how big ideas are embedded in a worldview.
Ascension is coming up in the church calendar.
i’ve thought in the past how the 3 temptation in the wilderness represent a movement from lower to higher, reflecting the Hebrew words direction UP. from anywhere in the world, Israel is up, from anywhere in Israel Jerusalem is up, from anywhere in Jerusalem the temple mount is up.
the temptations begin in the Galilean desert, stones into bread. go up to the pinnacle of the temple, cast yourself down. then to the highest place in the world where all the kingdoms are visible, this must be near God’s throne in the Holy of Holies.
the ascension is the fulfillment of the 3rd temptation. God is lifting Jesus up so that everyone can see He is powerful. The Return, the Parousia, is pictured as the inverse. what i see interesting is how these things are embedded in a flat earth worldview. there is no mountain high enough(music playing in mind) from which to see all kingdoms. even that famous blue marble of the earthrise over the moon only shows 1/2 of a planet. but we are so much children of our time, so familiar with our dominant paradigms, that never does the Ascension or the progression of the 3 temptations feel jarring, despite the fact that they are impossible given our spherical earth. no such Archimedean point exists where we can see everyone or everyone see an ascending Messiah, someone will always remain in the dark.
but these thoughts must of felt wrong to those generations where flat earth was being replaced by spherical earth. i’ve read defenses of the Christian ideal of the flat earth versus the pagan spherical written as late as the 7thC AD. it is these folks who can feel the discontinuity, the way the older way of thinking-flat earth was intimately tied to the message. and how jarring it must have been to re-interpret with the new underlying ideal-spherical.
now the change from geocentric to heliocentric occurred much closer to our time. we can read how people fought and defended the old ways-as physics/astronomy misplaced the central role of humanity. the same thing will happen when we meet creatures from other worlds, that will jar loose many old paradigms.
for a 150 years the dominant paradigms of life have been changing in the West from a designer Paley-type God with Aristotelian fixity of the species and a theodicy built around the Fall, to something else with deep time, life as bricolage, common ancestor, and God as something else. it’s jarring to live in these times, steeped in the older ways of thinking yet feeling comfortable with the new. the YEC fight that feeling of being misplaced, of being out of sync with the world. they fight it by recapitulating the past paradigms, accenting the elements most in conflict with the new ways of thinking, and constantly reminding themselves that loyalty to God requires this stand.
it’s noble and futile, for the world is not flat, the earth is not the center of the music of the spheres, and life did evolve.
http://theaquilareport.com/index.php?option=com_content&view=article&id=7298%3Areview-the-evolution-of-adam-by-peter-enns&catid=63%3Abooks&Itemid=139
http://www.urbanghostsmedia.com/2012/05/rubjerg-knude-lighthouse-buried-shifting-sand/
http://www.urbanghostsmedia.com/2010/02/photograph-of-the-day-submerged-church-at-curon-venosta/
http://www.alternet.org/rights/155487/tasing_a_pregnant_woman_in_front_of_her_kid_the_outrageous_–_and_dangerous_–_abuse_of_tasers_by_police/?page=entire
http://worldcrunch.com/where-grandma-needs-permit-have-grandkids-stay-over/5375
http://bigthink.com/ideas/why-opinion-on-same-sex-marriage-evolves-and-abortion-opinion-doesnt?page=all
http://truth-out.org/news/item/9174-the-spectacle-of-military-commissions-for-alleged-9-11-masterminds
> I would add that we assume maximal heterozygosity
> of alleles in the 8 humans and the kinds of organisms
> that would have been on the ark.
i’m curious how you would do this. with 8 people you can have 16 variant allelles in any particular amino acid, yet in something like the thalassemias we have literally hundreds of variants.
look at iceland, it shows founders effects in the genetics of it’s population even though those events got down into the low thousands(1k-2k) can you imagine the consequences of an 8 individual bottleneck? this idea of “maximal heterozygosity” is a pipe dream.
i appreciate the discussion and the attempt to model, but guys, we have good modern examples of founders effects destroying populations with far more than just 8.
