Protein coding genes are just raw data


(Tomi Aalto) #1

An astonishing similarity of protein coding genes in humans, pigs, mice, dolphins, kangaroos, spiders etc.

https://proteomics.cancer.gov/whatisproteomics

Excerpt: “The human genome contains about 21,000 protein-encoding genes, but the total number of proteins in human cells is estimated to be between 250,000 to one MILLION.”

My comment: Newest studies have confirmed the number of human protein coding genes to be about 19,000. RNA-directed cellular mechanisms are able to build thousands of different proteins by using raw data of one gene, without changing the gene’s sequence. Mechanism is called alternative mRNA splicing. Based on DSCAM gene in Drosophila Melanogaster, the fruit fly’s cell is able to build even 38,016 different proteins, without changing the sequence. The way of how the cell uses protein coding genes tells us that genes are not drivers. Instead, they are just raw data, libraries for RNA-directed mechanisms.

http://www.sciencedirect.com/science/article/pii/S0092867400001288

The alternative splicing is the most significant mechanism inducing the ecological adaptation and organisms’ variation. The clever question arises: how come variation of organisms happen if the sequences of protein coding genes are not to be changed? Mutations in protein coding genes could be extremely harmful and they would cause a huge mess in genomic stability and integrity.

Serious science has the answer:
Epigenetic Control of Gene Expression. The alternative splicing mechanism is regulated by several epigenetic factors. The three main regulators are:

  1. The DNA methylation.
    http://www.cell.com/trends/genetics/abstract/S0168-9525(15)00040-2

  2. MicroRNA downregulation.
    https://www.lakeforest.edu/live/news/4451-co-regulation-of-mirna-biogenesis-and-alternative

  3. Histone methylation
    https://www.ncbi.nlm.nih.gov/pubmed/27606339

By the way, did you know that the C. Elegans, a tiny multicellular nematode worm, that is assumed to be a simple type of organism, has 20,450 protein coding genes? More than us! It is not a simple life form! It also uses the alternative splicing machinery for regulating its proteins in 1031 cells it has.

Protein coding genes are very similar in most animals. For example, human and mice genomes differ only at 2.5%.

https://www.newscientist.com/article/dn2352-just-2-5-of-dna-turns-mice-into-men/

Human and pig genomes are also extremely similar.

“We took the human genome, cut it into 173 puzzle pieces and rearranged it to make a pig,” explains animal geneticist Lawrence Schook. “Everything matches up perfectly. The pig is genetically very close to humans.”

Human protein coding genes are also very similar to kangaroos, dolphins, spiders etc. These are very inconvenient facts for believers of the evolutionary theory that is misleading people by maintaining the heresy of human-chimp genomic similarity. They don’t tell you that the famous 98% is true only with these protein coding genes. But when we compare the alternative splicing mechanism and epigenomes, the differences are quite remarkable.

Everything points to Design and Creation. Don’t get misled.


(Phil) #2

Interesting information. It is truly amazing to consider the way life is put together, and the kinship we have with creation. Sort of reminds you of Legos. Of course, it is also remarkable how with DNA studies, we can follow where those blocks came from and where they went. God is truly amazing in his creation.


#3

Only a small fraction of protein diversity is due to functional alternative mRNA splicing. The vast majority of protein diversity is due to antibodies which are produced by gene shuffling early in embryonic development. The bulk of the remaining protein diversity is due to post-translation modification in the form of phosphorylation, glycosylation, and proteolytic processing to name a few. Of the splice variants that are known, it is suspected that many are errors mRNA processing and don’t produce functional protein.


(Tomi Aalto) #4

Wrong.

Mechanisms known to affect the phenotype

  1. RNA methylation
  2. DNA dinucleotide methylation
  3. DNA CpG island methylation
  4. Histone methylation
  5. Chromatin remodeling
  6. DNA coiling
  7. MicroRNA regulation
  8. Alternative splicing
  9. Flanking binding sites of the DNA

No gene sequence alterations in the list, because

  • Deletions, insertions and frameshift mutations during protein synthesis are misinterpretations of the alternative splicing mechanism
  • Retrogenes and genetic recombinations are misinterpretations of microRNAs and the alternative splicing mechanism
  • RNA based gene duplications are misinterpretations of the alternative splicing mechanism

So, what do the evolutionists have for supporting their idea of random mutations and natural selection?

Point mutations, which don’t occur randomly. Methylated cytosine may flip to thymine and this alteration will not be repaired by the repair mechanisms. This is a designed feature. Hydroxymethylated cytosine turns to Guanine and this seems to be another epigenetic based mechanism. The immune system is a dynamic part of the genome and some genes may be altered due to defense mechanism against pathogens.


