2016/11/23

Diet affects epigenome through gut microbiota

Diet affects epigenome through gut microbiota

http://medicalxpress.com/news/2016-11-diet-affect-epigenetics-microbiota.html

Excerpt: "You are what you eat, the old saying goes, but why is that so? Researchers have known for some time that diet affects the balance of microbes in our bodies, but how that translates into an effect on the host has not been understood. Now, research in mice is showing that microbes communicate with their hosts by sending out metabolites that act on histones—thus influencing gene transcription not only in the colon but also in tissues in other parts of the body. The findings publish November 23 in Molecular Cell.

In the study, the researchers first compared germ-free mice with those that have active gut microbes and discovered that gut microbiota alter the host's epigenome in several tissues. Next, they compared mice that were fed a normal chow diet to mice fed a Western-type diet—one that was low in complex carbohydrates and fiber and high in fat and simple sugars. Consistent with previous studies from other researchers, they found that the  of mice fed the normal chow diet differed from those fed the Western-type diet.


"When the host consumes a diet that's rich in complex plant polysaccharides (such as fiber), there's more food available for microbes in the gut, because unlike , our human cells cannot use them," explains Federico Rey, an assistant professor of bacteriology at UW-Madison and the study's other senior author.
Furthermore, they found that mice given a Western diet didn't produce certain metabolites at the same levels as mice who ate the healthier diet. "We thought that those metabolites—the short-chain  acetate, propionate, and butyrate, which are mostly produced by microbial fermentation of fiber—may be important for driving some of the epigenetic effects that we observed in mouse tissues," Denu says.
The next step was to connect changes in metabolite production to . When they looked at tissues in the mice, they found differences in global histone acetylation and methylation based on which diet the mice consumed. "Our findings suggest a fairly profound effect on the host at the level of chromatin alteration," Denu explains. "This mechanism affects host health through differential gene expression."

"Fruits and vegetables are a lot more than complex polysaccharides," Rey says. "They have many other components, including polyphenols, that are also metabolized in the gut and can potentially affect chromatin in the  in ways that we don't yet understand. Short-chain fatty acids are the tip of the iceberg, but they're not the whole story."

My comment: Diet is the most significant factor causing changes in the genome. There are several mechanisms known how nutrients impact the epigenome but microbiota mediated gene regulation is one of the most interesting types. This discovery provides a perfect example of cause and effect, signal and response, laws that organisms use within ecological adaptation. These mechanisms have nothing to do with random mutations or natural selection. A couple of living examples:

http://www.sciencemag.org/news/2016/06/how-does-lizard-go-vegetarian-growing-its-gut
https://www.eurekalert.org/pub_releases/2016-05/iu-yaw051116.php
https://www.ncbi.nlm.nih.gov/pubmed/25217047
http://journal.frontiersin.org/article/10.3389/fgene.2013.00049/full

