nuDAN

John Cuthber called it. The offspring from each parents' first cousins would be YOUR Second Cousins (NOT removed).

I don't think there is any inbreeding here. Different grandparents, different offspring who each had a first cousin. Happens all the time. The two first cousins who married are from two completely different family lines. This person's grandparents are not related (assumption) so each of this person's parents and their respective first cousins are also not related. At least that's how I read the OP.

They talk about double-stranded DNA integration. What loop do mean here? It's only how I visualize the application. I would seem to me that if both LTR's are plugged into the same target then it may not mean the target is more than an insertion into a single base pair in the DNA strand? What I do know is that there a lot science doesn't know about this process. I mean, if cholesterol acts as an inhibitor to the flippage, or even an inhibitor to reversing the flippage to a floppage? Then it could be an answer to what you initially were asking about? I really don't know enough to keep from asking questions myself, though. Such as: Is this a dynamic that one could use, or is using, as a way of performing gene splicing using a string of genes instead of just one? I know there is information out there, but as with any such finer detailed subjects, I would have to learn a whole set of terminologies to follow what the data is explaining. But for some reason I gather that science hasn't really worked out all of the processes regarding LTR insertion mechanisms? But I might agree with you that non concerted DNA insertion involves one LTR end applied to one target. But the other LTR end wouldn't be left hanging so it should be involved in it's own insertion process somewhere? And there may be a limit to where along the DNA molecule that could physically happen depending on the length of the gene string and the number of base pairs in the LTR itself. The possibilities may also differ in respect to whether or not one is talking about mtDNA loops or nuDNA strings that are open ended. So much for what at first looked like a simple (on the surface) OP question, eh?

I'm certainly not up on this subject, so please excuse my rudimentary knowledge. I also do not like answering a question with a question, why would a cell NOT want a phosphatidylinositol to return to the cytoplasm side? I mean isn't most flip-flopping necessary in the bilayer for cell growth or cell shape?

Let's start off with an example using a string of viral genes with identical long terminal repeats (LTR's) on each end containing a few hundred base pairs. Concerted DNA integration takes both LTR ends and plugs them into a single target. Essentially making a loop. The purpose of which is that when one LTR gets mutated the second will automatically be mutated. And to tell you the truth, that's all I know about it.

No it doesn't. Bigger brains do NOT mean more neurons. If that was the case Elephants would be ruling the world. Example: duplication of base pairs in the Human NOTCH2NLB gene, which resides at the 1q21.1 locus of chromosome 1, can cause macrocephaly (large head/brain) and lead to autism and other mental issues and neurological disorders. It has nothing to do with the number of neurons. It's like most things, generalities can work until one begins to talk about an individual. But according to you large brain individuals are what? Better Humans? I've known plenty of folks with large brains that are down right stupid. Academia all over the world is filled with big brains and small brains. You're just going to have to come up with something better than brain size to anchor your beliefs. Maybe look more at the slower rate of brain development in fetuses that allow stem cells more time to produce more progenitors than neurons. In Great Apes the fetus grows a brain much quicker than a Human brain. As a result, more neurons than progenitors get created. What that means is there won't be enough progenitors in the long run to grow the number neurons need to match the Human brain. It's why Chimps will never build an iPhone. It's easy to pass judgement after everything's in place but it's critical that one understands that brain development and function doesn't happen in the bubble of a perfect world. How about looking at malnourishment which is at epidemic levels in third world countries as well as developed countries. You can't tell me that a country or region that has experienced war and famine for years id going to have nutritionally perfect brain and body development. Bottom line? The world is flawed and it's peoples aren't cookie cutter perfect. There's 8 billion people in this world. Sample half, sample a quarter, not the small numbers of individuals I've seen in the research papers- many of which are dated- and then get back to me

Good post, DrmDoc, and you take it back to the OP which/who has slipped away from the OP's initial presentation to one more based in sociology (as the more recent postings would suggest). Which, IMHO, is more pertinent the thread's title anyway. Because I've seen little but bias involved in any evidence correlating intelligence capacities with race. But the sociological evidence is overwhelming I would like to add that, with respect to brain size, the development of the number of neurons in the neocortex is far more important than brain size. If it wasn't for that, I would be pulling termites out of a hole with a stick with my Chimpanzee and Bonobo cousins.

I'm not quite sure what you're saying here? I was leaving the thread but saw that I needed some clarity on that sentence. You said it was a truth but it's not reading well. At least not to me.

There is a real sociological danger when one pursues equating race to some degree of perceived Human imperfection. Personally, I'll have no truck with such concepts. So....done here.

It's not a good thing to do.

Decided to say 'never mind'.

Thank you, studiot, nice to be here, small brain and all Maybe I'll even stumble onto a thread that could inform me how I can produce more progenitors cells than neurons? Then perhaps I'll get lucky enough to have it result in even more neurons and hopefully get a smarter, bigger brain. Race, ethnicity, intelligence tests not withstanding.

