2018/01/26

Disease-causing genetic mutations in human DNA are in an explosive growth

Disease-causing genetic mutations in human DNA are in an explosive growth

http://www.hgmd.cf.ac.uk/ac/index.php

The human genetic mutation database (HGMD) maintains a database of disease-causing genetic mutations in human DNA at population level. The page will be updated every 2-3 months. Even yesterday (26th Jan 2018) the number was 214,158 but today, after the update, the figure is 220,270. Over three months, more than 6,000 new harmful genetic mutations were registered, which is an annual growth of over 24,000.

It's noteworthy to understand the direct consequences of these genetic mutations:

https://rareundiagnosed.org/rare-disease-facts/

  • Rare diseases affect 1 in 10 people, more than 350 million people worldwide
  • Approximately 50% of the people affected by Rare Disease are children
  • 30% of children with rare disease will not live to see their 5th birthday
  • There are more Americans who live with a rare disease than ALL of those who have either HIV, Heart Disease or Stroke.
  • 95% of rare diseases are without an FDA approved treatment or therapy.
 
Genetic degradation is a scientific fact and it occurs all over nature. There is no mechanism for evolution because any change in organisms is based on epigenetic regulation of existing, preprogrammed biological information OR degradation of information. Don't be deceived.

2018/01/23

Digital-to-Analogue Converter in the Cell points to Design

Digital-to-Analogue Converter in the Cell points to Design

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4082330/

Excerpt: "Cells must coordinate responses to many stimuli, including signalling cues from other cells, the extracellular matrix, hormones and active compounds. As they are subject to feedback control, these response pathways are usually ‘on’ or ‘off’ in nature. By contrast, transcriptional changes can be ‘dialled’ up or down and provide a composite response to multiple inputs over time. In line with this, signal transmission to chromatin can be compared to a digital-to-analogue converter (DAC) that takes ‘on’ and ‘off’ signals and converts them into a continuous output that can vary in amplitude over time. We speculate that histone tails may function in this way, acting as a site that stores signals and integrates them to regulate the transcriptional programme. Indeed, the pure density and variety of post-translational modifications on histones suggests that they are uniquely placed to act as signal integration devices.
 
Histone modifications work in combination, which adds to the diversity of outputs that they might facilitate. Crosstalk between histone modifications occur in cis and trans, by: influencing the binding of reader molecules to adjacent residues; precluding or recruiting enzymes that modify additional sites; or through combined effects on complex docking (termed ‘multiple site display’). Although the underlying mechanisms are not fully understood, the modification landscape can be fully or partially maintained throughout replication, allowing past signalling events to influence the current state of transcription. As a result, the transcriptional output of a single gene over a time course, or even over the life of a cell, follows a continuous wave pattern that can be dialled up or down, but that differs from the inputs received at any specific time point. Circadian gene expression is one example of this, whereby chromatin surrounding the CLOCK gene promoter is methylated, acetylated, then deacetylated to control fluctuations in the amplitude of CLOCK gene expression over a 24-hour period. Thus, histone tail posttranslational modification has all the features of a ‘storage and output’ device for epigenetic information. Nevertheless, it is ill defined how long a signal can be stored on chromatin. In addition, it is still largely unknown how the chromatin landscape is preserved during DNA replication and cellular division. Thus, determining the variables that define the longevity of marks on histones is critical for understanding the storage capacity for these marks."
 
My comment: CD player is a nice example of a device that needs a DAC, digital-to-analogue converter for the player being able to convert digital data to analogue format. A lot of research and design were needed before the standard for proper information handling was established in 1980. This kind of complex information protocols don't appear by chance or accident. They need perfect design. That's why the theory of evolution is the most serious heresy of our time. Don't be deceived.

