2018/11/30

Scientists claim: "All humans are descended from just TWO people and a catastrophic event almost wiped out ALL species"

MtDNA mutation rate is much higher than scientists claim

https://www.dailymail.co.uk/news/article-6424407/Every-person-spawned-single-pair-adults-living-200-000-years-ago-scientists-claim.html?fbclid=IwAR1LLXG8V2QEB6zyvuHR39u-8ZYCxdX1z8__Lli1cdHe5ftuDOjI7ZXXTQQ

Excerpt: "Scientists surveyed the genetic 'bar codes' of five million animals - including humans - from 100,000 different species and deduced that we sprang from a single pair of adults after a catastrophic event almost wiped out the human race.

These bar codes, or snippets of DNA that reside outside the nuclei of living cells, suggest that it's not just people who came from a single pair of beings, but nine out of every 10 animal species, too

Stoeckle and Thaler, the scientists who headed the study, concluded that ninety percent of all animal species alive today come from parents that all began giving birth at roughly the same time, less than 250 thousand years ago - throwing into doubt the patterns of human evolution.

'This conclusion is very surprising,' Thaler admitted, 'and I fought against it as hard as I could.'

The new report from experts at the Rockefeller University along with from the University of Basel published the extraordinary findings in Human Evolution.

The research was led by Senior Research Associate Mark Stoeckle and Research Associate David Thaler of the University of Basel, Switzerland.

They mined 'big data' insights from the world's fast-growing genetic databases and reviewed a large literature in evolutionary theory, including Darwin.

Dr Stoeckle said: 'At a time when humans place so much emphasis on individual and group differences, maybe we should spend more time on the ways in which we resemble one another and the rest of the animal kingdom.'
 
We're also surprisingly similar to not just every other human, but every other species.

'If a Martian landed on Earth and met a flock of pigeons and a crowd of humans, one would not seem more diverse than the other according to the basic measure of mitochondrial DNA,' said Jesse Ausubel, Director of the Program for the Human Environment at The Rockefeller University.

'Culture, life experience and other things can make people very different but in terms of basic biology, we're like the birds,' Dr Stoeckle added.

The 'mitochondrial DNA' examined in the research is that which mothers pass down from generation to generation and it showed the 'absence of human exceptionalism.'

'One might have thought that, due to their high population numbers and wide geographic distribution, humans might have led to greater genetic diversity than other animal species,' added Stoeckle.

'At least for mitochondrial DNA, humans turn out to be low to average in genetic diversity.' "

My comment: Previous studies over human mtDNA mutation rates have been quite controversial. The observed mtDNA mutation rate is much higher than what scientists claim. This was discovered by researchers who were studying mtDNA mutation rates from samples of Romanov family members. They noticed that human mtDNA mutation rate can be 20 times faster than other studies claim. Here's a study:

http://www.dnai.org/teacherguide/pdf/reference_romanovs.pdf

Excerpt: " And because heteroplasmy is caused by mutations, this unexpectedly high incidence suggests that mtDNA mutates much more often than previously estimated--as much as 20-fold faster, according to two studies that are causing a stir.

Regardless of the cause, evolutionists are most concerned about the effect of a faster mutation rate. For example, researchers have calculated that "mitochondrial Eve"--the woman whose mtDNA was ancestral to that in all living people--lived 100,000 to 200,000 years ago in Africa. Using the new clock, she would be a mere 6000 years old."


Mitochondrial DNA appears to mutate much faster than expected, prompting new DNA forensics procedures and raising troubling questions about the dating of evolutionary events.

2018/11/24

Metamorphosis helps us understand why evolution is impossible


Butterfly metamorphosis reveals that DNA has no control over cellular processes

Metamorphosis of insects, especially fantastic butterflies, is a nightmare for evolutionists. A more detailed examination of the mechanisms of metamorphosis also points out that metamorphosis can not be evolved. Metamorphosis also helps scientists to understand what is DNA's role in the cell and how the cell uses DNA at different stages of metamorphosis.

The butterfly, as in most insects, has four different stages; the egg, caterpillar, pupa and adult. In all four phases, DNA of the insect is exactly the same. So how is it possible that the same genes have four completely different forms? If the DNA dictated the phenotype of the organism, the insect form change would not occur. There is therefore another information layer controlling the DNA. This information layer on and outside the DNA is called epigenetic information. ('Epi' is Greek and means 'on top of'.)



