The entire concept of “gene” has to be reconsidered

New discoveries change our understanding of genes and their purposes



"But, now multiple vast networks of regulation have been found that include more than forty different types of tags placed on both DNA and the protective histone proteins that allow access to DNA strands. All of these tags alter genetic function and are based on the actions of protein enzymes."

Another type of regulation involves the shape of the DNA both in small loops and large placement inside of highly structured nucleus scaffolds with dramatic influence on genetic functions.

The very complex editing of messenger RNA can make up to 500 different proteins from a single strand of DNA—what used to be called a gene, but now is hard to define. Genes can overlap and triggers of regulation can happen in the gene or in the regulatory strand.

What is equally amazing is that mental events—thought—almost instantly triggers large networks of many genes at the same time. How does this happen?

Now entirely new sets of factors have appeared that are based on physical properties of the coding of RNA and the liquid phase transitions that separate active and inactive sections of the chromosomes. The first unusual new physical properties occur when there are repeated patterns of code. The regions of regulatory code where there are large amounts of repeats have been correlated with multiple different degenerative diseases such as Huntington’s and ALS. The second is the way that active and inactive sections of the DNA are in different regions of the nucleus.

It is not known how many overlapping layers of regulation there are:

Some include:

  • Histones protect DNA and must be opened to be used. There are now forty different tags that determine whether histones can be opened or not to utilize DNA.
  • There are many newly discovered tags on DNA itself that alter function.
  • Thousands of proteins called promoters and enhancers start and stop DNA function.
  • Promoters work in many different places for each gene and in different places for each type of human cell. Also, for even more complexity, multiple promoters combine into larger machines, some touching the DNA and some only combining with the other promoters. Multiple structures exist for each gene in different places.
  • There are multiple different places where transcription starts for each “gene”, again undermining the notion of the simple “gene.”
  • Thousands of large and small RNAs interact in multiple ways to regulate what pieces of DNA are used.
  • Many different mechanisms are used to repair DNA errors without obvious direction.
  • Eight million factors affect the RNA particles that are made from at least 20% of all DNA (maybe up to 50%). Messenger RNA somehow determines multiple different edits from the same pieces of DNA.
  • Pieces of DNA and RNA are taken from multiple places, strands are cut out and others sewn together without clear direction.
  • In some DNA there are two superimposed codes at once in one section of DNA. These are related to new messenger RNA folding, and multi-use codons called “duons.” The first purpose is to transcribe DNA code to RNA code to make proteins. The second purpose is to bind regulatory factors, as the regulatory regions do to trigger other genes.
  • Transcription factors bind inside at least 13% of “genes” themselves, not just the regulatory regions nearby. This finding was truly shocking since the DNA in the gene, then, must code for two meanings at once for two entirely different purposes.
  • RNA splicing, can make up to 500 different proteins from the same pieces of DNA. The RNA cuts out sections and sews others together. Recently, it has been demonstrated that the pieces that are sewn together by the messenger RNA may come from multiple different areas that used to be called individual genes.
  • Four million different switches are active, often operating in multiple places at once; 18,000 places where active RNA is made; and 8 million different particles interacting to regulate these RNAs.
  • The entire concept of “gene” has to be reconsidered because messenger RNA takes pieces from different regions to make one RNA edit for a protein.
  • The 3D shape of the DNA chromosome is correlated with the activity of the genes inside.
    • The links exist at multiple levels.
    • Loops of chromatin make space for enhancers to land. A larger relationship exists for specific places in the nucleus to impact on particular active DNA sites.
    • Special protein structures alter polymerase activity.
    • Chromosomes with fewer active genes are placed at the edge of the nucleus while the active ones are near the center.
    • Less active sections are placed near the nuclear lamina, which is close to membrane.
    • The location can suppress the genetic machinery.
    • If the chromatin is opened but not used, the entire section is moved to a different location.
    • The exact location of the gene in space in the nucleus influences its activity.
    • To fit 2 yards of DNA into a tiny nucleus is a monumental engineering feat. DNA is highly compacted yet has to be instantly available to rapidly make proteins in neurons with a momentary change of thought."
My comment: Messenger RNA takes pieces of genes from different locations to make one RNA edit for a required protein. Where is the regulation for this? Certainly not in gene sequences. These epigenetic mechanisms, 3D genome, overlapping genes and codon duons tell us about an extremely complex language that points to perfect design. There is no such a thing as mutation driven evolution. Gene centric population genetics and the theory of evolution have seriously failed. Again.

