labeled primers. Samples containing no DNA were included in all plates as negative controls. We then resolved PCR products in a MegaBACE 1000 capillary sequencer and determined allele sizes with the Fragment Profiler soft- ware (Amersham Biosciences, Germany).
Genetic Diversity Measures and Reconstruction of Queen Genotypes Foreachsampleset,weconstructedtableswiththegeno- types of all drones (obtained either directly, by genotyp- ing drones caught in a DCA, or indirectly, by inferring their genotype from worker offspring of a single queen). Per locus allelic richness (AR) and gene diversity (ex- pected heterozygosity, He) were calculated with FSTAT (version 188.8.131.52; Goudet 2002). Because drones are pro- duced parthenogenetically and only carry alleles from their mother, genotyping drones allows for their assign- ment to specific queens. To reconstruct the genotype of individual drone-producing queens, we performed a sibshipreconstructionanalysisemployingCOLONY(ver- sion 1.3; Wang 2004).
multilocus genotypes of the samples analyzed by Moritz et al. (2007) were directly introduced into COLONY to assign drones to colonies. In the samples analyzed with the linked markers, we first grouped all in- dividuals sharing the same allelic combination at all loci within each linkage group. Individuals sharing a partic- ular allelic combination were assigned to a single haplo- type. Individuals that could not be assigned to a specific haplotype in at least one linkage group (because of low polymorphism or missamplifications at some loci) were excluded from all subsequent analyses. The haplotypes found in each linkage group were then used as individual alleles so that they could be introduced into COLONY. In the six samples in which only one set of linked markers was used for genotyping, we did not use COLONY be- cause we did not have unlinked sets of markers. Instead, given that queens are diploid, we calculated a conserva- tive estimate of the number of drone-producing queens by halving the sample-size-corrected number of haplo- types found in each population.
At any point in the document?
Or are you making the assumption that that's somehow implicit?
How do you answer my point that what you propose is equivalent to supposing that all caucasians, on that basis, are equally fast runners? Do you not see that because all caucasians are clearly not equally fast runners, there must be critical differences in genetic makeup? And that that applies equally to bees?
What do you suppose 'genetic diversity' means?
You really haven't thought this through Jonathan.
Last edited by Juhani Lunden; 04-03-2014 at 11:03 AM. Reason: spelling mistake (alleles)
Treatment free, honey production, isolation mated queens, www.saunalahti.fi/lunden/varroakertomus.html
I never met a guy who takes so many words to state the obvious.
Don't forget nurture and epigenetics as well - as your understanding of genetics appears to be at a very basic level like the stuff we were taught around age 15 about Mendel's pea plant experiments. That and wiki.
There are many people posting about genetics on Beesource you could learn from but you are determined to take on all comers with your 'husbandry' and 'best to best' simple conception of things.
Those who have studied genetics in a University setting could teach you a bit if you were prepared to stop and listen
Bees which show resistance traits in one area sometimes lose them when they are moved to another area. Go read Seeley.
One set of workers has the trait for uncapping a mite infested cell. Another set of half sister workers has the gene for dragging out the mite infested pupa.
Some others will have the independent trait of biting and grooming the mites.
Try and get you head around what Peter Loring Borst is posting about on the other thread.
Keep your ego in check and see what you can learn.
Go read the paper. It is not a paper specifically about ferals but there are some interesting comments which relate to your interest in these.
Its you who is declining to address one or two very direct questions that expose the very obvious contradictions in your position.
Simple evolutionary biology is all you need to understand how nature works with diversity, through the recombination bought about by sexual reproduction, to make each new generation from the best of the old. And its all you need to understand how to husband genes in a population, in like fashion, to raise resistance - and other traits.
It isn't rocket science. But you do have to put the horse before the cart. Some things are basic to the processes, and understanding them to be basic is important.
Here remains your problem Jonathan. What you said, and are standing by, is this:
"There was no difference genetically between the managed colonies and the ferals sampled from the nature reserves. Draw your own conclusions if you like but if the genetics is the same there is likely no adaptation in terms of varroa tolerance."
The conclusion you've drawn is that because the two populations have similar 'genetics' they will have similar qualities in terms of mite resistance. What I've been trying hard to explain to you is: you cannot make that inference. Its fallacious. Its equivalent to saying that, because you and I are both caucasion, we'll both have the same qualites, in any field you like. And reality just isn't like that, and so you need to adjust your thinking to take account of the fact. I've tried to show you where you're going wrong. But you're not going to acknowledge it. Suit yourself. You stand in plain contradiction of the realities.
Last edited by mike bispham; 04-04-2014 at 03:12 AM.
a) Degree of diversity
b) Colony density.
That's what the papers says. It goes on to suggest that the former feature (a) implies a likelihood that the natural population is derived from the agricultural. Nothing much new there.
I haven't read it thoroughly, but from what I have read I see no statement about the relative degrees of mite resistance between the two populations. Or any other trait. And there is no implication that similarities in observed rates of diversity imply similarities in any variable traits - like mite resistance.
Consider this. Lets assume two populations of Russian bees, same in racial type and sub-type, are divided by a long inland lake. Along comes varroa, hitting the western population, but not the eastern.
After a few years of natural selection the western population will have aquired a measure of resistance. |The eastern will have none at all.
They are still the same species, same subspecies, and will have similar measures of genetic diversity.
The difference is that the western population will have higher levels of alleles controlling mite managing behaviours.
If you measure genetic diversity you will find no difference
If you measure the rates of those specific alleles you will find a marked difference.
I think you agree with me on this.
You are right: those alleles don't fall from the sky; they are present in all bee populations, at a 'resting' level -until natural selection raises them in response to mite infection.
Last edited by mike bispham; 04-04-2014 at 03:14 AM.