Skin remembers wounds and heals faster the second time around by using 3D genome

Skin remembers wounds and heals faster the second time around by using 3D genome

https://www.the-scientist.com/?articles.view/articleNo/51153/title/Skin--Remembers--Wounds--Heals-Faster-the-Second-Time-Around/

Excerpt: "

Inflammatory Memory

Our body is routinely assaulted by ultraviolet radiation, irritants, and pathogens.
Shruti Naik, an immunologist at Rockefeller University, wondered: “Do these stressors have any kind of lasting impact on cells?” Immune cells are known to “remember” infections and inflammatory events so that they can respond faster to future insults, but what about the epithelial stem cells that maintain the skin and promote wound healing?

Multiple Assaults

Naik and her colleagues induced inflammation in mice by exposing the animals’ skin to chemicals, fungal infection, or mechanical wounding. Then they measured the time it took for the skin to heal after injuring it in the same place a second time. On average, regardless of the type of injury, skin that had been previously inflamed healed about 2.5 times faster than the skin of mice that were wounded for the first time.
 


Swift Repair

To uncover the genetic basis for an “inflammatory memory,” the researchers searched for genetic loci in the epithelial stem cells that were maintained in a chromosomally accessible state after the first injury. Multiple regions of chromatin were left “open” for up to 180 days after an assault, allowing rapid transcription of key stress response genes following a second injury.

Beneath the Skin

Epithelial stem cells are the first nonimmune cells found to have a memory, and the findings point to “a primitive basic response to jazz up the cells quickly and make them heal the wound,” says George Cotsarelis, a dermatologist at the University of Pennsylvania’s Perelman School of Medicine who was not involved in the study. “It changes the way people think about the skin now.” "

My comment: Skin having an epigenetic memory that helps it heal wounds more rapidly is a very interesting mechanism that points to design. The mechanism by which this is done is amazing, the cell uses the 3D formation of chromatin to maintain a memory. Open regions of chromatin are ended up into transcription, so this is an epigenetic mechanism. This is a nice example of how our immune system functions.

2018/01/19

Previous Sexual Partners Can Influence Another Male's Offspring

Telegony (microchimerism) is not studied by pseudoscientists because it refutes the theory of evolution

http://www.theneonnettle.com/features/1006-study-women-store-dna-from-every-male-they-have-sex-with

"A new study by the University of Seattle and the Fred Hutchinson Cancer Research Center has revealed that Women absorb and retain living DNA of every single man they have sex with. When scientists were trying to determine if women who had been pregnant with a son might be more predisposed to diseases usually found in men, then also found in the study that the female brain also absorbs male DNA."

"Le Dantec wrote that some farmer told him that once his swine copulated with a boar and their pigs absolutely resembled the father in color. But when the same swine copulated with another boar some pigs of the second farrow still resembled the color of the male pig the swine had copulated first."
 
http://modernnotion.com/is-telegony-real/
"Scientists believe the phenomenon occurs because molecules from the first partner’s seminal fluid absorbs into the female’s immature eggs, and manifests in them once they’ve matured. In other words, previous partners’ semen may actually affect female eggs, regardless of whether they’re fertilized or not.

“Our discovery complicates our entire view of how variation is transmitted across generations, but also opens up exciting new possibilities and avenues of research. Just as we think we have things figured out, nature throws us a curve ball and shows us how much we still have to learn,” said lead researcher Dr. Angela Crean."

http://www.telegraph.co.uk/news/science/science-news/11133203/Could-previous-lovers-influence-appearance-of-future-children.html

"Certainly until recently it would have been thought impossible because the DNA genome of the sperm was thought to be the only thing passed down to future generations by the male.

“However, there is now evidence that so-called ‘epigenetic’ changes, can be passed down at least one or two generations, and such changes can be influenced by diet and other lifestyle differences."

 
http://www.dailymail.co.uk/sciencetech/article-3475637/Can-babies-looks-mother-s-ex-lovers-Study-fruit-flies-suggests-chemicals-previous-partner-s-semen-lingering-effect.html

"And size might not matter as much as previously thought. Seminal fluid is chemically complex, with proteins and tic messengers called RNA floating in the liquid outside of the sperm.

So even the effects of a small ejaculate could be significant, giving females a largely unexplored bonus from sex.