Life is not driven by gene sequences. Genes are driven by lifestyle. Don't get lost.


Why a mother's baby might look like her EX? Embryonic development is regulated by RNA molecules

Epigenetic information layers are established by macromolecules - Embryo-uterine crosstalk guided by RNA molecules from extracellular vesicles


Excerpts: "Once considered a simple medium for sperm and embryo transport, the functional spectrum of uterine fluid is now expanding. Novel molecular players, such as extracellular vesicles and mobile RNAs, have been detected in the uterine fluid of livestock, rodents, and humans. These novel molecules, together with previously known ions and proteins, ensure uterine fluid homeostasis and facilitate embryo–maternal interactions. Here, we propose that these molecules may also carry information that mirrors maternal environmental exposure and possibly relay such information to the embryo via uterine fluid, generating long-term epigenetic effects on the offspring via embryonic and placental programming.

...Extracellular vesicles (EVs) that carry a variety of macromolecules (e.g., proteins or RNAs) have been detected in the uterine fluid of mammalian species, including humans, and have the potential to mediate embryo–uterine interactions.

Functional noncoding (nc)RNAs encapsulated within and floating outside EVs can be transferred into floating blastocysts, suggesting a putative function in the genetic and/or epigenetic regulation of embryonic features, which might modulate embryonic and placental development.

Maternal exposures or eating habits have been reported to change the intrauterine (uterine fluid) environment, which might influence embryo quality and epigenetic regulation of gene expression. This mechanism might help explain the observed epigenetic inheritance of maternally acquired traits, as in the case of metabolic disorders.

Before and during embryo implantation, uterine fluid is the liquid medium that connects the floating embryo(s) and the uterus, and has the potential to transfer vital information between the embryo and the uterus. Indeed, recent studies are shedding light on new forms of embryo–maternal communication via the delivery and/or exchange of extracellular vesicles (EVs) and mobile RNAs, newly identified information carriers that exist in the uterine fluid.

Among the various cargos of EVs, ncRNAs are of particular interest given their well-known functions in genetic and epigenetic regulation. Studies of circulating EVs (exosomes) have revealed that they contain different types of ncRNAs, including miRNAs, tRNA-derived small RNAs (tsRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs).

...Over the past several years, growing evidence has robustly demonstrated that the epigenetic information carried in parental gametes can transfer acquired information to offspring.

The impact on the ICM might affect the trajectory of fetal development and may cause disease predispositions in the offspring via a butterfly effect, in which the initial small bias (for example, in essential gene expression) is amplified throughout development and causes long-lasting effects in the offspring. This might occur via transcriptional changes or be regulated via epigenetic changes, such as DNA methylation or various histone modifications, as shown in recent mouse studies."

My comment: After fertilization nearly all epigenetic markers are wiped out of the embryo which means there are only stem cells left that lack all information required for cellular differentiation and specialization. This means that individual traits have also been erased. They are established by maternal macromolecules carried by maternal EVs. From father's side, there are thousands of different RNA molecules in the sperm that stay inside the mother and affect embryonic development. This is how inheritance of traits functions.

The following might be a shocking news:

Excerpt: "This has very important ramifications for women. Every male you absorb spermatazoa from becomes a living part of you for life. The women autopsied in this study were elderly. Some had been carrying the living male DNA inside them for well over 50 years.

Sperm is alive. It is living cells. When it is injected into you it swims and swims until it crashes headlong into a wall, and then it attaches and burrows into your flesh. If it’s in your mouth it swims and climbs into your nasal passages, inner ear, and behind your eyes. Then it digs in. It enters your blood stream and collects in your brain and spine.

Like something out of a scifi movie, it becomes a part of you and you can’t get rid of it.

We are only now beginning to understand the full power and ramifications of sexual intercourse."

My comment: This is why a mother's baby might look like her ex. And this is exactly what the Bible tells about this:

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?"