2016/11/22

Researchers map diet induced epigenetic inheritability

Researchers map diet induced epigenetic inheritability 


Excerpt: "A fundamental law of genetics states that progenies do not inherit epigenetically-based adaptive, pathological or neural features acquired in response to environmental conditions. However, recent studies seem to contradict this dogma.Now, two new studies in mice from University of Massachusetts and Beijing University, respectively, demonstrate how a father’s diet affects levels of specific small RNAs in his sperm, which in turn can affect gene regulation in offspring. The researchers state that these results add to the growing list of ways in which a male’s lifestyle can influence his offspring, including through the sperm epigenome, microbiome transfer and seminal fluid signalling.
The group state that their findings suggest that RNAs from sperm of HFD males contain the information to induce glucose intolerance, but not insulin resistance. Further investigation identified tRNAs fragments, containing about 30-34 nucleotides, as the class of small RNA that caused the glucose intolerance observed in HFD offspring. Results show that a genome-wide comparison between ND and HFD offspring found significantly less expression of genes involved with ketone, carbohydrate, and monosaccharide metabolism in the HFD group.
In the second study, a team of researchers from the University of Massachusetts tested whether the sperm of mice on a low protein (LP) diet experienced any changes in RNA levels. Results show that small RNAs from immature sperm in the testis did not correlate with dietary effects; yet, sequencing of small RNA in mature sperm in the epididymus revealed great expression of certain RNAs. The lab then isolated RNA in sperm from LP mice and controls, finding particularly high levels of a RNA, tRNA-Gly-GCC, in the LP group. Data findings show that tRNA-Gly-GCC suppresses a subset of genes, including a gene that contributes to the plasticity of mouse embryonic stem cells.
The researchers surmise that although tRNAs are best known for roles in protein synthesis, their fragments are turning up in other cellular situations.  They go on to add that both studies suggest that the RNA bits alter gene activity with the UMass team blocking one of the tRNA fragments inside embryonic stem cells to increase the activity of about 70 genes.  For the future, the groups state that they to investigate how permanent these changes are and how quickly they can be reversed by changing diet. They go on to conclude that the effects of the RNA fragments don’t have to be harmful and state that if a bad diet can influence a person, a healthy diet can do it in the same way."
My comment: These studies demonstrate how RNA in sperm can be affected by diet, and that this can cause changes in gene regulation of offspring. Several other studies have recently reported also that organisms are able to inherit some acquired traits through sperm RNAs:
http://qichen-lab.info/assets/2016_NRG_Chen_et.al.pdf
http://phys.org/news/2016-10-biologists-inheritance-gene-silencing-rna.html

Diet is the most significant factor causing alterations to organisms. But there are other energy associated factors 
such as climate, stress etc. affecting the epitranscriptome.   Random mutations are not the reason for rich and rapidly changing biodiversity. Changes and variation are based on designed and created mechanisms. Modern scientists understand this fact. Mechanisms for ecological adaptation and variation are soon well known. Large scale evolution has no mechanism. The evolutionary theory is a major lie.

2016/11/18

Energy efficient cells

Cities operating at 100% energy efficiency - The Cell has factories, it's a supercomputer and a complex city


Excerpt: ""The miniature cities are fully equipped with all of the facilities, or organelles, that are necessary for a smooth-running operation."
Administration center, factories and even recycling centers are all there, running at 100-percent efficiency. In contrast to the infrastructures and city buildings in cells, however, the organelles, are not built on static foundations. They are huge, mobile cellular cargos that travel rapidly to reach resources and deliver products. When organelles go off the rails and mobility is disrupted, bad things happen.
"In human neurons, glitches in these movements result in severe neuro diseases," said Brandizzi, an MSU AgBioResearch scientist. "But before our paper, scientists had little idea about how the organelles moved on their tracks in plant cells beyond the conventional proteins that make up the cytoskeleton."
Brandizzi and her team of MSU scientists, focused on the largest factory in a cell -- the endoplasmic reticulum. Earlier studies had proven that the ER moved around the cell on a track, known as actin cytoskeleton propelled by myosin, structures that give cells their shape as well as serve as a rail and motor system at the molecular level."
My comment: Realizing the perfection of how cellular mechanisms function has led many scientists to support Intelligent design and creation. For example Jerry Fodor and Massimo Piattelli-Palmarini criticize neo-darwinism after studying a few perfectly functioning organisms:
http://www.patheos.com/blogs/geneveith/2011/12/non-creationist-critiques-of-darwinism/
"
Fibonacci patterns, in which each term is equal to the sum of the two preceding ones, seem to be prior to all evolutionary developments; scaling factors in organisms are multiples of a quarter, not of a third, according to the “one-quarter power law”; computational analysis of nervous systems of organisms show that their “connection economies” are perfect; “cost versus speed” analyses of the respiratory patterns of the song of canaries show the most efficient use of energy; tests of the ratio of foraging honeybees to those staying in the hives show perfect solutions in all situations. There is perfection everywhere. They also offer an example of a type of wasp whose patterns of feeding her young competes with ID theorist Michael Behe’s notion of “irreducible complexity.”
But the major neo-Darwinist problem, they conclude, is that natural selection, in analogy to artificial selection, depends on the existence of a mythical “Mother Nature.” But since there is no Mother Nature, “she is a frail reed for [adaptationists] to lean on. Ditto, the Tooth Fairy; ditto the Great Pumpkin; ditto God. Only agents have minds, and only agents act out of their intentions, and natural selection isn’t an agent.”"

