A soldier or a worker ant? Epigenetic programming makes the difference, not random mutations.

When an ant colony is under attack, the queen transmits epigenetic markers on developing ants so that ants will become soldiers


Excerpt: "In our recent Stuff to Blow Your Mind episode on "The Science of Ant-Man," we discussed the physics of shrinking, the anatomical strength of a half-inch tall human and the possibility of a quantum realm. But we couldn't quite figure out how Ant-Man communicated with his arthropod friends, especially given the complex way ants use pheromones and other nonverbal cues to "talk." But a team of researchers in the January issue of Science may have found an answer.

By using epigenetic manipulation, Daniel Simola, Riley Graham, Shelly Berger and more were able to change the behaviors of ants, so they performed different roles than their nature normally allows. In the carpenter ant Camponotus floridanus there are distinct castes called "minors" and "majors" that perform different tasks for their colony.

The major ants are larger than minors and act as the colony's soldiers. They rarely search for food. The minor ants primarily forage. Minors also scout, leaving the nest first to discover a food source before bringing in labor reinforcements to haul the goods back to base. While both majors and minors can scout, by the time they're 14 days old the minors exhibit this behavior more than the majors.

Observations led the research team to conclude that these roles were molecularly innate to the ants. This division of labor allows colonies to adapt to crises such as famine or predators. 

So how did these researchers get the ants to change their innate behavior? It would be easy to just say "epigenetics," but let's do a brief primer on what this actually means. Essentially, epigenetics is when environmental factors affect DNA, changing how genes are expressed. Imagine identical twins, but one develops cancer and the other does not. What environmental, nutritional and social exposures triggered this development? Epigenetics aims to find out.

The research team noticed that the carpenter ants' propensity for foraging seemed to be affected by their exposure to histone proteins, what Berger refers to as "the packaging material" for DNA. To get information from each gene, DNA has to loosen like a spool of thread in a process called "acetylation." So the team began their experiment by feeding the ants a compound that increased their acetylation of the histone H3K27ac. Sure enough, after consuming the compound minor ants foraged even more than normal.

Next, the team developed a technique to inject the chemicals directly into the ants' brains. Changing the dose to a more potent compound called trichostatin A, they noticed the injections increased the major ants' foraging behavior as well. Soldiers became farmers. Even 30 to 50 days after a single injection, majors displayed lasting effects and continued to forage. It should be noted however that these treatments were only effective when applied to very young major ants. This implies that as they age, ants conform to their roles rigidly.

Given these results, we could speculate that Ant-Man controls his ants in a similar, but more complex epigenetic manner. Is Ant-Man constantly injecting baby ant brains with weird chemicals so they'll let a tiny person ride on their backs? Maybe. But another possibility Berger pitched is that he emits an odor like the ant queen, which regulates the brain physiology of each ant, essentially telling them, "Everything is fine." Berger refers to the queen's odor emission as an example of a "pure epigenetic signal."

Of course, the ramifications of this study are much bigger than solving the mysteries of a fictional superhero. The researchers speculate that their study's findings may be applicable to other eusocial insects like honeybees and possibly even to some mammals. But what about humans? Can chemical exposure epigenetically change our behaviors?
According to Berger, the same histone deacetylases (HDACs) used in this study are already widely used in humans for both cancer and psychiatric treatments. So there could be many applications for this research, especially in the early windows of human brain development. In the 1990s, a National Institutes of Health (NIH) project scanned hundreds of human brains and found that they're still developing until we're 25 years old. Berger argues that the molecular nature of this development comes from epigenetic changes within the brain. So maybe ants aren't the only ones with malleable societal roles regulated by chemicals?"

My comment: Soldier and worker ants have the same DNA. The major differences between their behavior and outcome are determined by epigenetic factors and mechanisms. These changes are not random occurrences but accurately programmed procedures. 
When an ant colony is under attack, the queen transmits epigenetic markers on developing ants so that ants will become soldiers. If their living environment is food-poor and the colony is starving, the queen puts epigenetic tags on developing ants to create more ant workers.This is done either by diet type or using chemical odors, pheromones, that triggers signal routing mechanisms in the brain. Further, gene expression patterns are changed by using histone epigenetic markers. Just one histone tag, acetylation for example, can have a major impact on how chromatin is folded and DNA transcribed. This kind of complex programming system points to Intelligent Design and Creation and refutes hollow claims of random mutations, selection and evolution.