Neo-Darwinism has failed as an evolutionary theory

One in five 'healthy' adults may carry disease-related genetic mutations


Excerpt: "The first genome screening study looked at 100 healthy adults who initially reported their family history to their own primary care physician. Then half were randomly assigned to undergo an additional full genomic workup, which cost about $5000 each and examined some 5 million subtle DNA sequence changes, known as single-nucleotide variants, across 4600 genes—such genome screening goes far beyond that currently recommended by the American College of Medical Genetics and Genomics (ACMG), which suggests informing people of results for just 59 genes known or strongly expected to cause disease.

Of the 50 participants whose genomes were sequenced, 11 had alterations in at least one letter of DNA suspected to cause—usually rare—diseases, researchers report today in The Annals of Internal Medicine. But only two exhibited clear symptoms. One was a patient with extreme sensitivity to the sun. Their DNA revealed a skin condition called variegate porphyria. “Now that patient knows they will be much less likely to get bad sunburns or rashes if they avoid the sun and certain medications,” says Jason Vassy, a primary care clinician-investigator at Veteran Affairs Boston Healthcare System and lead author of the study.

The team also found that every sequenced patient carried at least one recessive mutation linked to a disease—a single copy of a mutant gene that could cause an illness if two copies are present. That knowledge can be used to make reproductive decisions—a partner may get tested to see if they have a matching mutation—and prompt family members to test themselves for carrier status. And in what Vassy calls a “slightly more controversial result,” the team examined participants’ chances of developing eight polygenic diseases, conditions that are rarely attributed to a single genetic mutation. Here, they compiled the collective effects of multiple genes—up to 70 for type II diabetes and 60 for coronary heart disease—to predict a patient’s relative risk of developing the disease."

My comment: This is the end of the pseudoscientific theory of evolution. Genetic mutations are not resulting in any kind of evolution or adaptation. Genetic mutations lead to diseases and disorders. So called natural selection is not able to weed out genetic errors.

People need to choose their partners and screen for their genomes for avoiding genetic diseases to break out within their children. There are 203,885 disease-causing genomic mutations in the human genome and the number is increasing very rapidly. Scientists urgently need help in making CRISPR gene editing more accurate and reliable.

The theory of evolution is the major heresy. Stop maintaining pseudoscience.


Sulforaphane in broccoli sprouts found to improve glucose levels in diabetics

Eating raw veggies best for balancing your genome


Excerpt: "A team of researchers from Sweden, the U.S. and Switzerland has found that treating rat liver cells with a compound called sulforaphane, which is found in cruciferous vegetables, reduced production of glucose. In their paper published in Science Translational Medicine, the group outlines the methods they used to isolate the compound and what they found when testing it with liver cells and in human patients.

Type 2 diabetes has been in the news a lot in the past several years due to its ties to the obesity epidemic in several countries, particularly the U.S. Prior research has shown that it is a condition in which the body mishandles glucose—cells fail to use insulin properly, leading to higher glucose levels, which can cause a wide variety of health problems. Current treatment includes modifying the diet and taking drugs such as metformin. But because the drugs used to treat diabetes can cause other problems, such as liver damage, researchers continue to look for alternatives. In this new effort, the researchers sought to find a compound that could alleviate symptoms in a more natural way. They created a genetic signature for the disease based on 50 genes that have previously been linked to the disorder and fed the results into a database, which used the genetic signature to look for compounds specifically related to gene expression in liver cells—sulforaphane showed the strongest known effects.

The researchers then cultured liver cells from rats with type 2 diabetes and applied sulforaphane to see what would happen—doing so caused the cells to produce less glucose. Optimistic about their results, the researchers next tested the compound on 97 obese human volunteers with type 2 diabetes over a 12-week period—this was possible because sulforaphane is a compound naturally occurring in cruciferous vegetables such as broccoli sprouts. The researchers report that those given the compound showed a significant reduction in glucose levels (while fasting).

The researchers acknowledge that their results are preliminary and that more testing of the compound will be needed to prove that the compound or simply eating the right vegetables might someday replace drugs used to treat type 2 diabetes. They note also that their technique for discovering the compound's usefulness in treating the disease could very well be applied to other diseases."