Distal control regions switch genes on and off

Distal control regions switch genes on and off by chromosomal folding and touching


Excerpt: "Image shows a cut-away cell nucleus (top left) with one chromosome highlighted and enlarged on the right. Each chromosome contains hundreds of genes. Enlarged section of the chromosome (bottom left) shows how chromosome folds to allow distal control regions of the DNA thread (yellow) to directly interact with a gene (blue). These distal control regions switch genes on and off. Small changes in the DNA sequence of the control regions may interfere with normal gene expression and lead to disease susceptibility.
Credit: Drs C. Varnai and P. Fraser, © The Babraham Institute 2016
My comment: There are several types of biological information in the cell. Gene sequences make a digital information platform, epigenetic layers, chemical tags and markers make an analog information layer. Chromosomal folding, 3D-genome and touching by distal control regions constitute a complex analog information layer that is very difficult to understand, measure or predict. But it tells us how the cell takes use of genes. Genes are raw library material and RNA mediated cellular processes use them along the needs of ecological adaptation. Even the slightest erroneous changes in this regulation architecture can be harmful and lead to diseases. That's why random mutations can never lead to adaptation or evolution.  

Bacteria quorum sensing

Bacteria can boost their own immune system by talking to each other


Excerpt: "People have long understood the advantages of living in communities and bacteria are no different, often residing in close quarters to share resources. However, there are also potential drawbacks to community life as high-density bacterial populations are more vulnerable to the spread of viruses - just like people in a crowded bus or a daycare centre," he says.
The breakthrough came when the researchers discovered that the ability of bacteria to gauge the number of cells in their communities enabled the bacteria to boost the power of their CRISPR-Cas immune systems to prevent viral outbreaks.
Associate Professor Fineran says the bacteria sense the population density by "talking" to each other using a form of chemical communication known as quorum sensing.
"The higher the population density, the stronger the communication between cells becomes, which results in greater coordination of immune defenses," he says.
Adrian Patterson, a PhD student and first author on the paper, says the study shows that bacterial cells preemptively elevate their immunity when they are most at risk of a virus spreading through the population.
"They both increase their ability to generate new immune memories and strengthen existing immunity by up to 500-fold," Mr Patterson says.
The role of CRISPR-Cas in providing bacteria with viral immunity was only discovered in the past decade.
The systems create genetic memories of specific past viral infections by taking little snippets of the viruses' DNA and storing them in memory banks to aid in recognising and destroying future infections.
One of the least understood aspects of the CRISPR-Cas field is how bacteria control the activity of these systems. Too much activity can result in an autoimmune-like disease, killing the host cell, but too little activity might allow viruses to wipe out entire bacterial communities. The team's research shows that by openly communicating with each other, bacteria strike the right balance between these two outcomes.
Dr Simon Jackson, second author of the study, says bacterial immune systems are fascinating to study.
"Lately we have made significant advances in understanding how they function. The really exciting part of our most recent discovery is that we predict the communication-based coordination of CRISPR-Cas immunity to be widespread throughout bacterial species." "

My comment: Even unicellular life forms seem to use complex mechanisms for securing life. There is not such a thing as a simple life form. Bacteria also have genetic memory and they are able to transfer information to each other by using the quorum sensing mechanism. Snippets of viral DNA are stored in the memory for future generations to be prepared for viral attacks. By this way they can fight back using mechanisms, not random mutations. This points to Intelligent Design. The evolutionary theory is a big lie.