Prof Bonduriansky said: 'It is pretty clear now seminal fluid is packed with paternal RNA. And this would be in humans, mice, fruit flies and nematode worms at least.'

He added: 'In some systems, mostly nematodes and mice, there is evidence these RNAs can play a role in early embryonic development.' "

My comment: Telegony is an inconvenient subject for evolutionary biologists. That's why it's been studied only by few scientists. But some serious researchers have already revealed the complex mechanisms that prove these scientific facts. For example:

http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004296

Traits of an organisms are not determined by DNA of the semen. Cellular programming and differentiation is directed by non coding RNA molecules such as microRNAs and lncRNAs. These molecules are rich in seminal fluid and they absorb and attach into woman's tissues and cells. They might affect epigenetic programming of embryonic cells making their own imprinting on the cells. This is why a white couple might have a black baby. DNA sequences don't determine the skin color. Human traits are determined by epigenetic information layers.

Interesting is, that the Bible teaches us about this phenomenon:

Matthew 19:5 "And said, For this cause shall a man leave father and mother, and shall cleave to his wife: and they twain shall be one flesh."

2018/01/18

Rapid human genome degradation - Evolution is not happening

About 20,000 new disease-causing genetic mutations in 2017 in the human DNA at population level - Today the total number is 214,158

https://www.ncbi.nlm.nih.gov/pubmed/28349240?dopt=Abstract

Excerpt from abstract: "The Human Gene Mutation Database (HGMD®) constitutes a comprehensive collection of published germline mutations in nuclear genes that underlie, or are closely associated with human inherited disease. At the time of writing (March 2017), the database contained in excess of 203,000 different gene lesions identified in over 8000 genes manually curated from over 2600 journals. With new mutation entries currently accumulating at a rate exceeding 17,000 per annum, HGMD represents de facto the central unified gene/disease-oriented repository of heritable mutations causing human genetic disease used worldwide by researchers, clinicians, diagnostic laboratories and genetic counsellors, and is an essential tool for the annotation of next-generation sequencing data. The public version of HGMD ( http://www.hgmd.org ) is freely available to registered users from academic institutions and non-profit organisations whilst the subscription version (HGMD Professional) is available to academic, clinical and commercial users under license via QIAGEN Inc."
 

My comment: Modern scientists are not aware of random beneficial mutations in the human DNA. Even the famous lactose tolerance is not based on genetic mutations, but different methylation levels of the MCM6 regulatory gene.

http://sciencerefutesevolution.blogspot.fi/2017/02/lactase-persistence-genotype-data-is.html


Rapid genetic degradation is a scientific fact all over nature. It can be observed as gene loss, decreasing number of chromosomes, increasing amounts of heterochromatin in genomes, shortening life spans, susceptibility to diseases, bacteria turning to parasitic or pathogenic bacteria etc. You can easily find information about the Madeira Mouse who lost over half of its chromosomes just in 500 years or the Red Fox who has 1,500 protein coding genes fewer than its descendants. Or the Red Muntjac who has only 3 pairs of chromosomes left. There are no mechanisms resulting in evolution due to rapid genetic degradation. Changes we can observe in organisms are due to epigenetic control of gene expression OR loss of genetic information. Don't be deceived.

2018/01/16

An unexpected role for transcription factors: They promote architectural changes of the genome

An unexpected role for transcription factors: They promote architectural changes of the genome

https://medicalxpress.com/news/2018-01-role-gene-architecture-cell-fate.html

Excerpt: "Scientists read the code of life—the genome—as a sequence of letters, but now researchers have also started exploring its three-dimensional organisation. In a paper published in Nature Genetics, an interdisciplinary research team of scientists from the Centre for Genomic Regulation (CRG) in Barcelona, Spain, shows that the three-dimensional organisation of the genome plays a key role in gene expression and consequently in determining cell fate.