Epigenetic factors and mechanisms include, for example, DNA methylation profiles, non-coding RNA molecules, transcription factors, and in particular chemical markers of histones, which serve as a biological database. Histone epigenetic markers, known for many different types of chemical markers, guide and control how actively certain areas of DNA are read and when. Thus, the cell selects DNA sequences as needed into transcription. In the insect transformation, it is important to have a precise timing and this is accurately regulated by the histone markers. The timing of DNA reading is influenced by, for example, nutrition as well as various growth factors from which cells receive information via RNA molecules.

The butterfly metamorphosis is the best example of how the cell utilizes passive DNA to produce active RNA molecules. DNA does not control cellular processes and does not dictate the appearance or behavior of the organism. DNA is controlled by epigenetic factors and mechanisms.

Due to its passive nature, mutations in DNA do not lead to any evolution because the cell is capable, under the control of epigenetic mechanisms, to select the most suitable DNA sequences for use. If the DNA sequence had an error or a wrong dinucleotide, the cell at the RNA level may still be capable of several complex repair and editing activities before the final RNA product is manufactured. For evolution to occur, there should happen tens or probably hundreds of simultaneous information increasing events in the cells, especially in germ cells, that would result in controlled change in the entire epigenetic regulatory system.  This is impossible and has never been observed. Therefore, there is no evolution. We can observe the controlled epigenetic adaptation of food and other environmental factors in organisms, but it is always based on carefully regulated mechanisms. New biological information that would lead to the growth of functional or structural complexity would not come to organisms. As we can still observe the corruption and disappearance of biological information, it is clear that there is no mechanism for evolution. And because there is no evidence of the alleged evolution of butterfly fossil record, it also confirms our understanding that evolutionary theory is the most serious heresy of our time.

2018/11/20

Open chromatin exposed to major genetic disruption

How epigenetic regulation of chromatin openness might result in DNA errors

https://www.labroots.com/trending/cell-and-molecular-biology/13307/warning-using-epigenetic-modifiers-therapeutic-targets

Excerpt: "Organisms are built from a genome, but that genome is more than just a collection of genes. The proper expression of those genes is an essential part of a healthy life, and the genome also contains many features that can help control gene expression. The structure of the genome and its shape at any given time can influence gene expression, as can epigenetic tags - a variety of different markers that can be added to genes by complexes called epigenetic modifiers. Researchers have found that in cancer samples, mutations are often found in epigenetic modifiers.

The acquisition of genetic mutations is a natural part of life. The human body has to generate billions of new cells every day to replace ones that are old or dysfunctional. Every time a cell divides to make two new ones, the genome in its nucleus has to be copied. Between all that copying, plus environmental influences like pollutants or UV rays, we can accumulate plenty of errors in our genome. Those genetic errors can lead to cancer, which becomes more likely to develop as more mutations appear in a cell. But some regions acquire mutations at a faster rate than others.
 
Since many cancer cells are known to carry epigenetic mutations, epigenetic modifiers have become a therapeutic target. Scientists at the Institute for Research in Biomedicine (IRB Barcelona) wanted to know more about why mutations accumulate in certain areas, and what the potential consequences of targeting epigenetic modifiers are.

The research, which was reported in Nature Cell Biology, indicated that chromatin, a structure formed by DNA and modifying proteins that help package it, has a major influence on how mutations are collected in certain areas. When chromatin is more 'open,' major genetic disruption is more likely. And when the researchers inhibited an epigenetic modifier called G9a, they found that chromatin accessibility, or openness, increased substantially.
Because the G9a is sometimes inhibited as a therapy, the researchers warn that this may actually be increasing the level of instability in the genome, increasing the likelihood that mutations will happen, and resulting in the growth of aggressive cancer.

Targeting epigenetic factors can have a positive effect; when used, the researchers saw that cancer cells will stop growing. "This finding would make you think that epigenetic factors are good therapeutic targets. But the genomic instability that occurred also brought about the appearance of mutated tumor cells, which eventually developed highly aggressive tumors,” explained first and co-corresponding author Alexandra Avgustinova, a postdoctoral fellow at IRB Barcelona."