2016/11/17

One genome - Two structures

THE CATERPILLAR AND THE BUTTERFLY
ONE Genome - TWO Structures


http://multivu.prnewswire.com/mnr/mds-foundation/37124/docs/37124-epigenetics_unbranded.pdf

Excerpt: "When the caterpillar changes into a butterfl y, its genome – its basic genetic sequence – does not change. The differences between its two forms result from turning on and off different genes. These changes in GENE EXPRESSION (turning a gene on) and GENE SILENCING (turning a gene off), which do not change the underlying DNA sequence, are collectively referred to as EPIGENETICS. In some cases – the caterpillar and butterfl y, for example – these changes are normal and expected and may be required for development. But diet, environmental effects or even pre-natal factors can create unintended, reversible chemical modifications that mark a gene to be expressed or to be silenced. Some of these epigenetic changes may be benign. But when they allow cells to multiply uncontrollably, the result can be cancer!"

My comment: The genome of butterfly eggs contains all information necessary for every four forms for metamorphosis. This makes us realize that this kind of way to use biological information is not possible to evolve. Perfect timing of those phases is directed by diet induced microRNA regulation.

Metamorphosis is a perfect example of a power of epigenetic control of gene expression. Organisms have silenced genes and activated genes. Genes can be switched on or off rapidly with needs of adaptation. These clever mechanisms point to creation and Intelligent design.

2016/11/15

DIET CHANGES THE GENOME

DIET CHANGES THE GENOME

https://www.sciencedaily.com/releases/2016/11/161115111720.htm

Excerpt: "Researchers at the University of Oxford have demonstrated that the diets of organisms can affect the DNA sequences of their genes.
In a study on two groups of parasites, the team detected differences in DNA sequences that could be attributed to the composition of their food.
The results are published in the journal Genome Biology.
Study co-author Dr Steven Kelly, from Oxford's Department of Plant Sciences, said: 'Organisms construct their DNA using building blocks they get from food. Our hypothesis was that the composition of this food could alter an organism's DNA. For example, could a vegetarian panda have predictable genetic differences from a meat-eating polar bear?
'To test this hypothesis, we picked simple groups of parasites to use as a model system. These parasites share a common ancestor but have evolved to infect different hosts and eat very different foods.
'We found that different levels of nitrogen in a parasite's diet contributed to changes in its DNA. Specifically, parasites with low-nitrogen, high-sugar diets had DNA sequences that used less nitrogen than parasites with nitrogen-rich, high-protein diets.'
The study involved groups of eukaryotic parasites (Kinetoplastida) and bacterial parasites (Mollicutes) that infect different plant or animal hosts.
The results, based on novel mathematical models developed by the researchers, reveal a previously hidden relationship between cellular metabolism and evolution. They provide new insights into how DNA sequences can be influenced by adaptation to different diets.
Furthermore, the team found it is possible to predict the diets of related organisms by analysing the DNA sequence of their genes.
Study co-author Emily Seward, a doctoral candidate in Oxford's Department of Plant Sciences, said: 'It has been unclear why very closely related organisms can look so different in their genetic makeup. By bringing together two fundamental aspects of biology -- metabolism and genetics -- we have advanced our understanding of this area.
'It's a difficult question to answer, because there are so many factors that can influence the DNA sequence of an organism. But our study explains a very high percentage of these differences and provides evidence that we really are what we eat.
'We are now looking at more complex organisms to see if we will find the same thing.'"

My comment: The ecological adaptation is based on designed mechanisms. Organisms adapt to changing environment. Nutrition changes the epigenome and this may cause changes in base sequences, too. There is always a cause and an effect in biology. The main principles of the evolutionary theory are random genetic mutations and natural selection. Modern scientists understand that organisms may experience changes due to Intelligently designed mechanisms, not by random mutations. Don't get lost.

Bacteria don't evolve

Bacteria don't evolve, they only adapt due to Intelligent mechanisms

1. Bacteria have a maximum number of simultaneous traits by which they can resist medicines. This means that although modern medicines don't work, it's possible that old type medicine is again effective. This seems to be true according to newest findings:

http://medicalxpress.com/news/2016-11-simple-antibiotic-treatment-mrsa-bacteria.html
http://www.bbc.com/news/uk-england-nottinghamshire-32117815

2. Ancient bacteria are able to rapidly adapt to modern medicine. This points out that bacteria don't evolve. They just switch between limited number of simultaneous genetic and epigenetic combinations.

