Each of our cells has the same gene sequences


(Tomi Aalto) #1

Traits are not determined by gene sequences - Epigenetic information layer is used for cellular differentiation

Each of our cells has the same gene sequences. However, there are hundreds of different cell types in our bodies. By which mechanism is a skin cell specialized into its own function? Why does a nerve cell have its own identity? Hundreds of different cell types are capable of producing hundreds of thousands of different proteins even though they have the same gene sequences. How is this possible?

There are several forms of biological information in our cells. Gene sequences constitute a digital body and a platform for other forms of biological information. For their successful differentiation, the cells need a specific information layer that functions on top of the genes. This kind of information is called epigenetic control of gene expression. If the epigenetic information layer is removed from the cell, it becomes a pluripotent stem cell that is in an open state to specialize in any task. Our genome has only about 19,600 protein encoding genes, but different proteins in our bodies are up to one million. Epigenetic control of gene expression and transcription makes this possible.

An epigenetic data structure consists mainly of chemical markers on top of genes. The most significant epigenetic marking of DNA is a methyl group (CH3) attached to a cytosine base. Also, methylation of DNA packaging proteins, i.e. histones, greatly affects the identity of the cell and the structure of the protein it produces. The number of different epigenetic markers on the DNA is not so high compared to RNA, whose epigenetic markers science has only started to understand in recent years. There are over a hundred different epigenetic markers of the RNA and they have a significant effect on protein production and embryonic development. Long and short non-coding RNA molecules form a significant group of epigenetic regulatory elements that participate in many vital regulatory tasks in our body.

The cell uses epigenetic information for many different functions. Genes can be suppressed, silenced or activated by methylating certain regions of them. The number of methyl groups in a gene and its different regions also plays a decisive role in the type and quality of the cell-produced protein. There are also genes in which only one addition or deletion of one methyl group has a significant influence on cell activity and identity. About 95% of plant genes are epigenetically suppressed, which explains their enormous potential for variation.

Perhaps the most interesting feature of epigenetic information is its analog nature. The team of McGill researchers, led by Professor Moshe Szyf of the Department of Pharmacology and Therapeutics, and Professor Ehab Abouheif, from the Department of Biology, found that the size of the Florida Carpenter Ants changed based on the amount of DNA methylation of a certain gene. Thus, the amount of methylation in the gene can act as a control knob, such as a volume regulator.

An example of epigenetic control of gene expression: Skin color.

If skin cells are programmed to produce white pigment instead of black, then which one is being changed, the gene sequences or the epigenome? The correct answer is: the epigenome.

This fact has been studied only by a few scientists, because it’s too inconvenient fact for the theory of evolution. Here’s one example:

Unfortunately this group doesn’t realize that point mutations don’t modulate methylation patterns or levels on genes and histones. It’s done by non coding RNA molecules.

Others have tried to find the reason for human skin color variation by examining sequence changes with poor results. They claim that light skin is determined by sequence changes in SLC45A2 gene, but do they tell that this claimed mutation is nearly absent in East Asia? So, they try to use another pseudoscientific explanation: Convergent evolution. This is the level of population genetics. It’s false science.

There is no such a thing as mutation driven evolution or different human races. We all are created by loving God. Don’t get misled.


(George Brooks) #2

Well… T., you lost me. I can’t even begin to wonder why you think any of this stuff changes the purpose of BioLogos, or the relevance of Evolutionary theory to the Book of Genesis.

But have a nice time anyway. I’m sure there must be some folks you haven’t burned out yet … but I congratulate you for being able to accomplish this result with me in less than 24 hours.


(Curtis Henderson) #3

It is clear that epigentic control of gene expression is an important modifying factor. But I’m really not understanding your point. Are you aware that methyl groups (and acetyl groups, for that matter) are added and removed by enzymes that are encoded in the genome? Gene sequences and what they encode (mRNA for proteins, or miRNA, or ncRNA) determine traits. Even if epigentic mechanisms were as important as you suggest, how would this in any way detract from the plausibility of evolution?

And I’m sorry, but I just can’t pass up on this nugget… [quote=“Tomi_Aalto, post:1, topic:35836”]
Our genome has only about 19,600 protein encoding genes, but different proteins in our bodies are up to one million. Epigenetic control of gene expression and transcription makes this possible.
[/quote]

If epigenetics only determines whether or not genes are expressed, how could it possibly account for the production of hundreds of thousands of proteins from 19,600 genes? @Tomi_Aalto I challenge you to research and find a more plausible explanation.

A bit off-topic, but based on the volume of posts fighting the “evil hordes of evolutionists”, please know it is possible to love and follow Jesus Christ AND accept the scientific evidence supporting the science of evolution.


(Benjamin Kirk) #4

False. Our T and B cells rearrange their genes to produce receptors and antibodies respectively.[quote=“Tomi_Aalto, post:1, topic:35836”]
Hundreds of different cell types are capable of producing hundreds of thousands of different proteins even though they have the same gene sequences. How is this possible?
[/quote]Differential gene expression. Splicing.[quote=“Tomi_Aalto, post:1, topic:35836”]
This fact has been studied only by a few scientists, because it’s too inconvenient fact for the theory of evolution.
[/quote]
Again, false. None of the many people I know who study epigenetics agrees with you.


(Jay Johnson) #5

Are you trying to discuss anything, or has the forum become your personal blogging space now?


(Lynn Munter) #6

Wow, I’ve seen some amazing non sequiters before but this one is spectacular!