My comment: As we can see, epigenetic modifications might result in genetic errors. This is one reason for why ecological adaptation can lead to genetic degradation. Every time when epigenetic modifiers are altered or disrupted, they might left the chromatin in open position and expose it to genetic errors. This is why any change in organisms is due to epigenetic regulation of pre-existing information OR gradual but inevitable loss of information. There's no mechanism for evolution. Don't get lost.

2018/11/15

Histone modifications - the most significant reversible factors for cell differentiation and biodiversity

Histone modifications regulate pre-existing biological information but they don't result in any kind of evolution

https://www.the-scientist.com/uncategorized/the-nucleosome-untangled-47599

Excerpt: "Histones serve as slates to a dizzying array of modifications, but researchers are confident they can decipher the epigenetic puzzle.

Roughly two meters of DNA gets packed into every cell nucleus in the human body. In addition to stuffing all that information into a sphere 3 to 10 microns across, the proteins that perform this task must also ensure that in each cell certain genes are constantly transcribed, while others lie ready, and other regions remain dormant, practically inaccessible. Within this cramped, chaotic space, an army of proteins must manage cellular information, decide cell fate with a moment's notice and maintain it, often passing that fate to daughter cells.

This regulation takes place in the context of the histone proteins. Two each of the four standard histones - H3, H4, H2A, and H2B - join together to form an octameric nucleosome, a spool around which roughly 146 nucleotides wind in a near double loop. By no means inert packing material, the nucleosome serves as a slate for a rich variety of modifications or "marks" that appear to play a role in managing the genome. Acetylation, methylation, phosphorylation, ubiquitination, sumoylation - the list of modifications grows monthly. Researchers have mapped as many as 50 different marks to specific amino acid residues on the histones' highly conserved N-terminal tails and elsewhere on the molecules, says Thomas Jenuwein from the Research Institute of Molecular Pathology in Vienna. "One of the challenges, I think, is to identify all of the modifications that exist," says Tony Kouzarides, of the Wellcome Trust/Cancer Research UK Gurdon Institute.

 
The list of known histone epigenetic modifications.

Constant additions to the cast of histone marks, and the regulatory proteins that make them, remove them, or act upon their presence, put the number of potential combinations in the astronomical range. Say there were 30 different residues marked in a given nucleosome, 230 gives a billion possible combinations. A human cell has approximately only 40 million incorporated nucleosomes. Nevertheless, many appear to act together. Take one oft-described scenario on histone H3: Methylated lysine 4 (H3K4Me) and an acetylated lysine 14 (H3K14Ac) together produce an active gene state similar to a phosphorylated serine 10 in combination with acetylated lysines 14 and 9. Methylated lysine 9 is antagonistic to the serine 10 phosphorylation acting like a switch to shut down expression. And, adjacent serine-lysine pairs appear elsewhere in the histone tails.

Epigenetic markers function also as dials or knobs. In this way digital information (markers) is converted to analogue form of information. 

These "cross-talking" units and other signaling cascades (see image below) have an alluring quality to many researchers. A layer of information is definitely encoded in these signals, says C. David Allis, a Howard Hughes Medical Institute investigator at Rockefeller University. "As you develop from a totipotent or pluriopotent cell to a developmentally differentiated cell ... the DNA is remaining constant. It sort of tells us [that] something non-DNA is going on," says Allis, but just how much information is stored in these signals has been a matter of debate.

Epigenetic modifications are reversible


https://www.sciencedirect.com/topics/neuroscience/epigenetic-modification


Excerpt: "Epigenetic modifications play an important role in gene expression and regulation, and are involved in numerous cellular processes such as differentiation, development, and tumorigenesis. Epigenomics is the study of the complete set of epigenetic modifications on the genetic material of a cell. Epigenetic modifications are reversible modifications on a cell's DNA or histones that affect gene expression without altering the DNA sequence. Epigenomic maintenance is a continuous process that plays an important role in the stability of eukaryotic genomes by taking part in crucial biological mechanisms such as DNA repair. Two of the most characterized epigenetic modifications are DNA methylation and histone modification."

