Sorry about that. But as you learned, much of what you thought was "junk DNA"has other functions.
Only about 1 percent of DNA is made up of protein-coding genes; the other 99 percent is noncoding. Noncoding DNA does not provide instructions for making proteins. Scientists once thought noncoding DNA was “junk,” with no known purpose. However, it is becoming clear that at least some of it is integral to the function of cells, particularly the control of gene activity. For example, noncoding DNA contains sequences that act as regulatory elements, determining when and where genes are turned on and off. Such elements provide sites for specialized proteins (called transcription factors) to attach (bind) and either activate or repress the process by which the information from genes is turned into proteins (transcription). Noncoding DNA contains many types of regulatory elements:
- Promoters provide binding sites for the protein machinery that carries out transcription. Promoters are typically found just ahead of the gene on the DNA strand.
- Enhancers provide binding sites for proteins that help activate transcription. Enhancers can be found on the DNA strand before or after the gene they control, sometimes far away.
- Silencers provide binding sites for proteins that repress transcription. Like enhancers, silencers can be found before or after the gene they control and can be some distance away on the DNA strand.
- Insulators provide binding sites for proteins that control transcription in a number of ways. Some prevent enhancers from aiding in transcription (enhancer-blocker insulators). Others prevent structural changes in the DNA that repress gene activity (barrier insulators). Some insulators can function as both an enhancer blocker and a barrier.
Other regions of noncoding DNA provide instructions for the formation of certain kinds of RNA molecules. RNA is a chemical cousin of DNA. Examples of specialized RNA molecules produced from noncoding DNA include transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), which help assemble protein building blocks (amino acids) into a chain that forms a protein; microRNAs (miRNAs), which are short lengths of RNA that block the process of protein production; and long noncoding RNAs (lncRNAs), which are longer lengths of RNA that have diverse roles in regulating gene activity.
Some structural elements of chromosomes are also part of noncoding DNA. For example, repeated noncoding DNA sequences at the ends of chromosomes form telomeres. Telomeres protect the ends of chromosomes from being degraded during the copying of genetic material. Repetitive noncoding DNA sequences also form satellite DNA, which is a part of other structural elements. Satellite DNA is the basis of the centromere, which is the constriction point of the X-shaped chromosome pair. Satellite DNA also forms heterochromatin, which is densely packed DNA that is important for controlling gene activity and maintaining the structure of chromosomes.
Some noncoding DNA regions, called introns, are located within protein-coding genes but are removed before a protein is made. Regulatory elements, such as enhancers, can be located in introns. Other noncoding regions are found between genes and are known as intergenic regions.
The identity of regulatory elements and other functional regions in noncoding DNA is not completely understood. Researchers are working to understand the location and role of these genetic components.
https://ghr.nlm.nih.gov/primer/basics/noncodingdna
Well, let's take a look...
Transposon-Derived Non-coding RNAs and Their Function in Plants
Jungnam Cho*
- The Sainsbury Laboratory, University of Cambridge, Cambridge, United Kingdom
Transposable elements (TEs) are often regarded as harmful genomic factors and indeed they are strongly suppressed by the epigenetic silencing mechanisms. On the other hand, the mobilization of TEs brings about variability of genome and transcriptome which are essential in the survival and evolution of the host species. The vast majority of such controlling TEs influence the neighboring genes in cis by either promoting or repressing the transcriptional activities. Although TEs are highly repetitive in the genomes and transcribed in specific stress conditions or developmental stages, the trans-acting regulatory roles of TE-derived RNAs have been rarely studied. It was only recently that TEs were investigated for their regulatory roles as a form of RNA. Particularly in plants, TEs are ample source of small RNAs such as small interfering (si) RNAs and micro (mi) RNAs. Those TE-derived small RNAs have potentials to affect non-TE transcripts by sequence complementarity, thereby generating novel gene regulatory networks including stress resistance and hybridization barrier. Apart from the small RNAs, a number of long non-coding RNAs (lncRNAs) are originated from TEs in plants. For example, a retrotransposon-derived lncRNA expressed in rice root acts as a decoy RNA or miRNA target mimic which negatively controls miRNA171. The post-transcriptional suppression of miRNA171 in roots ensures the stabilization of the target transcripts encoding SCARECROW-LIKE transcription factors, the key regulators of root development. In this review article, the recent discoveries of the regulatory roles of TE-derived RNAs in plants will be highlighted.
Sorry. TE's are not what you assumed they are.
Perhaps you could help your case by showing us that most non-coding DNA sequences are remnants of other alleles for various existing genes. What do you have?
Development. 2017 Jun 1;144(11):1959-1965. doi: 10.1242/dev.146407. Epub 2017 Apr 28.
New alleles of the wheat domestication gene Q reveal multiple roles in growth and reproductive development.
Greenwood JR1,2, Finnegan EJ1, Watanabe N3, Trevaskis B1, Swain SM4.