It all began with the 4-D Genome project, an ambitious and innovative research initiative aimed at understanding how the spatial organisation of the genome contributes to decisions made by cells. What scientists wanted to find out was whether genome architecture plays an active function or whether it is a mere side effect of the genome's activity. The model that the 4-D Genome team used was cell reprogramming, a process that allows the scientists to revert white blood cells back to a state of pluripotency in which they can differentiate into any other cell type. Proteins that control gene activity (known as transcription factors) play a key role in this process, which the 4-D Genome team studied in great detail, assessing how they induce changes in gene expression, modifications of chromatin (the structure around which DNA is wrapped), and changes in the 3-D organisation of the genome.

Understanding how stem cells are formed and how they can convert into different cell types is a major challenge in modern biology. It has been known since the 1950s that all specialized cells in the body contain the same genome. So what then distinguishes one cell type from another? The answer is that different cells read the information contained in different parts of the genome. The machinery required to achieve this selective information recall resides primarily in so called transcription factors, molecules that switch genes on or off. Many other molecules are also involved in this process, including epigenetic regulators that help to densely pack the genome into the nucleus of a cell, or locally unpack it to allow gene expression. The scientists used a reprogramming method discovered by CRG senior researcher Thomas Graf and his team. With this precision tool in hand, they were able to study the dynamics of genome organization by comparing the changes in genome architecture and transcription at different times during reprogramming.
 
"We expected that transcription factors would first switch on certain genes, which then afterwards may force a re-organisation of the 3-D structure of the chromosome. Surprisingly, what we found is that in a large proportion of the genome, the transcription factors were actually promoting this re-organisation before the genes were switched on," explains Ralph Stadhouders, co-first author of the paper together with computational biologist Enrique Vidal.

"Our paper shows that transcription factors may play a completely new role in cell reprogramming. They do not only switch genes on and off, but also promote the architectural changes necessary to modify gene expression," says Thomas Graf, senior CRG group leader and lead investigator of this study. "It may have relevant implications for researchers worldwide studying gene regulation in general since we know now that the large-scale organization of the genome cannot be ignored. It also raises new questions about how these large changes can be brought about: possibly new mechanisms, perhaps even new machineries that are necessary to change certain areas of the genome," says Graf.

The findings, reported in Nature Genetics, indicate that genome architecture has important informational value for controlling gene expression during cell reprogramming, and is thus required for the specialized functions of a cell. "We are only scratching the surface of what could be critical, as-yet unrecognized mechanisms by which cells regulate gene expression," says co-principal investigator Marc A. Martí-Renom. "The new discovery might also be fundamental for development and for some development-related diseases and cancer," he concludes."

My comment: I'm wordless. We can observe incredible piece of design and creation within this amazing mechanism. How does the cell mediate the transcription factors to correctly promote the 3D architecture of the genome? After this discovery, it's ridiculous for evolutionists to tell fairytales about random mutations and selection leading to evolution. Oh no. These amazing cellular mechanisms point to Intelligent Design and Creation. Don't get lost.

2018/01/13

Epigenetics - The reasons why organisms can quickly adapt to changing environment

Random mutations and selection are not the reasons why organisms adapt to changing conditions

https://www.forbes.com/sites/grrlscientist/2017/09/06/how-do-darwins-finches-respond-so-quickly-to-environmental-changes/#37f1f45a5810

Excerpt: "How does a population adapt to sudden changes in the environment? According to the most widely accepted paradigm, random genetic changes (mutations) are the source of heritable changes in a plant or animal’s observable characteristics (phenotype). Phenotype, in turn, is the raw material that is acted upon by natural selection, and the most beneficial adaptations are passed on to successive generations. But there is a problem with this paradigm: adaptive genetic mutations are so infrequent that this scenario cannot adequately explain the speed at which adaptation can occur.

One well-known example of speedy adaptation is seen in “Darwin’s finches”; a group of approximately 15 bird species that live in the Galápagos Islands Archipelago, which are located on the equator in the Pacific Ocean. Ongoing field studies have documented rapid changes in these birds’ beak sizes and shapes in response to sudden environmental variations -- drought, or human disturbances, for example -- yet very few genetic changes have been found that accompany those physical differences between finch species, nor between populations. What guides these important changes and the speed which they can occur in these iconic birds?