My comment: Evolution believers claim that epigenetic modifications are subject to evolution and selection. This is a pseudoscientific claim. Why? Here's because:

1. Epigenetic modifications are based on mechanisms where readers, writers and erasers are accurately doing their job along the needs of ecological adaptation. These processes are highly controlled by RNA-mediated information transmission. Nothing to do with randomness and selection.

2. Epigenetic modifications don't result in increase in biological information because they regulate how DNA is condensed and how actively it is read into transcription. Epigenetic modifications mean regulation of pre-existing biological information.

3. Epigenetic modifications are reversible. This means highly dynamic information layers.

4. Epigenetic modifications actually often result in subtle DNA errors and this leads to gradual but inevitable DNA degradation.

The theory of evolution is the most serious heresy of our time. Don't get lost.

2018/11/11

Epigenetic inheritance under attack - What does serious science say?

There are several factors and mechanisms affecting transgenerational epigenetic inheritance

In recent days we have seen several articles about transgenerational epigenetic inheritance. Typically these articles are based on research made by population geneticists who try to belittle the importance of epigenetic inheritance. Here's a couple of examples:

https://www.cell.com/cell/fulltext/S0092-8674(18)31255-8#.W-VG7yzrTNw.twitter

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6065375/

Serious science takes account of all known factors and mechanisms regarding epigenetic inheritance. This is a much better paper:

https://humgenomics.biomedcentral.com/articles/10.1186/s40246-015-0041-3


Excerpt from abstract: "Genome-wide association studies of complex physiological traits and diseases consistently found that associated genetic factors, such as allelic polymorphisms or DNA mutations, only explained a minority of the expected heritable fraction. This discrepancy is known as “missing heritability”, and its underlying factors and molecular mechanisms are not established. Epigenetic programs may account for a significant fraction of the “missing heritability.” Epigenetic modifications, such as DNA methylation and chromatin assembly states, reflect the high plasticity of the genome and contribute to stably alter gene expression without modifying genomic DNA sequences.

Consistent components of complex traits, such as those linked to human stature/height, fertility, and food metabolism or to hereditary defects, have been shown to respond to environmental or nutritional condition and to be epigenetically inherited. The knowledge acquired from epigenetic genome reprogramming during development, stem cell differentiation/de-differentiation, and model organisms is today shedding light on the mechanisms of (a) mitotic inheritance of epigenetic traits from cell to cell, (b) meiotic epigenetic inheritance from generation to generation, and (c) true transgenerational inheritance. Such mechanisms have been shown to include incomplete erasure of DNA methylation, parental effects, transmission of distinct RNA types (mRNA, non-coding RNA, miRNA, siRNA, piRNA), and persistence of subsets of histone marks."

My comment: So, modern science is aware of at least 25 different molecular mechanisms affecting transgenerational epigenetic inheritance. These are:

Category
Molecular mechanism
DNA sequence-invariant heritable traits
DNA methylation/histone post-translational modifications
DNA methylation maintenance across cell division cycles
Hemimethylated DNA-guided, DNMT1-mediated CpG methylation pattern maintenance
DNA demethylation
Passive DNA demethylation
   -5-mC to 5-hmC conversion
Active DNA demethylation
   -Glycosylase-mediated base removal and base excision repair mechanisms
Histone code
Condensed chromatin
   -HAT inactivation
   -HMT activation
Relaxed chromatin
   -HAT activation
   -HMT inactivation
Epigenetic modulation of mother-to-fetus transmission
Maternal nutrition status
Maternal exposure to environmental toxins and food contaminants
   -BPA
   -Phthalates
   -Dioxins
   -Tobacco smoke
Cell differentiation and body development
Epigenetic signature reprogramming
   -Erasure/reprogramming in the zygote (mitotic   transmission)
   -Erasure/reprogramming in PGCs (meiotic transmission)
Gamete-carried transmission
   -DNA methylation profiles in sperm and oocytes
   -H3K4 and H3K27 histone methylation in sperm  cells
   -RNA molecules carried by sperm cells (mRNA, non-coding RNA, miRNA, siRNA, piRNA)
Stem cell reprogramming
Epigenetic signature of induced pluripotency
   -Decreased TETs/decreased hydroxymethylation at ES gene promoters
   -Reprogramming-resistant regions enriched for H3K9me3

Especially the role of non coding RNA molecules in the epigenetic inheritance is understudied. Serious scientists are focusing on histone epigenetic markers because they seem to be a biological database having a strong influence on how DNA is read and transcribed. We have seen several articles about switching genes on or off but this is too narrow view about how DNA is used by cellular mechanisms. Reading and transcribing of DNA is just the first step in making a functional product, an RNA molecule.
 