My comment: Broccoli contains sulphoraphane (
C6H11NOS2) which is broken down into methyl groups and other important compounds in the gut. DNA, histones and long non-coding RNA-molecules need these CH3 groups for their epigenetic markers. These are used for correct and successful gene expression and several regulatory functions in our cells. Lack of methyl and abnormal methylation profiles are linked to unsuccessful cellular differentiation and malignant cellular behavior. This means diseases. Diet changes our genomes and poor nutrition exposes our genome to genetic errors.

Life is not driven by gene sequences. Genes are driven by lifestyle. There is no such a thing as mutation driven evolution. Don't get misled.


No signs of the big bang particle

Physicists find no sign of the particle that made the universe explode

So, what caused it?


Excerpt: "A recent attempt to find a theoretical particle responsible for the Universe's early rapid expansion has come up empty handed, throwing a question mark over whether it really exists.

While there is still a low chance that the particle could be heavier than expected, or look a little different, physicists are preparing themselves for going back to the drawing board on one of the Universe's biggest mysteries.

Physicists from the Institute of Nuclear Physics at the Polish Academy of Sciences and the University of Zurich hunted for traces of a light form of a particle dubbed the inflaton in data collected during experiments using the Large Hadron Collider at CERN near Geneva in 2011 and 2012.

Much as its name suggests, inflatons are particles that, well, inflate space.

To be more precise, it helps to know why we're looking for them in the first place.

When we look up in the sky and measure the haze of microwave radiation, we find there's a background static that looks eerily the same no matter which way we look.

This background radiation, or cosmic microwave background, is the remnants of light that existed when the Universe was still just a few hundred thousand years old and not yet cool enough for particles to form.

As the Universe expanded, the radiation stretched into microwave lengths, which we can still see.

But given the scale of space, and the fact light from one side of the Universe hasn't yet had had time to make it to the other side, it seems odd that all of the light is spread out in such a similar way.

"When we look into the sky, the deep space fragments visible in one direction may be so distant from those visible in another direction that light has not yet had time to pass between them," researcher Marcin Chrzaszcz from the Polish Academy of Sciences explained.

"So nothing that has happened in one of these areas should affect the other. But wherever we look, the temperature of distant regions of the cosmos is almost identical! How could it have become so uniform?"

In 1981, a physicist by the name of Alan Guth suggested if the Universe grew rapidly for a short amount of time while still young and hot, the background radiation would still reflect that uniformity."


The Paternal Epigenome Makes Its Mark

Father's lifestyle affects his child's epigenome


Excerpt: "Researchers now understand that sperm contains a memory of a male’s life experiences, ranging from his nutritional status to his exposure to toxic chemicals, said Michael Skinner, PhD, a professor in the school of biological sciences at Washington State University. This information is captured in alterations to the epigenome, the suite ofmolecular on-off switches that regulate gene expression.

Epigenetic information can be embedded in sperm in the form of changes in DNA methylation—the addition of chemical “tags” that switch genes “on” or “off”—or histone modifications—chemical tags on histone proteins, which regulate how DNA is condensed. In addition to these epigenetic marks, researchers also have become increasingly interested in changes in noncoding RNAs, such as microRNAs (miRNAs), which are involved in gene silencing and can be present in sperm.

Last year, a review of human and animal research suggested that epigenetic changes may be the underlying mechanism by which paternal factors such as age, diet, weight, stress, and alcohol consumption contribute to a range of health outcomes in offspring including birth defects, behavioral problems, developmental disorders, obesity, diabetes, cardiovascular disease, and cancer.

A series of studies of historic cohorts from Överkalix in northern Sweden published last decade suggested that information about life experiences could be passed down several generations through the male line and could influence descendants’ health. In 2001 Lars Olov Bygren and coinvestigators from Umeå University in Sweden demonstrated that men born in 1905 who experienced food scarcity before puberty—when primordial sperm cells are developing into mature sperm—had paternal grandchildren with a lower relative risk of early death. The reverse was true for men who had plenty to eat: Their sons’ children were more likely to die young. 
...When the collaboration began, Pembrey was director of genetics on the landmark Avon Longitudinal Study of Parents and Children (ALSPAC) at the University of Bristol. In the 2006 article, he and his coauthors also presented data from a cohort of fathers in the ALSPAC study. In this group, men who took up smoking before puberty had 9-year-old sons with higher BMIs than men who first lit up later in life, suggesting that the timing of the ancestral exposure matters. A follow-up study published in 2014 found that the sons of early smokers—who themselves were not necessarily overweight—had an average of 5 to 10 kg more body fat in their teens than their peers.