Also human monozygotic twins have identical DNA but they might have different colors of skin, eyes and hair. These traits are also regulated by epigenetic factors and mechanisms. Don't get misled.

Another article about epigenetic control of ant phenotypes can be found from here:


Your brain is like 100 billion mini-computers all working together

Your brain is like 100 billion mini-computers all working together


Excerpt: "Each of our brain cells could work like a mini-computer, according to the first recording of electrical activity in human cells at a super-fine level of detail.

The study has revealed a key structural difference between human and mouse neurons that could help explain our superior powers of intelligence.

Brain cells, or neurons, communicate by firing electrical impulses down their length, which researchers can detect and measure by putting microscopic electrodes inside them. Most such studies have been done on rodent neurons kept alive in a dish, where the cells can live for several hours. But Mark Harnett at the Massachusetts Institute of Technology in Cambridge wanted to see how human neurons compared with those of mice, so he used live tissue obtained from surgeons who were removing small chunks of brain from people with epilepsy.

While people have recorded signals from inside human neurons before, it has always been inside the main “trunk” of their tree-like structure. Harnett’s team used thinner electrodes to record activity inside the fine branches, known as dendrites, at the end of the trunk.
Each neuron may have about 50 dendrites, and each dendrite has hundreds of synapses, or connection points with other neurons. It’s signals running across these synapses and into the dendrite that make it more or less likely that the dendrite itself will fire an electrical signal along its length.

Compared with mice, the dendrites of human neurons turn out to have fewer ion channels, molecules studded in the cell’s outer membrane that let electricity flow along the dendrite.

While this might sound bad, it could give greater computing powers to each brain cell. Imagine a mouse neuron: if a signal starts down one dendrite, there are so many ion channels to conduct electricity that the signal will probably continue into the main trunk of the neuron. In a human neuron, by contrast, it’s less certain that the signal will conduct into the main trunk: whether it does will probably depend on activity in other dendrites, says Harnett.

This lets the thousands of synapses on each neuron’s dendrites collectively determine the final “decision” on whether the main branch should fire. “They’re looking for specific patterns of input to come together to produce [a signal],” says Harnett."

My comment: Human brain cells are unique as also this study confirms. 100 billion mini-computers working in a single human brain means more computing capacity than in all computing devices in the world together. There is no random force being able to create this kind of design. Incredible human brain points to Intelligent Design and Creation!


Food ark is needed due to rapid genetic degradation

About 93% of seed varieties sold in the US in 1903 were extinct by 1983



  • Food varieties extinction is happening all over the world—and it’s happening fast. In the United States an estimated 90 percent of our historic fruit and vegetable varieties have vanished. 
  • Of the 7,000 apple varieties that were grown in the 1800s, fewer than a hundred remain. 
  • In the Philippines thousands of varieties of rice once thrived; now only up to a hundred are grown there. 
  • In China 90 percent of the wheat varieties cultivated just a century ago have disappeared. 
  • Experts estimate that we have lost more than half of the world’s food varieties over the past century. As for the 8,000 known livestock breeds, 1,600 are endangered or already extinct.
  • In 1983, we found that about 93% of seed varieties sold in the US in 1903 were extinct by 1983. For example, commercial seed catalogues in 1903 offered 497 varieties of lettuce. In 1983, on 36 of those varieties were found in our national seed collection.
  • Seed banks are critical to protecting our fast-disappearing crop diversity, because they preserve varieties that might otherwise disappear forever.
My comment: Both artificial selection and genetic editing 
of plant breeds have resulted in rapid genetic degradation. This is why scientists have built a Food Ark where to store plant seeds that have not experienced so heavy loss of genetic diversity. When do scientists understand that every time an organism experiences variation, artificial or ecological, biological information is at some rate lost? There is no mechanism for evolution.