Major biological functions of lncRNAs in epigenetic, transcriptional, and posttranscriptional regulation. (a) DNA methylation, (b) genomic imprinting, (c) chromatin remodeling, (d) histone modifications, (e) transcriptional regulation, and (f) posttranscriptional regulation.

Here's a good example of how epigenetic markers, especially the histone code is affecting one of the most significant human traits, the height:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4208652/

Modern scientists know that histone code is established during embryonic development and non coding RNA molecules have a strong impact on this process. According to NONCODE, there are over 167,000 different long non coding RNAs (lncRNAs) functioning in a human body. The number of different lncRNAs in human sperm is also up to several thousands, probably tens of thousands. They are carried by extracellular vesicles such as exosomes and they have a significant role in establishing the histone code that mostly determines organismal characteristics and traits. DNA methylation profiles are also meaningful regarding epigenetic inheritance but most of them are erased during embryonic development. Here's a great study over histone code and long non coding RNA molecules:

http://tcr.amegroups.com/article/view/15283/html

So, before claiming that transgenerational epigenetic inheritance is just a minor contributor regarding inheritance, scientists should carefully investigate these several epigenetic factors and mechanisms, especially the role of histone code and non coding RNA molecules. 

2018/11/09

Biological Meltdown: The Loss of Agricultural Biodiversity

Biological meltdown - The loss of genetic diversity is caused by intense breeding and gene editing

https://www.reimaginerpe.org/node/921

Excerpts: "This story illustrates not only the tremendous value of rapidly disappearing crop genetic diversity, but also the fact that it is impossible to talk about the conservation of species and ecosystems separate from farm communities and indigenous peoples. The world's main food and livestock species have their centers of genetic diversity in the South. Generations of farmers in the tropics and sub-tropics have consciously selected and improved plants and animals that are uniquely adapted to thousands of micro-environments. Today, farming communities in Africa, Asia and Latin America are the primary custodians of most of the earth's remaining agricultural biodiversity. They are also carriers of unique knowledge about genetic resources and entire ecosystems.

Agricultural biodiversity refers to that part of biodiversity that feeds and nurtures people--whether it is derived from the genetic resources of plants, animals, fish or forests. We are losing genetic resources for food and agriculture at an unprecedented rate. It can best be described as a biological meltdown. The statistics are numbing:

Crop genetic resources are being wiped out at the rate of 1-2% every year. Since the beginning of this century, about 75% of the genetic diversity of agricultural crops has been lost.

Livestock breeds are disappearing at an annual rate of 5%, or 6 breeds per month. In Europe, half of all breeds of domestic animals that existed at the turn of the century have become extinct, and 43% of the remaining breeds are endangered.


Whether in farmers' fields, forests, or fisheries, the genetic variation needed to meet human food needs is slipping into oblivion. Equally alarming, genetic resources are being privatized and their natural habitats plundered. We are losing the biological options we need to strengthen food security and to survive global climate change. The consequences, warns the United Nations, are "serious, irreversible and global."


 

Effect of Domestication and Plant Breeding on Genetic Diversity of Maize Genes. Reduction of gene pool is a result of intense breeding.




























Erosion of crop and animal diversity threatens the existence and stability of our global food supply because genetic diversity (found primarily in the South) is vital for the maintenance and improvement of agriculture. To maintain pest and disease resistance in our major food crops, for instance, or to develop other needed traits like drought tolerance or improved flavor, plant breeders constantly require fresh infusions of genes from the farms, fields and forests of the South. But agricultural biodiversity is not just a raw material for industrial agriculture; it is also the key to food security and sustainable agriculture because it enables poor farmers to adapt crops and animals to their own ecological needs and cultural traditions. Without this diversity, options for long-term sustainability and agricultural self reliance are lost.