http://news.nationalgeographic.com/news/2012/04/120411-drug-resistance-bacteria-caves-diseases-human-health-science/
http://blog.eoscu.com/blog/mrsa-an-ancient-bacteria-adapts-to-modern-medicine


3. Bacteria stay as bacteria, they don't evolve into another life form. The evolutionary theory is a big lie.

2016/11/13

Plant microRNAs play a role in gene expression

Plant microRNAs play a role in gene expression


Excerpt from the abstract: "Our previous studies have demonstrated that stable microRNAs (miRNAs) in mammalian serum and plasma are actively secreted from tissues and cells and can serve as a novel class of biomarkers for diseases, and act as signaling molecules in intercellular communication. Here, we report the surprising finding that exogenous plant miRNAs are present in the sera and tissues of various animals and that these exogenous plant miRNAs are primarily acquired orally, through food intake. MIR168a is abundant in rice and is one of the most highly enriched exogenous plant miRNAs in the sera of Chinese subjects. Functional studies in vitro and in vivo demonstrated that MIR168a could bind to the human/mouse low-density lipoprotein receptor adapter protein 1 (LDLRAP1) mRNA, inhibit LDLRAP1 expression in liver, and consequently decrease LDL removal from mouse plasma. These findings demonstrate that exogenous plant miRNAs in food can regulate the expression of target genes in mammals."

Here's another example: 

http://www.greenmedinfo.com/blog/amazing-food-science-discovery-edible-plants-talk-animal-cells-promote-healing



Excerpt: "A groundbreaking new study published in Molecular Nutrition & Food Research titled, "Interspecies communication between plant and mouse gut host cells through edible plant derived exosome-like nanoparticles," reveals a new way that food components 'talk' to animal cells by regulating gene expression and conferring significant therapeutic effects. With the recent discovery that non-coding microRNA's in food are capable of directly altering gene expression within human physiology, this new study further concretizes the notion that the age old aphorism 'you are what you eat' is now consistent with cutting edge molecular biology.

"Our findings show that exosome-like nanoparticles are present in edible fruits and vegetables and reveal a previously unrecognized strategy by which plants communicate with mammalian cells via exosome-like nanoparticles in the gut, and in particular intestinal macrophages and stem cells. We found that edible plants contain large amounts of nanoparticles. Like mammalian exosomes, further characterization of the plant nanoparticles led to identifying them as exosome- like nanoparticles based on the nanoparticles being com- posed of proteins, lipids, and miRNAs. EPDENs from different types of plants have different biological effects on the recipient mammalian cells. This finding opens up a new avenue to further study the molecular mechanisms underlying how the plant kingdom crosstalks with mammalian cells such as intestinal macrophages and stem cells via EPDENs. This information may provide the molecular basis of using multiple plant-derived agents for better therapeutic effect than any single plant-derived agent."

Can we observe the plant miRNA induced gene expression to occur in nature? Yes, we have several examples. One of the best examples is rapid adaptation of the Italian wall lizard:

http://news.nationalgeographic.com/news/2008/04/080421-lizard-evolution_2.html

Excerpt: "Italian wall lizards introduced to a tiny island off the coast of Croatia are evolving in ways that would normally take millions of years to play out, new research shows.

In just a few decades the 5-inch-long (13-centimeter-long) lizards have developed a completely new gut structure, larger heads, and a harder bite, researchers say. In 1971, scientists transplanted five adult pairs of the reptiles from their original island home in Pod Kopiste to the tiny neighboring island of Pod Mrcaru, both in the south Adriatic Sea.

The transplanted lizards adapted to their new environment in ways that expedited their evolution physically, Irschick explained.
Pod Mrcaru, for example, had an abundance of plants for the primarily insect-eating lizards to munch on. Physically, however, the lizards were not built to digest a vegetarian diet.

Researchers found that the lizards developed cecal valves—muscles between the large and small intestine—that slowed down food digestion in fermenting chambers, which allowed their bodies to process the vegetation's cellulose into volatile fatty acids.

"They evolved an expanded gut to allow them to process these leaves," Irschick said, adding it was something that had not been documented before. "This was a brand-new structure."