Enormous and rapid loss of genetic diversity after intense breeding

Intense breeding of crops and livestock has resulted in enormous loss of genetic diversity


Excerpt: "In his classic 1973 overview of U.S. agribusiness and its effects on the food we eat, Hard Tomatoes, Hard Times, Jim Hightower discusses how the search for market efficiencies had changed the tomatoes Americans could buy in their local supermarkets. Tomatoes posed a number of problems for modern industrial agriculture; in particular, they tended to get bruised or smashed when harvested by machine and transported long distances. To facilitate mechanical harvest and shipping, varieties were developed that were harder and tougher — often at the expense of other qualities, such as taste. This same process has occurred with many crops. For instance, I can buy huge, bright red strawberries year-round in the U.S. these days, as long as I don’t mind that they have only a hint of the rich taste of the strawberries my grandma used to grow.

As a result of concentration in agribusiness (including grocery chains) and selection of varieties that can withstand the mechanical harvesting and long-distance shipping required by the industrial food system, we see fewer and fewer varieties of crops on the shelf. Despite the efforts of heritage seed banks and heirloom variety enthusiasts, many have disappeared altogether; others are dangerously close to doing so. It’s an enormous loss of genetic diversity, of varieties that were developed over many years based on flavor, resistance to pests, ability to withstand drought, frosts, or other environmental stresses, and so on.

Dolores R. let us know that National Geographic posted an image based on a 1983 study by the Rural Advancement Foundation International that illustrates the loss of this genetic diversity. RAFI looked at a typical commercial seed catalog from 1903 — that is, a catalog of seeds targeting farmers producing for the market. They found a large number of varieties available. But then they looked at the seed collection at the National Seed Storage Laboratory (now the National Center for Genetic Resources Preservation). This government entity is in charge of collecting and storing seeds to preserve genetic diversity among crops and livestock. The bottom half of this image shows how many of the varieties in the 1903 catalog were in the lab’s collection as of 1983:
Of course, the NCGRP isn’t the only organization storing seeds; many private groups, such as Seed Savers Exchange, preserve heirloom varieties. And many varieties have been introduced, such as the Round-Up Ready crops developed by Monsanto to be compatible with Round-Up weed killer. The NCGRP has also added greatly to its collection over time. Nonetheless, many varieties have simply disappeared, reducing the genetic diversity available in our current agricultural system and increasing the risks should a virulent pest or disease attack the dominant varieties of crops and livestock. "

My comment: The more variation or adaptation, the more genetic degradation. This same phenomenon can be observed in nature and in artificially selected breeds of plants or animals. There is no mechanism for evolution.


Darwin's Finches - Icons of Evolution turned into the best evidence for Intelligent Design and Creation

Random mutations and selection have nothing to do with rapid adaptation of Darwin's Finches


Excerpt: "Researchers have uncovered epigenetic variation between urban and rural populations of Darwin's finches that could underlie their adaptation to a new environment.

The Galápagos Islands only recently underwent urbanization, leading the researchers to wonder how organisms there are coping with speedy environmental change. By examining populations of two species of Darwin's finches, researchers from Washington State University and the University of Utah uncovered morphological differences between urban and rural populations of Geospiza fortis as well as epigenetic differences between urban and rural populations of G. fortis and G. fuliginosa. However, as they reported in BMC Evolutionary Biology last night, they found little genetic variation.

"In the finches that we studied, epigenetic alterations between the populations were dramatic, but minimal genetic changes where observed. We believe that the epigenetic differences may be a heritable component that might explain the rapid adaptation of Darwin's finches to an urban environment," senior author Michael Skinner, a biology professor at Washington State, said in a statement.

The researchers captured nearly 1,100 ground finches belonging to either G. fortis or G. fuliginosa from two sites some 10 kilometers apart that differ in degree of urbanization. They measured the birds' beak size, tarsus length, body mass, and more, and also collected blood and sperm for genetic and epigenetic analysis from a subset.

Through their morphological comparisons, Skinner and his colleagues found the medium ground finch, G. fortis,to be larger than the small ground finch, G. fuliginosa. But they also reported that the urban population of G. fortis was larger than the rural population on nearly all measures. The researchers noted that food is more abundant in urban areas.

However, they observed no size differences between G. fuliginosa from urban and rural regions. They suggested that this lack of size difference could be due to a lower starting degree of variation among G. fuliginosa, as compared to G. fortis. Also, they noted that urbanization could have had a greater selective effect on G. fortis than on G. fuliginosa.

Additionally, the researchers compared copy-number variation among the finches to find that while there was within-population variation in copy number in the two species, there were no fixed differences between the urban and rural populations of either species.

