I will try to clear-up the points being raised here. For what it is worth, molecular genetics and population genetics in oncology and immunology are a major part of my everyday professional life.
Bob, on one level you are correct. These results do not demonstrate that the cultivars showing identity by these tests are completely identical throughout their genome. You are also correct that they are focusing on areas of significant variation to define relatedness and not sequencing entire genomes. One aspect of that is cost (money, man power and time) as you point out. But another reason, and I'd say the primary one, is to as efficiently as possible define genetic relatedness in a scientifically rigorous way. I believe the group at Davis has done that in their publication.
Most of the genes from fig cultivar to fig cultivar vary very little. So, to examine relatedness, it is useful to find loci (specific places in a genome) where there is significant variability. Microsatellite DNA sequences (also known as VNTRs) fit this bill. What has been demonstrated repeatedly in both mammalian and plant systems, is that the amount of sequence variation associated with a microsatellite allele found on a particular chromosome is orders of magnitude (factors of 10) less than the variation in sequence associated with a different allele on the same chromosome. Let me try to give an example. Lets say the Chromosome 1 I got from my mother has a microsatellite locus that has 7 variants in the human population. Lets call the microsatellite variant I got from my mom 1A. If you DNA sequenced the entire genome from 100 other people carrying the 1A allele on their chromosome 1, you would find from to tens to maybe a couple of thousand base pair differences in the >103 million base pairs on Chromosome 1. A very small percentage (<10%) of that chromosome is DNA that codes for 3141 structural genes found on chromosome 1. So, the likelihood that there are meaningful phenotypic differences between people that carry the 1A allele is very low. When you then sequence the DNA of chromosome 1 from people who carry different alleles (versions) of the microsatellite loci (place on the chromosome), what you find is a MUCH higher rate of variation between allele 1A and 1B or 1C or 1D on to 1G, but essentially the SAME amount of variation among individuals that are 1B or 1C or 1D, etc. So, you would see tens of thousands to hundreds of thousands variations between the sequences from a 1A chromosome versus a 1B or 1C or 1D etc. If you pick loci where the variants (alleles) are broadly distributed within fig populations and any individual fig cultivar is likely to be heterozygous at that loci (that is have 2 different alleles), then you have a spot that measures diversity within the population of figs. If you next find a series of those alleles that behave independently relative to each other, you will hopefully generate a set that covers all 13 ficus carica chromosomes. There are 26 chromosomes in diploid cells. This is what the group at Davis has done. The math they use is strongly supported by experimental data. I am unaware of "different ways of building these models" that would "produce different results." To be sure, there has been refinement in the mathematics used to determine genomic relatedness over the past 30 years. But those refinements simply give better accuracy in determining relatedness and do not measure a new or different underlying phenomena. Based on my experience in looking at complete chromosome sequences from microsatellite loci identical individuals and microsatellite loci different individuals in human & mouse systems, my expectation is that, if you were to sequence 100 different Vista plants and 100 different Violette de Bordeaux plants from around the world or even just the US, the amount of variation between any 2 Vistas or any 2 VdBs would be no different than between any Vista and any VdB. On that basis it is hard to differentiate a Vista from a VdB. The same comparison would have no trouble differentiating a VdB or Vista from the closely related Negro Largo for instance.
I think the work with the microsatellite alleles does give a very clear view of cultivar relatedness at the genomic level. I agree there is a long way to go in defining individual genes in figs and how they function. And I got a real kick out of your historical analogies! I am still cracking up over (fig) Newton!!! I agree we are on our way and we just have to keep going.
Jon, I hope I've given some answer to your first statement. With respect to the "sameness" between Beer's Black, VdB and Vista, let me first say that I am very, very happy that I got a Vista from you instead of a VdB! It is certainly possible that there are minor genomic differences between Orphan, 278-128 and Deanna that result in Orphan producing a superior fig to your taste. However, you can also hypothesize explanations other than genetic differences. For instance, differences in watering or fertilizing or sun exposure might result in the difference you observe. Orphan could have a less damaging case of FMD from the Deanna and 278-128 you tasted. The process of going from tree genetics to how any individual rates the fruit is way complex with tons of factors other than genetic ones that might drive the outcome. Or it could all be genetic. Fodder for endless debate.
Good luck with your trees!