Several other epidemiological associations between a father’s health prior to conceiving and the health of his children have emerged. For example, there are also some indications that a father’s drinking may contribute to fetal alcohol syndrome– like symptoms, specifically low birth weight, congenital heart defects, and mild cognitive impairments.

Early this decade, a spate of animal studies demonstrated that, in addition to toxins and alcohol, paternal weight and eating patterns—such as high-fat or lowprotein diets—also appear to alter the sperm epigenome and offspring health. In one mouse study, a paternal diet low in folate was associated with an increase in birth defects in offspring compared with a paternal diet sufficient in folate. The fathers who consumed less folate had abnormal methylation of genes implicated in development and chronic disease such as diabetes and cancer.

Studies published last year also suggest a link between paternaldietary patterns or diet-induced weight gain and increased birth weight and breast cancer risk in female offspring.One of these studies identified shared epigenetic changes present in both the sperm of overweightmalemice and the breast tissue of their female offspring. These alterations included reduced expression of miRNAs that regulate insulin receptor signaling, among several other wellcharacterized signaling pathways known to play a role in tumorigenesis. Alterations in miRNA expression may therefore underlie the metabolic reprogramming that, in turn, increases breast cancer risk.

Researchers are just beginning to tease out these underlying epigenetic mechanisms in humans. Investigators on the Newborn Epigenetics Study (NEST) at Duke University provided the first molecular evidence in 2013 and 2015 that a man’s lifestyle may be imprinted on his child’s epigenome.

Soubry suggested that physicians can encourage male patients who plan on conceiving to eat a nutritious diet, quit smoking (even temporarily), drink moderately, and manage stress—all of which the Centers for Disease Control and Prevention already recommends for fathers-to-be. “That advice cannot harm, and I think it can even help to reduce the risks later on for the child,” Soubry said. Of course, behavior matters during pregnancy, too. Fathers—along with mothers and domestic partners—can have a profound effect on the health of pregnancies."

My comment: Abnormal methylation profiles of genes and histones result from poor nutrition, lack of exercise, smoking, alcohol consumption, toxicants and even negative thoughts. Epigenome is your molecular memory and there are several mechanisms in the cell that makes epigenetic memories inheritable. The most stable epigenetic markings are maintained by histone methylation/acetylation and by piRNA-mediated epigenetic silencing. Modern science is aware of lifestyle driven 
epigenetic changes that are the underlying mechanism by which paternal factors such as age, diet, weight, stress, and alcohol consumption contribute to a range of health outcomes in offspring including birth defects, behavioral problems, developmental disorders, obesity, diabetes, cardiovascular disease, and cancer.

Life is not driven by gene sequences. Genes are driven by lifestyle. Don't get lost.


Bacteria are not simple life forms

Several bacterial senses point to Intelligent Design and Creation

You may have heard about an idea that complex life forms evolved from simple life forms such as bacteria. Does observed biology support such claim? No, because actually bacteria are not simple life forms. In my previous posts, I have told about MO-1 marine bacterium that has seven ion flow motors synchronized with a 24 gear-wheel planetary gearbox.


Bacteria also have different kind of sensors by which they are able to sense the surrounding environment. The assortment of different senses within bacteria might be surprising:

1. Sense of smell

4. Sense of light

"Using the world’s most powerful X-ray laser at the Department of Energy’s SLAC National Accelerator Laboratory, they were able to see atomic motions as fast as 100 quadrillionths of a second – 1,000 times faster than ever before.

Further, “We’re the first to succeed in taking real-time snapshots of an ultrafast structure transition in a protein, in which a molecule excited by light relaxes by rearranging its structure in what is known as trans-to-cis isomerization,” says the study’s principal investigator, Marius Schmidt from the University of Wisconsin, Milwaukee."