And once again, you see that being abusive has damaged you here. Try to do better.
Barbarian, regarding the notion that Adam and Eve were "perfect" because they had more than 2 alleles for each gene:
There actually are some cases where humans have more than two copies of each gene. It doesn't make them "perfect", though. It usually makes them dead. And when it doesn't kill them, it usually causes some serious damage. Trisomy 21 (Down's Syndrome) is one such case that isn't lethal.
Hardly perfection.
Nope. You're confusing polyploidy with a new allele. You, for example, have at least a dozen new alleles, but you are unlikely to be polyploid, since you're alive.
Instead of getting upset and abusive, focus on what you're trying to persuade us about. It can only make you more credible.
Normal humans have 2 copies of each gene, which may be different alleles. Those who have more than 2 copies usually end up dead before birth, and those that don't are most often mentally or physically impaired. So the notion that Adam and Eve could have had all existing human alleles is completely wrong.
On the other hand, when it's positive, it can provide good immunity to malaria, stronger bones, resistance to arteriosclerosis, immunity to HIV, and so on. As you just learned, natural selection tends to remove the harmful ones and increase the good ones.
The HbS gene is an instructive case, because when one has two HbS alleles one has a debilitating and often fatal disorder. But if one has one HbS allele, one has very good immunity to malaria, which is a debilitating and often fatal disease. In areas where malaria is common, HbS is prevalent, because people who are heterozygous for HbS will have about 3/4 of their children immune to malaria. About 1/4 will have a severe disease that will make them unlikely to live long enough to have children. But those parents without one HbS allele will have most of their children contract malaria with much the same outcome. Hence, HbS is favored where malaria is common, because those with one copy of it will tend to leave more offspring capable of reproducing. Recently, another mutation produced the HbC allele, which is increasing at the expense of HbS. The reason is that homozygotes for HbC, although protected from malaria, are also much more healthy than homozygotes for HbS, and often live productive lives, and reproduce.
What I see is blah, blah, blah, blah.
Gibberish about polymorphism would kill or harm you....
"HLA genes are highly
polymorphic, which means that they have many different
alleles, allowing them to fine-tune the
adaptive immune system."
That polymorphic ability is what keeps you alive, not kills you.....
Here's more double-talk from you.
"Only about 1 percent of DNA is made up of protein-coding genes; the other 99 percent is noncoding. Noncoding DNA does not provide instructions for making proteins. Scientists once thought noncoding DNA was “junk,” with no known purpose. However, it is becoming clear that
at least some of it is integral to the function of cells, particularly the control of gene activity. For example, noncoding DNA contains sequences that act as regulatory elements, determining when and where genes are turned on and off. Such elements provide sites for specialized proteins (called transcription factors) to attach (bind) and either activate or repress the process by which the information from genes is turned into proteins (transcription). Noncoding DNA contains many types of regulatory elements:"
And "some of it" is completely unknown because it no longer does anything because mutations "highly degraded it"....
But I notice you still ignored that part from Berkley.... along with the large fraction who's function was still "unknown".
Experiments have already shown that E coli already had the ability to survive in aerobic conditions, as tested long ago with antibacterials.
1. Bacteria are spread out on a plate, called the "original plate."
2. They are allowed to grow into several different colonies.
3. This layout of colonies is stamped from the original plate onto a new plate that contains the antibiotic penicillin.
4. Colonies X and Y on the stamped plate survive. They must carry a mutation for penicillin resistance.
5. The Lederbergs set out to answer the question, "did the colonies on the new plate evolve antibiotic resistance because they were exposed to penicillin?" The answer is no:
When the original plate is washed with penicillin, the same colonies (those in position X and Y) live — even though these colonies on the original plate have never encountered penicillin before."
Colonies x and y survived 31,000 generations before they developed any mutations. All the mutation did was take an ability that already existed and make it dominant.
On the other hand, mutations in humans have taken what was once active and highly degraded it to the point that quite a bit of it is now non-functional. Another large portion is "unknown"
New alleles are discovered every day in the human leukocyte antigen genome. This is because this portion of the genome is the most commonly studied due to diseases capable of infecting the human body.
Now lets cover your strawman.
Here is your stance - double genomes, which was never brought up by me to begin with.
Here is my stance. Now non-functioning genomes added variation we do not see today. their function is unknown, because they are no longer functional..... If their function is unknown, because they are now non-functional, any claims they did not do something when functional is deluded at best....
They coded for all the different races, which is why the population can now only get different varieties of races by mixing. No new races have ever formed in the history of mankind from mutation. it has never been observed and is pure conjecture that it could have ever occurred.
Your theory always requires things to happen in the past where it can't be tested, because every test such as E coli, showed the ability already existed else they would not have survived to the 31,000 generation. But that was already shown to be the outcome back in 1952...... with bacteria and antigens......
Give up your false beliefs, they get you no where except round and round in circles.....