Why Are We Losing Agricultural Biodiversity?

The greatest factor contributing to the loss of crop and livestock genetic diversity is the spread of industrial agriculture and the displacement of more diverse, traditional agricultural systems. Beginning in the 1960s and 1970s, the Green Revolution introduced high-yielding varieties of rice and wheat to the developing world, replacing thousands of farmers' traditional crop varieties and their wild relatives on a massive scale. The same process continues today. New, uniform plant varieties are replacing farmer's traditional varieties - and the traditional ones are becoming extinct.

In the United States, more than 7000 apple varieties were grown in the last century. Today, over 85 percent of those varieties - more than 6000 - are extinct. Just two apple varieties account for more than 50% of the entire US crop. In the Philippines, where small farmers once cultivated thousands of traditional rice varieties, just two Green Revolution varieties occupied 98% of the entire rice growing area in the mid-1980s.

Industrial agriculture requires genetic uniformity. Vast areas are typically planted to a single, high-yielding variety or a handful of genetically similar cultivars using capital intensive inputs like irrigation, fertilizer and pesticides to maximize production. A uniform crop is a breeding ground for disaster because it is more vulnerable to epidemics of pests and diseases.

The same is true with livestock genetic resources. The introduction of "modern" breeds that are selected solely for maximizing industrial production has displaced or diluted indigenous livestock breeds worldwide."


My comment: The more variation or artificial selection of breeds, the more genetic degradation that can be observed as loss of genetic diversity. This same phenomenon is occurring in nature; when organisms adapt to changing environment they actually experience loss of genetic diversity. About 40,000 species become extinct every year. Why is this happening?

Every time when an organism adapts to a new environment or new diet type, its epigenetic information layers are altered. This shifting results in DNA errors (mutations). Gradually the gene pools of organisms are getting weaker and weaker. A weak genome can be observed as susceptibility to diseases or weak resistance to parasites and pathogens. We can observe rapid loss of biological information everywhere in nature. It's crystal clear that evolution is not happening. There is no mechanism for it. Don't be deceived.

2018/11/03

The most serious problems with the theory of evolution

The biggest holes in biological and chemical evolution - No new evolutionary innovations

http://www.ideacenter.org/contentmgr/showdetails.php/id/1551

Summary:

Problem 1: No Viable Mechanism to Generate a Primordial Soup

Problem 2: Unguided Chemical Processes Cannot Explain the Origin of the Genetic Code

Problem 3: Random Mutations Cannot Generate the Genetic Information Required for Irreducibly Complex Structures

Problem 4: Natural Selection Struggles to Fix Advantageous Traits into Populations

Problem 5: Abrupt Appearance of Species in the Fossil Record Does Not Support Darwinian Evolution

Problem 6: Molecular Biology has Failed to Yield a Grand "Tree of Life"

Problem 7: Convergent Evolution Challenges Darwinism and Destroys the Logic Behind Common Ancestry
 
Problem 8: Differences between Vertebrate Embryos Contradict the Predictions of Common Ancestry

Problem 9: Neo-Darwinism Struggles to Explain the Biogeographical Distribution of many Species

Problem 10: Neo-Darwinism has a Long History of Inaccurate Darwinian Predictions about Vestigial Organs and "Junk DNA"

My comment: There is no such mechanism for evolution being able to create new innovations, structures or functions. Atheists are desperately seeking 'evolutionary innovations by chance' but results have been miserable. In every case of so called 'new function' or 'new structure' we can observe the actual reason:

1. Alteration or regulation of pre-existing function.
2. Deletion or break-down of pre-existing function.

Here's a couple of examples:

a. The Italian wall lizard. So called new structures (Cecal valves) arose due to epigenetic switching which was regulated by changed diet type from insects to plants.
b. Nylonase bacteria. The nylonase enzyme was derived from a pre-existing esterase enzyme. (http://evolutiondismantled.com/nylonase)

Mutations in DNA never result in any kind of evolution but degradation of pre-existing information. DNA doesn't dictate body plan or even individual characteristics. Change in organisms is caused by epigenetic regulation of pre-existing biological information or loss of information. The theory of evolution has failed.