Along with the ability to digest plants came the ability to bite harder, powered by a head that had grown longer and wider."

My questions: 

1. Did the lizards eat the new type of food before these observed changes and new structures occurred?
2. What kind of genetic solution makes it possible for a lizard to get a new structure after few generations? Is the genetic material already present in the lizard's genome?
3. Does the ecological adaptation need millions of years?

If you are biologically uninformed and irrational, you buy the explanations of the evolutionists about random mutations and selection. If you understand something about biology, you admit that the changes that those lizards experienced were driven by the food type the lizards ate. The nutrition also caused morphological changes, like a head that had grown longer and wider. There's also a reason for that. The lizard is able to bite harder. 


The evolutionary theory is a laughable fairytale. The lizards are intelligently designed and created by God.

2016/11/12

Rapid adaptation refutes the evolutionary principles

Rapid adaptation refutes the evolutionary principles

http://www.polarbearsinternational.org/about-polar-bears/essentials/evolution

Excerpt: "Estimates of when polar bears began to split from brown bears continue to change as geneticists look further into the polar bear genome. Recent studies suggest that polar bears split from a common brown bear ancestor 350,000-6 million years ago."

Polar bears on land where there is little or no snow have slightly light brown fur. Seems that Polar bears are rapidly adapting into changing environment. Seems also that there are not so big differences between Brown bears and Polar bears. Ecological adaptation doesn't need millions of years. This kind of change can happen in a couple of generations.  

Newly discovered genetic code

Newly discovered genetic code controls bacterial survival during infections


http://phys.org/news/2016-11-newly-genetic-code-bacterial-survival.html

Excerpt: "
MIT researchers have now discovered another layer of control that helps cells to rapidly divert resources in emergency situations. Many bacteria, including strains that cause tuberculosis, use this strategy to enter a dormancy-like state that allows them to survive in hostile environments when deprived of oxygen or nutrients.


"What this study does is reveal a system that the bacteria use to shut themselves down and enter one of these persistent states when they get stressed," says Peter Dedon, the Underwood-Prescott Professor of Biological Engineering at MIT.

Rapid response
Dedon and colleagues have previously shown that stresses such as radiation or toxic chemicals provoke yeast cells to turn on a system that makes chemical modifications to transfer RNA (tRNA), which diverts the cells' protein-building machinery away from routine activities to emergency action.
In the new study, the researchers delved into how this switch influences the interactions between tRNA and messenger RNA (mRNA), which carries instructions for protein building from the nucleus to cell structures called ribosomes. The  in mRNA is "read" on the ribosome as a series of three-letter sequences known as codons, each of which calls for a specific amino acid (the building blocks of proteins).
Those amino acids are delivered to the ribosome by tRNA. Like other types of RNA, tRNA consists of a sequence of four main ribonucleosides—A, G, C, and U. (U in RNA substitutes for the T found in DNA.) Each tRNA molecule has an anticodon that matches an mRNA codon, ensuring that the correct amino acid is inserted into the protein sequence. However, many amino acids can be encoded by more than one codon. For example, the amino acid threonine can be encoded by ACU, ACC, ACA, or ACG. In total, the genetic code has 61 codons that correspond to only 20 .
Once a tRNA molecule is manufactured, it is altered with dozens of different chemical modifications. These modifications are believed to influence how tightly the tRNA anticodon binds to the mRNA codon at the ribosome.
In this study, Dedon and colleagues found that certain tRNA modifications went up dramatically when the bacteria were deprived of oxygen and stopped growing.
One of these modifications was found on the ACG threonine anticodon, so the researchers analyzed the entire genome of Mycobacterium bovis in search of genes that contain high percentages of that ACG codon compared to the other threonine codons. They found that genes with high levels of ACG included a family known as the DosR regulon, which consists of 48 genes that are needed for a cells to stop growing and survive in a dormancy-like state.
When oxygen is lacking, these bacterial cells begin churning out large quantities of the DosR regulon proteins, while production of proteins from genes containing one of the other codons for threonine drops. The DosR regulon proteins guide the cell into a dormancy-like state by shutting down cell metabolism and halting cell division.
"The authors present an impressive example of the new, emerging deep biology of transfer RNAs, which translate the genetic code in all living organisms to create proteins," says Paul Schimmel, a professor of cell and molecular biology at the Scripps Research Institute, who was not involved in the research. "This long-known function was viewed in a simple, straightforward way for decades. They present a powerful, comprehensive analysis to show there are layers and layers, ever deeper, to this function of translation."
"Alternative genetic code"
The researchers also showed that when they swapped different threonine codons into the genomic locations where ACG is usually found, the bacterial cells failed to enter a dormant state when oxygen levels were diminished. Because making this tRNA modification switch is critical to ' ability to respond to stress, the enzymes responsible for this switch could make good targets for new antibiotics, Dedon says.
Dedon suspects that other families of genes, such as those required to respond to starvation or to develop drug resistance, may be regulated in a similar way by other tRNA modifications.
"It is really an alternative genetic code, in which any gene family that is required to change a cell phenotype is enriched with specific codons" that correspond to specific modified tRNAs, he says.
The researchers have also seen this phenomenon in other species, including the parasite that causes malaria, and they are now studying it in humans."