7. Sense of gravity

8. Sense of changing temperature

9. Sense of salt stress (osmolarity)

11. Sense of chemicals (chemotaxis)

15. Sense of electron acceptors

16. Sense of metabolites

17. Sense of pathogens and viruses

All of these senses require perfect design in which receptors and response regulators were created simultaneously. Rapid bacterial adaptations and changes are based on designed mechanisms, not random mutations or selection. The theory of evolution is just an illusion.


Curcumin has anticancer effects

Anticancer effect of curcumin inhibits cell growth through miR-21/PTEN/Akt pathway in breast cancer cell

Excerpt from abstract: "Curcumin is a polyphenol extracted from turmeric, which that belongs to the Zingiberaceae family. Curcumin has numerous effects, including anti-inflammatory, antitumor, anti-oxidative and antimicrobial effects. However, the effects of curcumin on human breast cancer cells remain largely unknown. The aim of the present study was to investigate the anticancer effects and the mechanisms by which curcumin affects breast cancer cells. 

The anticancer effect of curcumin on cell viability and cytotoxicity on human breast cancer MCF-7 cells was analyzed using 3-(4,5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H-tetrazolium bromide and lactate dehydrogenase assays, respectively. Cell apoptosis of MCF-7 cells was detected using flow cytometry, 4',6-diamidino-2-phenylindolestaining assay and caspase-3/9 activity kits. Reverse transcription-quantitative polymerase chain reaction was used to analyze microRNA-21 (miR-21) expression in MCF-7 cells. The protein expression of phosphatase and tensin homolog (PTEN) and phospho-protein kinase B (pAkt) was determined by western blot analysis. miR-21 was transfected into MCF-7 cells and the anticancer effect of curcumin on cell viability and the expression of PTEN and pAkt was analyzed. 
The present results demonstrated that curcumin inhibited cell viability and induced cytotoxicity of MCF-7 cells in a concentration- and time-dependent manner, by inducing apoptosis and increasing caspase-3/9 activities. In addition, curcumin downregulated miR-21 expression in MCF-7 cells by upregulating the PTEN/Akt signaling pathway. The present study has for the first time, to the best of our knowledge, revealed the anticancer effect of curcumin in suppressing breast cancer cell growth, and has elucidated that the miR-21/PTEN/Akt signaling pathway is a key mechanism for the anticancer effects of curcumin."

My comment: Curcumin is a nice addon to our list of anticancer foods:

- Tomatoes
- Broccoli
- Berries
- Walnuts
- Garlic
- Beans


And apple peels and red grapes:

Curcumin induces apoptosis (programmed cell death), which is controlled by epigenetic mechanisms in cases where something goes wrong in the cell. Most cancers are not just bad luck, instead, we can take care of our epigenomes by eating healthy food and having good life habits. Have a healthy life!


Environmental genomic memories can be passed on for 14 generations

Over 100,000,000 histone modifications maintain stable epigenetic inheritance

Excerpt: "In multicellular organisms, specificity of cell types is maintained by mitotically heritable differences in gene expression, which are in part regulated by epigenetic mechanisms. These include RNA-based mechanisms, histone modifications, and DNA methylation. The full range of epigenetic marks is currently unknown but is potentially enormous, considering that the diploid human epigenome contains >108 Cytosines (of which >107 are CpGs) and >108 histone tails that can all potentially vary.

DNA methylation is one of the best understood epigenetic modification and has an important role in several biological processes such as genome imprinting, defence against viral sequences, inhibition of recombination, as well as assembly of heterochromatin.

Aberrant DNA methylation patterns have been linked to genomic instability and increased mutation rates. The role of DNA methylation has been mainly explored in the context of cancer. Findings from these studies have extensively demonstrated that cancer development is associated with gain of DNA methylation at CpG islands, loss-of-imprinting and epigenetic remodeling of repeat elements. Interestingly, altered DNA methylation seems to be involved in the pathogenesis of other age-related diseases, such as cardiovascular, neurological and metabolic disorders, and autoimmune diseases."

My comment: 108 histone tails, a biological bar-coding mechanism, can all potentially vary with several other epigenetic mechanisms in our cells. They all are affected by foods, stress, climate and other environmental factors. This is why we can only observe variation within created kinds but no evolution from a bacterium into something other form of life.