> I guess the discussion is over then.
not at all.
it’s a worthwhile enterprise, but look at the details.
>are you saying the amino acid sequences themselves are variants? Or are you talking phenotypes?
the genes give rise to the proteins, the term variants can apply to both. the proteins give rise to the phenotypes. which level the discussion concentrates: gene->amino acids that form the proteins->proteins that create the visible phenotype, depends on what you are interested in.
the thalassemias are an interesting example.
the phenotype is often driven by the success of resisting malaria vs how the oxygen carrying capacity is effected.
my point is that the variation just in the hemoglobin chains, complexity created certainly because of how many different chains there are, how many copies of each exist in our genome, and even how many pseudogenes exist, demonstrate how difficult it is to even imagine 8 individuals carrying enough variety to result in the incredible diversity we see now less that 6k years after the proposed event.
it’s one thing to propose “maximal heterozygosity” but get down and discuss what it would take for 8 individual to include enough variation so that given normal rates of mutation for 6k years produce the incredible variation since in human hemoglobin.
the task is made a bit easier because we know a lot about this class of mutations, it’s easy to detect, is often done in areas endemic for malaria. there’s data.
> On the one hand…, maximal heterozygosity of
> genes would indeed allow for something like skin
> tone to reach its continuum from light to dark
> tones in very few generations since the tone of
> the skin is determined by the numbers of dominants
> compared to the number of recessives.
i would dearly love to understand human skin color from a genetic basis. i once tried to look at mammalian fur color and was overwhelmed by the data. perhaps you could post a link to your favorite genetics of human skin color review article so i could learn some of the details you know.
i do not know which genes you are referring to with “numbers of dominants compared to the number of recessives”, i really just need to get up to speed on the genetics of human skin color. which genes are involved, what are the control pathways, how many chromatic proteins are involved (at least pheomelanin and eumelanin) what are the genetic mechanisms.
?> It seems to me you are conflating mutations with
> simply passing on what one currently has in regards
> to alleles.
afaik, the alleles are the various mutations.
for example, if i have red hair, i have the allele for “red hair” which is short hand for having the mutation
(from:http://en.wikipedia.org/wiki/Red_hair) ” the recessive gene on chromosome 16 which causes a mutation in the MC1R protein.”
which in turn is “The alleles Arg151Cys, Arg160Trp, Asp294His, and Arg142His on MC1R are shown to be recessives for the red hair phenotype.”
so the alleles are the variant mutations that give rise to the phenotype “red hair” (staying with color pigments to build on this learning curve.)
in this case, the 4 alleles are the mutations list above of amino acid substitutions in those specific sites on the MC1R protein
> Yes, I said that above that the alleles you are
> referring to are the mutations, but this simply
> means that multiple mutations can cause a problem…
i’m not sure we are talking about the same things.
in the red hair example above.
we have a gene on chromosome #16 which codes for the MC1R protein.
there is a wild type allele, which many of us have, which makes a normal functioning protein (http://herebedragons.weebly.com/mc1r-red-gene.html) there are 4 alleles, which are the four listed mutations.
i do not understand what you mean by ” that multiple mutations can cause a problem” for it is those various mutations that are the alleles that are necessary to include in the idea of “maximal heterozygosity” .
going back to out OP, if Noah and his family have “maximal heterozygosity” for the MC1R gene then these 4 alleles need to be distributed within those 8 individuals or can be explained by normal mutation rates over 6k years. which is why i choose this example, we have good evidence when and where one of those mutations occurred historically.
that is the kind of detail the model needs to deal with and why i propose the variants of hemoglobin chains as a structuring example. i think these far less complex than skin color, but i’ll read your review articles to learn more about human skin color genetics.