The process of adaptation is more subtle than originally thought

Scientists have recently become aware that adaptation is not solely dependent upon genetic mutations; it can also occur through “extra-genetic” mechanisms. At least some changes in gene function and expression patterns are independent of mutations in a gene’s DNA sequence, yet these changes may still be inherited. These alterations are known as “epigenetic changes” (epi comes from the Greek, and translates as “over, outside of, around”) because these changes are in addition to changes in the DNA sequence itself. Epigenetic changes can activate or intensify, lessen or even completely silence, the activity of a particular gene without changing its DNA sequence.

Epigenetic changes can be triggered by environmental events. The changes that dominate alterations in gene expression and function are biochemical in nature, including: addition of a biochemical tag (methylation) to DNA; addition of a biochemical tag (methylation or acetylation) to the histone proteins around which DNA spools; or regulation of gene expression patterns by small RNA molecules.

Probably the most common epigenetic modification is DNA methylation, and just as genetic mutations can be heritable, DNA methylation patterns can be heritable, too. For example, previous work found that some epigenetic variations in five closely related species of Darwin’s finches accompany genes associated with beak size and shape, as well as a number of other important physical traits. We also know that changes in DNA methylation patterns are more common than DNA mutations. Based on these clues, a team of researchers, led by evolutionary ecologist Sabrina McNew, a graduate student at the University of Utah, proposed that epigenetic mutations -- NOT genetic mutations -- may explain how Darwin’s finches rapidly adapt to new or highly variable environments, such as those created by urbanization.
 
“Darwin’s finches are known for being phenotypically very variable, yet [they are] genetically pretty similar,” Ms. McNew explained in email.

“We were interested in investigating epigenetic variation between urban and rural populations [of Darwin’s finches] because other exciting recent work suggests that epigenetic mechanisms, such as DNA methylation can be a source of heritable phenotypic variation.”

Are epigenetics the secret to Darwin’s finches’ speedy adaptation?

To test this hypothesis, Ms. McNew assembled a research team and they measured physical traits (morphology) of wild birds in the field, and examined both the genetics and the epigenetics of separate populations of two Darwin’s finch species living at El Garrapatero, a relatively rural, undisturbed locality. They compared these findings to those from urban finch populations living near Puerto Ayora (Academy Bay), the largest town in the Galápagos Islands.

The rural and urban study sites are separated by about 10km. Earlier long-term studies (2002–2012) established that the birds in these two finch populations stay put: only one bird (a female medium ground finch) out of 300 marked and recaptured individuals relocated between the two study sites in one decade.

“[T]he finches tend to be fairly sedentary and so we think that most of the birds we caught probably grew up at whichever site they were caught at and probably their parents lived there too,” Ms. McNew said in email.

Both sites are located on the southern and southeastern coast of Santa Cruz Island, and feature the same scrubby arid habitat. Despite the habitat similarities between the rural and urban sites, there is one big difference: urban-dwelling finches dine on a banquet of human foods that are new to them whereas their rural-living cousins do not. And it is well-known that, historically, food is the main driver of beak size and shape in Darwin’s finches.

When genetic analyses were conducted later in the lab, the research team found few genetic mutations in the genes encoding these measured traits in rural and urban representatives of both species, and none of those mutations were consistent. Since recent work showed that changes in the copy number of genes is linked to rapid evolution in pepper moths and in primates, Ms. McNew and her team looked to see whether differences in gene copy number may explain the measured differences between urban and rural populations of these two finch species. Once again, they uncovered no fixed differences in gene copy numbers between the urban and rural populations for either species.

“There’s been some evidence that certain genetic markers underlie variation in beak size and shape, but overall Geospiza finches are very difficult to distinguish genetically,” Ms. McNew said. “Could there be another source of phenotypic variation?”

When the team looked at epigenetics, they found a significant number of differences between urban and rural finches of both species.