Hey, where did this come from? Because now I'm confused. Could some PLEASE clarify an "American Race" for a small brained person like m'self? Because I had no idea. It HAS to be because I'm stuck with this small brain I have a small brain, and so apparently I'm left trapped here in the Department of Redundancy Department, LOL.

Hey, thanks for responding, CharonY. Yes, correct, as you say, the hypothetical could be aimed at any number of loci as many are Human specific. There are other primate loci that are, say, Chimp, Bonobo, or Gorilla, specific as well. To tell you the truth, there is so much going on with this hypothetical, I didn't know where to post it. Unknown DNA seemed like as good a place as any. I also agree that specific primers and assays, even if assays have to be tweaked depending on a certain geographical region due to something like soil composition,......I can easily paint myself into a corner if I write too much so I'll try to be brief. This is about Sasquatch existence vs. non existence. So much has been said about its advanced primate body coupled with a relatively primate, perhaps even ape-like brain. So targeting the NOTCH2NL gene is the focus since there are no NOTCH2NL ape genes in the Human genome. The Great Apes, minus the Orangutan, all have a NOTCH2NL defective copy. That copy got repaired at the Chimpanzee/Homo split. Humans now have the NOTCH2NL along with three more copies: A, B, and C. Two paper in May of 2018 attributed the larger brain and cognitive boost in Humans to there "newer" variations. Hypothetical: When getting Human contaminated samples from e-DNA field samples in North America, I propose looking deeper into the samples to see if any of the Human a, B, or C variations are present, OR if what is found is the Great Ape's NOTCH2NL's defective copy with could indicate an ape brain somewhere in the wild. It's never seems easy to articulate this concept, but that's what this is about. Nearly every piece of DNA that was initially suspected as coming from a Sasquatch source has been labeled as simply Human contamination. And yet I see no one thinking of ways to target either Human specific or Great specific genes. I don't think it is something that casting a wide net using a metarcoding protocol would catch. If the Sasquatch is that genetically close to Humans then why not run a cytochrome c oxidase barcode? At least that might work if the Sasquatch and the Human is thought to be that closely related. On the base pair front, Sapiens/Denisovans- about 400 base pair differences, Neanderthal- 200+, Chimpanzee- 1,400+. With what folks think regarding the Sasquatch, it might be somewhere around 800-1,000 base pairs different? This is a discussion I've been waiting to have for some time now. Academia, so far, has walked away after any initial correspondence. So who is there to run this by? That's why I'm here. It's about the NOTCH2NL and it variations with respect to using a COX1 barcode protocol and figuring out just what is needed to do that.....outside of getting a Sasquatch onto a slab, LOL!

An important point. Otherwise, Humans today might be pulling termites out of a hole, of fishing algae out of a pond, with a stick like their Chimp cousins.

Okay, I'm gone here.

I'm struggling a bit with the "superior gene" concept. There are too many factors involved in gene selection to make that kind of a qualitative assessment. As mentioned, environmental forcing is one, chemical is another which could include changes in crops composition with regional differences due to OTHER factors, both anthropogenic and non-anthropogenic. Latitude/altitude even can be a factor. And then there are carnivorous diets which can be a factor in gene selection due to whatever the prey's diet is, such as meat or plant material. Ultimately, phenotype through gene selection is a function of RNA which selects one of two genes (alleles) where one is maternal in origin and the other paternal. That determines which of the two genes goes on to express the protein that results in an organism's detailed phenotypes as well its overall phenotype. Nature experiments, as it always has, with success rates. Ligers might have been around a long time ago had it been successful. Whose to say that it WASN'T around and just didn't make the grade and so got selected out. Ultimately, most everything is a hybrid. Especially primates since Human ancestry is now known to be riddled with intermingling. And as long as genes make copies, which is what they do, then even something like a theoretical "superior gene" will eventually get altered by either adding or deleting base pairs. Just such a process occurs where deleting base pairs has resulted in microcephaly and added base pairs moved in the other direction, resulting in macrocephaly. Maybe "superior gene" is an inadequate, if not unfortunate, choice of terms?

I would like to add that I am aware that in order to zero in on the loci of a chromosome, I would need whole cells that have intact nuclei. Obviously, the question is in lieu of simply counting the number of chromosome pairs.

May I dig up this thread, please? 🙂 Though I am not a scientist, I have been pursuing this Sasquatch subject from the genetic angle for some time now. Oh yes, I have questions. This is on the subject of the NOTCH2NL gene, or should I say, its genetic variations? The question itself is hypothetical. If I take an environmental DNA sample and the metabarcoded test results includes Human, could I then run an barcode assay designed to target the NOTCH2NL gene? Specifically targeting, the Human NOTCH2NLA, B, or C gene variations at their 1q21.1 locus? And if so, what would it mean if none of those Human variations were present but the result did show a NOTCH2NL pseudo gene along with a defective copy at the 1p12 locus? i can give a bit more background on the question, but regardless of anything Sasquatch, I am looking at this as a purely scientific inquiry. Mostly to understand whether or not a lab can design an assay to target one, two, or more, of those Human specific gene variations. I'm not disappearing but it is late for me here so I'll check in again later. Thanks.