Let us suppose, for the sake of argument, that epigenetic factors are everything. You don’t get to stop there! The important question is: “Are they heritable?” If they are, evolution still works fine! If not, then where do they come from? Are they immune to mutation? Why?

Darwin described evolution without ever hearing about Mendel’s work on genes. I’m afraid you haven’t even begun to cast evolution into doubt.

And as for “different human races”—I must have missed some argument someone made somewhere, because I couldn’t begin to guess how it relates to anything!


(Benjamin Kirk) #7

It seems that you misunderstand evolutionary biology at the most basic level. Evolution is driven by genetic variation, but for diploids like humans, new mutations contribute only a tiny amount of additional variation each generation.


(Tomi Aalto) #8

If epigenetics only determines whether or not genes are expressed, how could it possibly account for the production of hundreds of thousands of proteins from 19,600 genes?

Epigenetics is much much more than just switching genes on or off. Sometimes just one addition of a methyl group is sufficient to result in significant changes in protein synthesis. Cells use alternative splicing mechanism for making millions of different proteins from our 19,600 gene libraries. For regulating that mechanism, several epigenetic factors are influencing on the procedure. DNA methylation, microRNA:s and histones especially are the most significant modulators of alternative splicing. It’s time to learn that gene sequences alone don’t determine traits. Population genetics has a serious missing heritability paradigm that can be solved through epigenetic inheritance only.

After fertilization, nearly all epigenetic markers are wiped out of embryonic cells making them pluripotent stem cells. An epigenetic reprogramming process is responsible for bringing necessary information for the ES cells. This is done by maternal and paternal non coding RNA molecules, such as lncRNAs, siRNAs, piRNAs and miRNAs.


(Tomi Aalto) #9

Unfortunately the Biologos server systems prevented me from commenting during the last 24 hours.


(Tomi Aalto) #10

False. Our T and B cells rearrange their genes to produce receptors and antibodies respectively.

Correct. And our neurons also have different gene sequences. And we also have mutated cells. But the point is to learn the basics about how cellular differentiation occurs.

Again, false. None of the many people I know who study epigenetics agrees with you.

Please show me a confirmed sequence mutation associated with skin color variation.


#11

There’s a whole Wikipedia page of the different human mutations linked to variations in skin color:


(Tomi Aalto) #12

Wikipedia is an insult upon intelligence.


#13

Therefore, the vast majority of epigenetic changes are not heritable and do not matter in the process of evolution. It is the DNA sequence of the genome that determines how the genome is methylated after fertilization.

Epigenetics poses no threat to the modern theory of evolution.


(Tomi Aalto) #14

Wrong.Traits are inherited by epigenetic mechanisms. Genetic errors are inherited by sequence level.


#15

Your post is a blatant attempt to avoid the ample evidence for the link between human skin color and DNA mutations.


#16

No, they aren’t. You said yourself that methylation patterns are wiped out prior to development. They aren’t inherited.


(Tomi Aalto) #17

You said yourself that methylation patterns are wiped out prior to development.

Wrong. Epigenetic markers are cleared out after the fertilization, but they are re-established by non coding RNA molecules. Only certain histone markers and immune system methyl markers are left without cleaning. It’s an incredible mechanism.


(Tomi Aalto) #18

No gene sequence alterations are needed for human skin colour variation. There’s not such a thing as a human race. We’re all the same human kind created by God.

The skin color variation is mainly based on alternative splicing of the OCA2 gene:
http://www.ncbi.nlm.nih.gov/gene/4948

“This gene encodes the human homolog of the mouse p (pink-eyed dilution) gene. The encoded protein is believed to be an integral membrane protein involved in small molecule transport, specifically tyrosine, which is a precursor to melanin synthesis. It is involved in mammalian pigmentation, where it may control skin color variation and act as a determinant of brown or blue eye color. Mutations in this gene result in type 2 oculocutaneous albinism. Alternative splicing results in multiple transcript variants.”

The level of UV radiation of the Sun and vitamin D in nutrition affect the epigenetic regulation of the genes that are in response of melanin production. Changes within skin color can be happen surprisingly quickly even within Australian aboriginals.

http://www.theaustralian.com.au/life/weekend-australian-magazine/no-so-black-and-white/story-e6frg8h6-1226305047298

“The arrival of the twins has proven to Scott how quickly skin colour can fade across the generations…”


(Phil) #19

Great article. Wikipedia articles vary, but well referenced articles like this save a lot of footwork in getting an overview of a subject, and provide references for deeper study if desired. Seems that the main problem I see with Wikipedia are in the obscure poorly referenced articles, and often they are flagged.


#20

Notice that it doesn’t say that alternative splicing is the cause of variations in skin color. Scientists have already identified the mutations in OCA2 related to differences in human eye color:

" Fifty-eight synonymous and nonsynonymous exonic single-nucleotide polymorphisms (SNPs) and tagging SNPs were typed in a collection of 3,839 adolescent twins, their siblings, and their parents. The highest association for blue/nonblue eye color was found with three OCA2 SNPs: rs7495174 T/C, rs6497268 G/T, and rs11855019 T/C (P values of 1.02×10-61, 1.57×10-96, and 4.45×10-54, respectively) in intron 1. These three SNPs are in one major haplotype block, with TGT representing 78.4% of alleles. The TGT/TGT diplotype found in 62.2% of samples was the major genotype seen to modify eye color, with a frequency of 0.905 in blue or green compared with only 0.095 in brown eye color. "
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1785344/

Getting a tan does not cause your children to be born with darker skin. Again, epigenetics is not heritable.