But when the researchers compared DNA methylation patterns — generated using methylated DNA immunoprecipitation (MeDIP) sequencing — they did find differences between rural and urban populations in both species.

The genes associated with the differentially methylated regions the researchers identified were typically involved in metabolism, cell signaling, and transcription, though they also differed by species. In particular, they noted that some differentially methylated regions were associated with genes in BMP/TGF-beta pathway. BMP4 expression, they added, has previously been linked to beak shape in Geospiza.

This, Skinner and his colleagues said, suggests that epigenetic changes could regulate the expression of genes involved in morphology. They added that their results are consistent with a role for epigenetic variation in rapid adaptation to environmental change.
However, they also cautioned that additional studies are needed to tease out the effects of the differentially methylation regions on phenotypes."

My comment: Different food sources are the main drivers of epigenetic modifications within Darwin's Finches. For example plants seeds contain nutritional compounds and microRNAs that modify the epigenome of Finches and in this way the offspring will be prepared for being able to eat hard seeds. These remarkable changes are based on intelligent mechanisms, not any random mutations or selection. These modifications are based on alternative biological programs and they happen very rapidly. These epigenetic alterations are also the main reason for speciation. Changing methylation profiles typically result in subtle genetic errors and this is why genetic degradation is a biological fact. The more adaptation and variation, the more genetic degradation will occur. There is no mechanism for evolution. Don't be deceived.


Epigenetic modifications often result in DNA errors

Methylation-Induced hypermutation changes definition of Epigenetics


Excerpt from abstract: "Methylation of DNA at the C5 position of cytosine occurs in diverse organisms. This modification can increase the rate of C->T transitions at the methylated position. In E. coli and related enteric bacteria, the inner C residues of the sequence CCWGG (W=A or T) are methylated by the Dcm enzyme. These sites are hotspots of mutation during rapid growth in the laboratory, but not in non dividing cells, in which repair by the Vsr protein is effective. It has been suggested that hypermutation at these sites is a laboratory artifact and does not occur in nature. Many other methyltransferases, with a variety of specificities, can be found in bacteria, usually associated with restriction enzymes and confined to a subset of the population. Their methylation targets are also possible sites of hypermutation. Here I show, using whole genome sequence data for thousands of isolates, that there is indeed considerable hypermutation at Dcm sites in natural populations: their transition rate is approximately eight times the average. I also demonstrate hypermutability of targets of restriction associated methyltransferases in several distantly related bacteria, ranging from a factor of 12 increase in transition rate to a factor of 58. In addition, I demonstrate how patterns of hypermutability inferred from massive sequence data can be used to determine previously unknown methylation patterns and methyltransferase specificities.

IMPORTANCE: A common type of DNA modification, addition of a methyl group to cytosine (C) at carbon atom C5, can greatly increase the rate of mutation of the C to a T. In mammals, methylation of CG sequences increases the rate of CG->TG mutations. It is unknown whether cytosine C5 methylation increases mutation rate in bacteria under natural conditions. I show that sites methylated by the Dcm enzyme exhibit an eight fold increase in mutation rate in natural bacterial populations. I also show that modifications at other sites in various bacteria also increase the mutation rate, in some cases by a factor of forty or more."

My comment: Epigenetics is understood as modifiable chemical layers on top of DNA that doesn't change DNA sequence. But as we can see, this is not the case. Epigenetic modifications, such as changing DNA methylation patterns, typically lead to errors (mutations) in underlying DNA sequences.  The most common genetic alteration occurring as a result from changing methylation patterns is CG --> TG mutation. This often results also in CG --> TA alterations. These are genetic errors and scientists try to repair these alterations in human genome, as we can read from here:


Excerpt: "Mutations that change C-G base pairs to T-A pairs happen 100 to 500 times every day in human cells. Most of those mutations are probably benign, but some may alter a protein’s structure and function, or interfere with gene activity, leading to disease. About half of the 32,000 mutations associated with human genetic diseases are this type of C-G to T-A change, says Liu, a Howard Hughes Medical Institute investigator at Harvard University. Until now, there was little anyone could do about it, he says."

Change occurring in organisms is due to epigenetic modifications and it often leads to genetic errors. This is why genetic degradation, genetic entropy is a biological fact. Evolution is not happening because there is no mechanism causing increase in biological information.