My comment: Cause and effect, signal and response, an altered factor and a reaction. This points out that organisms don't adapt to changing environment by random genetic changes but Intelligently designed and created mechanisms. "They present a powerful, comprehensive analysis to show there are layers and layers, ever deeper, to this function of translation." The evolutionary theory is a big lie.

2016/11/09

EPIGENETICS, DARWIN'S FINCHES AND DEFINITIONS OF SPECIATION


EPIGENETICS, DARWIN'S FINCHES AND DEFINITIONS OF SPECIATION


The genome within different species of Darwin's finches differs less from each other than does the genome between different breeds of dog. CNV (Copy Number Variation) is a comparison of the habit of too flimsy, but tell essentially genomic differences. Evolutionists use CNV-differences when there is a pressing need to find the differences between gene sequences. CNV does not really tell us more than that between the compared genetic sequences have some kind, even a small difference. So let's do a little comparison between genome similarities.

http://mappingignorance.org/2014/12/01/epigenetics-takes-us-back-galapagos/


At the Figure 3 you can have a look at the  CNV differences (blue color) and epigenetic differences (red color) within different finch species. The readings obtained from the species compared to reference species Geospiza fortis. We note that, for example Camarhyncus parvulus genome differs only by 52 CNV:s to the reference species. And yet, "science" has determined it as a separate species.

There are much larger differences between different dog breeds , such as the enclosed survey shows:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4053742/

Notably, the total number of CNVs identified in Boxers was lower than in any other breed, with an average of 64.5 loci different from the reference per sample, largely due to the reference being a Boxer. Of the remaining breeds, the average number of CNVs per sample varied from 116.5 (Swedish Elkhound) to 160 (English Springer Spaniel). On average, a sample differs from the reference at 130.9 CNV loci, of which 2.8 are specific to that breed. Fewer than 6% of CNVs found in any one breed are specific to that breed. These patterns are broadly consistent in the wolf samples, which exhibit a slightly lower than average number of CNVs per sample. On average, 2 dogs from the same breed differ at 83.1 CNV loci whereas 2 dogs from different breeds differ at 103 CNV loci.

That is, for example, the boxer's (reference breed) and english springer genome has 160 CNV:s difference. The human genome difference between human populations is also much larger, such as the enclosed survey shows; 1447 CNVr eligible. Yet the similarity between the human genome in various populations is 99.6% of the class.

http://www.nature.com/nature/journal/v444/n7118/full/nature05329.html

Evolutionists are absolutely lost with these definitions of speciation. They make the kind of configuration as a rule, on the basis of organism individuals to mate or not. And the geographical isolation is the second pseudoscientific criterion. This low threshold of the definition of the species has its reasons; by this way they keep the fossil discoveries separate of modern species and argue that evolution takes place.

Actual scientific research would make an appropriate question:

Why individuals in practice the same species do not seek to mate with each other, although certainly are capable of producing fertile offspring? Nature is not, after all, full of biological species, it is full of species breeds.