In the finches that we studied, epigenetic alterations between the populations were dramatic, but minimal genetic changes where observed,” said the study’s senior author, biologist Michael Skinner, a professor at Washington State University. Professor Skinner’s lab conducted the genetic and epigenetic analyses for this study.

The team also found these epigenetic differences were species-specific: few were shared between medium and small ground finches, in spite of their close family ties. This suggests that medium and small ground finches are each responding rapidly and in their own unique ways to environmental changes at the urban site.

Many of these observed epigenetic changes were associated with genes involved in metabolism and in intercellular communications. Other epigenetic mutations were associated with genes related to beak size and shape. These changes make intuitive sense in view of the fact that the diet of urban finches is diverging away from that consumed by rural populations.

“These species of finch have distinct diets which could explain the differences in methylation patterns as diet is known to influence epigenetics,” Professor Skinner said."

My comment: Scientists begin to understand the reasons why organisms are capable of adapting so rapidly to changing environment. Scientists themselves admit that the traditional bumper sticker, random mutations and selection doesn't explain the rapid and effective adaptation and variation of organisms. Rapid changes are caused by epigenetic mechanisms driven by nutrition, climate, stress factors, environmental toxicants, etc. Random mutations and selection have nothing to do with these ingenious mechanisms. The most common epigenetic mechanisms are DNA methylation, histone markers, and information transmitted by non-coding RNA molecules.

Epigenetic information layers are inherited, according to researchers. The study also confirms that changes in epigenetic information structures may also result in alterations in the DNA sequence. However, researchers did not find any consistent links between sequence changes and morphological changes experienced by birds. It is, therefore, clear that genetic defects in the modification of epigenetic information layers will occur in the DNA. Gradually, the genome of all organisms is degenerated and degraded. No new biological information will be added. All changes in organisms are based on epigenetic regulation of existing biological information or loss of information. Therefore there is no mechanism for evolution. Don't get lost.

2018/01/10

Alcohol found to boost cancer risk by damaging stem cell DNA

Alcohol found to boost cancer risk by causing genetic mutations in stem cell DNA

http://www.bionews.org.uk/page_920717.asp

Excerpt: "Drinking alcohol damages blood stem cells by altering their DNA, raising the risk of developing cancer, scientists have found.

A breakdown product of alcohol - acetaldehyde - is responsible for the damage, according to researchers at the MRC Laboratory of Molecular Biology in Cambridge. Acetaldehyde can cause irreversible DNA damage in blood stem cells, known as hematopoietic stem cells. These are the stem cells responsible for the constant production of fresh blood.

'How exactly alcohol causes damage to us is controversial,' said Professor Ketan Patel, who led the study which was published in Nature. 'This paper provides very strong evidence that an alcohol metabolite causes DNA damage [including] to the all-important stem cells that go on to make tissues.'

The link between alcohol and certain types of cancer has been known for some time, but exactly how drinking can raise cancer risk has been less clear. Acetaldehyde, a molecule produced by the breakdown of alcohol, badly damages DNA in cells, which in turn can lead to mutations and cancer, earlier studies have found. The cell has two ways of coping with the assault.
 
First, acetaldehyde can be cleared away by the enzyme ALDH2 (aldehyde dehydrogenase 2). However, if more alcohol is consumed than the ALDH2 can deal with, then excess acetaldehyde can damage DNA. The second coping mechanism is to repair some of the DNA damage with an enzyme called FANCD2 (Fanconi anemia group D2 protein).

In the study, the researchers used mice that did not possess either ALDH2 or FANCD2, or both, and gave them diluted alcohol for 10 days. They then sequenced the genome of their hematopoietic stem cells, to find that their DNA had been badly damaged. Hematopoietic stem cells from mice who had neither ALDH2 nor FANCD2 completely lost the ability to produce fresh blood.

'Our study highlights that not being able to process alcohol effectively can lead to an even higher risk of alcohol-related DNA damage and therefore certain cancers,' said Patel. 'But it's important to remember that alcohol clearance and DNA repair systems are not perfect and alcohol can still cause cancer in different ways, even in people whose defence mechanisms are intact.'