> For example the ABO blood typing likely includes
> only a single mutation…the O because it doesn’t
> have a marker of which to speak.
this is simply not true.
testing at 23&me predicts abo and rh blood types
https://www.23andme.com/you/labs/abo/results/?profile_id=408e637b5880ed2a
it might require sign in to read, here’s the highlights
“We use a set of 11 SNPs in the ABO gene to determine your ABO blood type: rs8176719, rs1053878, rs7853989, rs8176740, rs8176743, rs8176746, rs41302905, rs8176747, i4000504, rs8176749, i4000505. However, there are many other mutations and deletions in the ABO gene that can affect blood type. If you have one of these more rare mutations, your actual blood type could be different than that predicted by these SNPs.”
that’s 11 possible mutations for ABO
it gets much more complex, suffice it to say that they can predict abo/rh blood group for about 80% of people. based on mutations-specifically SNiPs.
“Your RH factor is called using the SNP i4001527, which tags the deletion of the RHD gene.”
it is usually just this one mutation for rh
they got my genotype right: a/o rh+/+
the devil is in the details.
biology is not common sense, it is important to do your homework, to study and learn. i find that under the hood in biology is always more complex and more fascinating than i could imagine before lifting that veil…..(i know mixing metaphors, again)
i believe the vocabulary is not that precise
http://lifesci.rutgers.edu/~mcguire/toolbox-demo/Arrays/representing_alleles.htm
quote:
For example, at the gene locus for the ABO blood type carbohydrate antigens in humans,[3] classical genetics recognizes three alleles, IA, IB, and IO, that determine compatibility of blood transfusions. Any individual has one of six possible genotypes (AA, AO, BB, BO, AB, and OO) that produce one of four possible phenotypes: “A” (produced by AA homozygous and AO heterozygous genotypes), “B” (produced by BB homozygous and BO heterozygous genotypes), “AB” heterozygotes, and “O” homozygotes. It is now known that each of the A, B, and O alleles is actually a class of multiple alleles with different DNA sequences that produce proteins with identical properties: more than 70 alleles are known at the ABO locus.[4] An individual with “Type A” blood may be an AO heterozygote, an AA homozygote, or an A’A heterozygote with two different ‘A’ alleles.
from: http://en.wikipedia.org/wiki/Allele
it really seems to vary depending upon the level of the discussion and how technical it is. and what you are trying to accomplish.
if i’m interested in the level of “11 SNPs in the ABO” system because i’m looking for which parent i inherited that entire segment from, i can refer to my mom’s allele or my dad’s allele A/O. but if i’m looking for a segment from a distant relation, i may very well compare individual SNiPs along the segment since crossover can occur within the abo gene. and correspondingly imagine each mutation a different genotypic but not necessarily a different phenotypic allele.
> Hopefully this made sense.
i think i understand most of the system under discussion.
the problem is the coarseness/fineness tuning of the thought experiment.
here’s the big objective:
can we explain the genetic diversity of human beings as descending from a group of 8 survivors of the Noahic flood?
if you set the knob to coarse selection and look at a-b-o as 1,2 or 3 alleles you get a very different result than if you set the knob on our simulator to fine and look at the 11 SNiPs that underlie the phenotypic alleles.
now if we simply draw blood from 100 people, test for a-b-o we get one set of mutation rates to create that group from noah. coarse.
if we look at their gross genotype a/a a/o etc. we turn the knob a little bit finer on our simulation and get a different answer. or a bit finer a`/a or a`/a“ distinguishing electrophoretic variants. yet another answer.
but if we look at the SNiPs along the ABO gene that actually create the genotype, we set the knob to finest distinguishing and really begin to see the actual genomic variation within those 100 people.
all are different tests.
from a-b-o to electrophoresis, to illumina chip.
which simulation most accurately captures the issue- is 6k years from 8 people to today’s populations doable?
http://herebedragons.weebly.com/index.html
http://thinkprogress.org/economy/2012/05/18/486742/house-gop-throws-out-entire-summer-of-debt-ceiling-negotiations-in-less-than-10-minutes/