Aberrant methylation patterns have been linked to genomic instability and increased mutation rates. This means that poor nutrition, alcohol consumption, smoking, toxins etc. expose us to genetic errors. Genetic mutations never result in adaptation or evolution. There are no mechanisms for large scale evolution. That's why creation and design. Don't get misled.



Not evolution but epigenetic variation of plants

These 6 Common Vegetables Are Actually All The Same Plant Species

Excerpt: "You may not have heard of the plant Brassica oleracea, but you've definitely eaten it. Many common vegetables that many people buy and eat on a regular basis are actually all derived from this plant, and are considered the same species.

Over the last few thousand years, farmers have bred Brassica oleracea into 'cultivars' (also known as subspecies) that eventually became these veggies:

Brassica is also known as the wild mustard plant.

"The wild plant is a weedy little herb that prefers to grow on limestone outcroppings all around the coastal Mediterranean region," Jeanne Osnas, a researcher at Purdue University who blogs as "The Botanist in the Kitchen," writes of Brassica oleracea.

"It is a biennial plant that uses food reserves stored over the winter in its rosette of leaves to produce a spike of a few yellow flowers at the end of its second summer before dying. Those nutritious leaves make its domesticated derivatives important food crops in much of the world now."

This one plant was selectively bred over hundreds of years to create dozens of wildly different vegetables.

By selecting and breeding plants with bigger leaves, or larger buds, the various cultivars were created.

Kale and collard greens, which are part of the same subspecies, were created by making the ancestor plant's leaves bigger, and were domesticated in Europe sometime before 300 BCE.

Red, green and savoy cabbages were created from a kale cultivar (likely the European collard greens) in the 1200s by selecting for a large terminal bud - the growing end at the top of the plant.

The leaves are tightly wound around a short, wide stem (the cabbage's core). Brussels sprouts are like tiny cabbages, except they grow from the buds along the plant's stem. They first hit the scene in the 1200s as well.

Kohlrabi was created by selecting for a thicker stalk in a kale plant around the 1400s. Chinese broccoli, another subspecies of B. oleracea, was domesticated in China and is distinct from broccoli, which was created from a kale predecessor in the 1500s.

Broccoli was developed by selecting for the larger flower clusters, which are then harvested before they bloom. Cauliflower was developed from one of hundreds of broccoli varieties."

My comment: About 95% of plants' genes are epigenetically silenced. This fact explains the huge potential for variation with them. Plants can experience rapid and versatile adaptation due to clever mechanisms. Phenotype variation is always based on epigenetic factors or loss of biological information. There are no mechanisms for large scale evolution. Don't get lost.


A comparison of two models of the origin of life and biodiversity

A comparison of two models of the origin of life and biodiversity

Darwinian tree of life
Creation orchard

A hypothetical model. Never observed.
Observational science.
Requires increase of biological information, new structures and functions. Never observed.
Genetic mutations are mostly harmful errors and result in degradation and loss of biological information. Genes are driven by life(style). Observed science.
Based on an assumption that organisms experience positive changes through random mutations and selection. Genes are drivers. Never observed.
Variation of organisms is based on existing information = Epigenetic mechanisms are induced by nutrition, climate, stress and other environmental factors. Observed science.
Not supported by the fossil record. A serious lack of the most important transitional fossils. Still missing link between apes and humans. The assumed ancestor of primates?
Confirmed by the fossil record. Fossils point to a global, catastrophic event and rapid burials.
Not supported by modern science, because:
- There are no mechanisms leading to simultaneous and synchronized increase of different forms (digital, analog, metadata) of biological information.
Supported by modern science, because:
- Changes in organisms are based on epigenetic mechanisms or loss of biological information.
Biggest problems:
- Abiogenesis
- Dinosaur bones’ soft tissues.
- 203,000 disease-causing genetic defects in the human DNA.
- Dog breeding shows the results of variation: a dead end.
- Molecular mechanisms and language of DNA are way too complex. Random lottery is not able to build such intelligent mechanisms.
- Receptors, signals and response regulators! Irreducible complexity.

Biggest problems:
- The most of created kinds are extinct.
Conclusion: Darwinian tree of life is not based on science.
Conclusion: Creation orchard is supported by discoveries made by modern science.