Evolution is not happening - Organisms need genetic rescue made by humans

A model example of why genetic degradation happens and how organisms can be rescued (temporarily)


Excerpt: "Genetic rescue of Norwegian Lundehund

Several wild animal populations have received individuals from closely related populations to increase the probability of survival of threatened populations. Genetic rescue contributes to the conservation of endangered populations both by increasing the number of individuals and the genetic variation for future selection.

An article published in the Finnish Kennel Club’s magazine “Koiramme” (9/2016) describes the history, characteristics and challenges of the highly endangered lundehund population.

Several severe bottlenecks in the history of the Lundehund have resulted in a severe loss of genetic variability in the current lundehund population. Low fertility and high frequency predisposition to intestinal disorder IL (intestinal lymphangiectasia) imply inbreeding depression. The Norwegian Lundehund Club has initiated a cross-breeding project where three foreign breeds are introduced in the population.
The article describes the first experiences of the cross-breeding project and highlights the issues relevant for populations in similar situation:
  • When is the right time to pursue a genetic rescue via introduction of foreign breeds?
  • How should phenotypic characters with possible negative effects on animal welfare be evaluated, and how should they affect breeding decisions?
  1. Cross-breeding gives a second chance for populations which are likely to become extinct; albeit with a cost of changing the genetic and phenotypic expression of the breed.
  2. Introduction of foreign breed(s) in reasonable time (relative to the amount of genetic variation and accumulation of genetic defects) allows us to reverse the detrimental development and rescue the population with fewer individuals introduced than if we wait until the genetic variation is fully depleted.
  3. Careful planning of cross-breeding followed by phenotypic selection enables the maintenance of the distinct characteristics of the Lundehund.
  4. Dog breeding programs should put more emphasis on the interaction between genetics, health and welfare both on the individual and population level."
My comment: Just in 200 years of intensive breeding of dogs has resulted in situation where several dog breeds need genetic rescue. Artificial selection of desired characteristics has led to rapid loss of biological information within dog breeds. At cellular level this means epigenetic amplification/silencing of epigenetic information patterns and it typically leads to strong rate of DNA mutations. This same phenomenon occurs in nature, but only slower.

There are synonyms for the term 'genetic degradation'. These are often used by evolutionary biologists.
  • Population bottleneck
  • Inbreeding depression
  • Genetic rescue
  • Genetic diseases
  • Low genetic diversity
Dog breeds suffering from low genetic diversity can only be rescued by cross-breeding. For this to be successful, dog breeds having healthier genome have to be used. But at the level of the whole Canidae kind, the genome will at any case get degraded. That's why evolution is not happening.


Enormous protein diversity results from alternative splicing - Not from random mutations

Alternative splicing is regulated by epigenetic factors - the most significant mechanism for organismal changes


Excerpt: "Alternative splicing allows more than one protein to be made from one gene.
Enormous protein diversity results from alternative splicing
. Mammals are much more complex than nematodes and fruit flies, yet the genomes of these organisms differ by less than 2 fold (about 25,000, 20,000 and 14,000 genes, respectively). The extent to which alternative splicing contributes to the complexity of eukaryotic organisms is a question that remains unanswered, but a strong correlation exists between complexity and intron number and alternative splicing. One fact that remains clear though, is that alternative splicing is important for generating protein diversity."

How many different proteins is it possible to produce by using only one DNA strand (a gene)?

An example: If all combinations were used, the cell is able to produce 38,016 different protein isoforms by editing and manipulating pre-mRNAs made from only one Dscam gene template.

Humans have fewer protein-coding genes (~19,600) than an earthworm (~20,470). This means that the genes we thought made us who we are, don't.

According to latest research, there are only ~19,000 DNA strands used for protein production in a human genome. But the number of different proteins in a human body is up to several millions.

What factors and mechanisms regulate this complex splicing procedure? 

1. DNA methylation profiles
2. Histone markers
3. Non coding RNA molecules
4. Transcription factors (proteins that bind to methylated regions).

These are epigenetic factors. Modifications in epigenetic information layers will never result in any kind of evolution, because it's only about switching between alternative biological programs.

Any change in organisms is due to epigenetic regulation of pre-existing biological information. DNA mutations are associated with genetic diseases and corruption of biological information. That's why there's no mechanism for evolution.