Around 8 percent of the world's population, especially people of East Asian origin, have very low levels of ALDH2. This can lead to 'flushing' after drinking. As a result, there is more pressure on FANCD2, and may lead to more missed DNA damage. This could be an explanation for the high incidence of esophageal cancer in countries such as China.

Professor Linda Bauld, an expert on cancer prevention at Cancer Research UK, said: 'This thought-provoking research highlights the damage alcohol can do to our cells, costing some people more than just a hangover. We know that alcohol contributes to over 12,000 cancer cases in the UK each year, so it's a good idea to think about cutting down on the amount you drink.'

Cancer Research UK estimates that about 4 percent of cancers in the UK are caused by alcohol. One pint of lager or a large glass of wine a day significantly increases the risk of developing cancer.
"

My comment: Acetaldehyde is an oxidative stressors for cells and DNA. Most genetic mutations are caused by poor diets, bad life habits, smoking and alcohol. One pint of lager or a large glass of wine a day significantly increases the risk of developing cancer, especially within people whose genome has already experienced significant genetic degradation. Alcohol consumption is one potential reason for 214,158 disease-causing genetic mutations in the human DNA at population level. Annual increase was about 20,000!! There's no mechanism for evolution. Don't get lost.

2018/01/06

Genetic degradation drives scientists to develop more accurate gene editing technology

Genetic degradation drives scientists to develop more accurate gene editing technology

https://www.wired.com/story/whats-next-for-crispr/

DNA consists mainly of four different bases: guanine (G), cytosine (C), adenine (A), and thymine (T). G makes a pair only with C and A forms a pair with T.

Genome's GC content is inclined to change to AT content. This is due to the special feature of the cytosine base: A methyl group (CH3), referred to as an epigenetic marker, may be attached to cytosine. The cell uses these markers for several tasks, the most important of which are gene suppression / activation, the secretion of the gene from transcription, and the modification of expression of the gene, i.e. the expression thereof, according to the adaptation of the organism. Also in cell differentiation, or identity, these markers play an important role. Without the epigenetic markers, the cell is a so-called a pluripotent stem cell that is ready to specialize in any task, as long as it is only programmed.

DNA may be exposed, for example, to oxidative stress as a result of dietary factors, environmental toxicants or poor lifestyle. Oxidative stress typically causes a reaction called deamination in DNA causing sequence changes. If the unmethylated cytosine deaminates, it becomes a different type of base, uracil. DNA repair mechanisms detect this error and correct the change at last in cell replication (base excision repair). But if the cytosine is methylated, it changes in deamination to thymine and this change is not corrected by DNA repair mechanisms. For genomic grammar to be correct, the original  pair of the cytosine is also replaced by changing guanine to adenine. This is how a genetic GC> AT mutation occurs.
 
Scientists are now developing accurate genomic editing methods that can restore the AT base pairs back to GC pairs. Approximately half of the 32,000 pathogenic point mutations in the human genome are due to the change in preference of the above GC pairs to AT pairs.

Excerpt: "Other scientists at Harvard and the Broad Institute have been working on an even more daring tweak to the Crispr system: editing individual base pairs, one at a time. To do so, they had to design a brand-new enzyme—one not found in nature—that could chemically convert an A-T nucleotide pairing to a G-C one. It’s a small change with potentially huge implications. David Liu, the Harvard chemist whose lab did the work, estimates that about half of the 32,000 known pathogenic point mutations in humans could be fixed by that single swap."

GC content turning to AT content is a phenomenon happening in all organisms and it causes rapid progressive genetic degradation. The specialty is eg. the fact that when bacteria start to have abundant AT content in its genome, they become harmful or pathogenic bacteria. A mammal, on the other hand, will typically be carnivorous when the GC content starts to run low.

Scientists' rush to develop these editing methods tells us that evolution is not happening. Mutations cause problems for the genome, such as information loss and diseases. Evolution theory is the most serious heresy of our time. Do not get lost, good people.