#5

Mechanisms known to affect phenotype is not the same as what is inherited. Methylation patterns in skin cells are not inherited by offspring.

Again, it is only HERITABLE changes that matter to evolution. The things you keep pointing to are NOT HERITABLE.

Pretty much the entire field of genetics.


(Steve Schaffner) #7

Almost all of which are affected by DNA sequence changes, aka random mutations. And heritable phenotypic changes are almost entirely driven by changes to DNA. (You do know that geneticists don’t only study the coding sequence of genes, right?)

Because you want to ignore gene sequence alterations. At least, that’s the only reason I can see. Numerous variants that change the protein sequence are known to affect phenotype. Denying this simply means that your comments about genetics are not engaged with reality.

Point mutations, which do occur randomly in the sense biologists mean: there is no mechanism for point mutations to favor beneficial phenotypic change.[quote=“Tomi_Aalto, post:4, topic:35843”]
Methylated cytosine may flip to thymine and this alteration will not be repaired by the repair mechanisms. This is a designed feature.
[/quote]
That last is an unsupported statement.


(George Brooks) #8

Oh brother … this fellow can turn any headline into a frenzied hysteria!
The paper could say: “Little Girl Rescued from Volcano!” … and have it read:
“Girl Abandoned by Parents Nearly Sacrificed to Volcano God!”

"Oh, Waiter! … check please!.. "

Everything points to God-Guided Evolution. Don’t be misled by untrained amateur scientists!


(Tomi Aalto) #9

http://www.atdbio.com/content/56/Epigenetics

“When the equivalent deamination reaction occurs on 5-methylcytosine, however, the product, thymine, is not repaired by DNA repair enzymes.”

Deamination is typically result of oxidative stress caused by poor diet or bad life habits.


(Curtis Henderson) #10

Deamination occurs VERY frequently and spontaneously in the DNA regardless of habits. The sentence that immediately precedes the one you quote reads “When cytosine is mutated to uracil by spontaneous deamination, the DNA glycosylase enzyme UDG (uracil DNA glycosylase) reverses the damage, in a base excision repair mechanism.” It appears to contrast with your assertion of the root cause of deamination.

Let me add one more fact in the interest of accuracy - deamination of 5-methylcytosine can indeed be repaired, but if DNA replication occurs prior to repair, substitution mutation typically occurs.

Now let’s move on to your last sentence and examine it. Do you know the primary cause of oxidative stress? The generation of reactive oxygen species (ROS) due to the electron transport chain transferring electrons to oxygen molecules. Is breathing oxygen also a bad habit?

@Tomi_Aalto , I applaud your tenacity, but the science is just not agreeing with you.


(Tomi Aalto) #11

“Several studies have shown that diet and some of its components could influence the intensity of OS damage.”


(Curtis Henderson) #12

There is a clear difference between “Several studies have shown that diet and some of its components could influence the intensity of OS damage.” and [quote=“Tomi_Aalto, post:9, topic:35843”]
Deamination is typically result of oxidative stress caused by poor diet or bad life habits.
[/quote]

“Could influence” is a far cry form being the “typical result”. The former is speculative while the latter is decidedly not. Are you admitting that breathing oxygen is not a bad habit?


(Tomi Aalto) #14

"Oxidation happens under a number of circumstances including:

  • when our cells use glucose to make energy
  • when the immune system is fighting off bacteria and creating inflammation
  • when our bodies detoxify pollutants, pesticides, and cigarette smoke

In fact, there are millions of processes taking place in our bodies at any one moment that can result in oxidation."

And oxidative stress result in deamination. Dietary factors are the most significant reason for aberrant methylation, genomic diseases and genetic errors.

Viruses also cause disruption on methylation patterns by stealing methyl from host cells. For example, HPV virus might cause cancer by this mechanism. 1 of 5 Americans are carrying cancer-causing HPV virus.


(Curtis Henderson) #16

You are picking factoids from a massive array of web material, and selecting a few sentences from each that you think support your position. You have not in any way adequately challenged any of the science supporting evolutionary theory and you still not have addressed why you continue to assert that evolution is heresy. I’m done pointing out the obvious flaws in your arguments, because I simply cannot refute every single assertion you make based on things like “Dr. Doni ND” that you cherry-pick from the internet and simultaneously maintain my sanity.

PS - No offense to Dr. Doni, I happen to agree with a lot of the article


(George Brooks) #17

The correctness of the article is just a secondary problem. What’s the point of even true articles of this category?

I wonder if Finland has a different kind of science … where discovering what causes things is the same as proving there are no other causes… Because Mr. T sure abuses that methodology to a considerable degree…


(Steve Schaffner) #18

The statement I commented on was, “This is a designed feature.” Your response has nothing to do with my comment.