Plant germ cells also go through methylation reprogramming

Plant germ cells also go through methylation reprogramming - and functionally it is essential


Excerpt: "A new study has revealed an undiscovered reprogramming mechanism that allows plants to maintain fitness down the generations.

The John Innes Centre team led by Dr Xiaoqi Feng made the discovery when studying germ cells - cells specialised for sexual reproduction - in flowering plants.

Germ cells are often referred to as “immortal” because they can pass their genetic material through the generations. They have been the subject of much scientific scrutiny.

This study aimed to solve a long-term debate on whether the germ cells in plants undergo an event of DNA methylation reprogramming at each reproductive cycle.

DNA methylation is a modification of DNA, which changes the activity of DNA without changing the genetic sequence.

It is a cornerstone epi-genetics – one of the fastest growing fields in life sciences with potential to deliver improvements in human and plant health.

DNA methylation reprogramming - known to exist in animals – occurs most dramatically in germ cells and regulates the reproductive success from generation to generation. Published in Nature Genetics the JIC team worked in collaboration with colleagues from the University of Leicester to reveal for the first time the existence of DNA methylation changes in the germline of flowering plants.

They also reveal the mechanism by which this reprogramming happens - via a process known as de novo (anew) DNA methylation and its biological significance in maintaining reproductive success.

Dr Feng, project leader at the John Innes Centre, explains: “We knew this DNA methylation re-setting is extensive and important in animals where methylation is erased and re-established between generations.

“But because plants carry DNA methylation information really well through generations, it was believed there was not much methylation reprogramming going on in plant germ cells. What we have discovered shows plant germ cells also go through methylation reprogramming and functionally it is essential.”

The John Innes Centre team made the discovery while applying genetic analysis to male sexual lineage in the reference plant Arabidopsis thaliana.

The research funded by BBSRC is a key breakthrough in fundamental understanding of epigenetic regulation of plant development.

Dr. Feng explained “Our research shows that developmentally regulated DNA methylation reprogramming can regulate plant development. Scientists have been searching for this for a long time. We show that genes can be regulated in specific cells via the de novo DNA methylation pathway, which is prevalent in many plant tissues, hence this mechanism may apply to many processes in plants.”
“Understanding how this naturally occurs during plant development is the first step in understanding how specific genes can be targeted by this epigenetic modification and hence regulated.

Additionally, understanding how DNA methylation is inherited through the germ cells is essential for understanding the transgenerational stability of incurred methylation changes. Both are essential to harness epigenetics for crop improvement.”"

My comment: Epigenetic reprogramming, like any kind of programming, points to Intelligent Design and Creation. DNA methylation patterns are erased during stages of reproduction and re-constituted by several clever and complex RNA-directed mechanisms. This is done for the organism to be able to efficiently adapt for changing environment. To observe epigenetic reprogramming occurring within plants, tells us about common design, not common ancestor because there is no mechanism for any kind of evolution. Information for the cellular differentiation and epigenetic reprogramming is given by the parents of an organism. The theory of evolution is the major heresy of our time. Don't get lost.


An epigenetic seesaw mechanism works like an analog regulator

An epigenetic seesaw mechanism works like an analog regulator


Excerpt from abstract: "


DNA methylation at promoters is largely correlated with inhibition of gene expression. However, the role of DNA methylation at enhancers is not fully understood, although a crosstalk with chromatin marks is expected. Actually, there exist contradictory reports about positive and negative correlations between DNA methylation and H3K4me1, a chromatin hallmark of enhancers.


We investigated the relationship between DNA methylation and active chromatin marks through genome-wide correlations, and found anti-correlation between H3K4me1 and H3K4me3 enrichment at low and intermediate DNA methylation loci. We hypothesized “seesaw” dynamics between H3K4me1 and H3K4me3 in the low and intermediate DNA methylation range, in which DNA methylation discriminates between enhancers and promoters, marked by H3K4me1 and H3K4me3, respectively. Low methylated regions are H3K4me3 enriched, while those with intermediate DNA methylation levels are progressively H3K4me1 enriched. Additionally, the enrichment of H3K27ac, distinguishing active from primed enhancers, follows a plateau in the lower range of the intermediate DNA methylation level, corresponding to active enhancers, and decreases linearly in the higher range of the intermediate DNA methylation. Thus, the decrease of the DNA methylation switches smoothly the state of the enhancers from a primed to an active state. We summarize these observations into a rule of thumb of one-out-of-three methylation marks: “In each genomic region only one out of these three methylation marks {DNA methylation, H3K4me1, H3K4me3} is high. If it is the DNA methylation, the region is inactive. If it is H3K4me1, the region is an enhancer, and if it is H3K4me3, the region is a promoter”. To test our model, we used available genome-wide datasets of H3K4 methyltransferases knockouts. Our analysis suggests that CXXC proteins, as readers of non-methylated CpGs would regulate the “seesaw” mechanism that focuses H3K4me3 to unmethylated sites, while being repulsed from H3K4me1 decorated enhancers and CpG island shores.


Our results show that DNA methylation discriminates promoters from enhancers through H3K4me1-H3K4me3 seesaw mechanism, and suggest its possible function in the inheritance of chromatin marks after cell division. Our analyses suggest aberrant formation of promoter-like regions and ectopic transcription of hypomethylated regions of DNA. Such mechanism process can have important implications in biological process in where it has been reported abnormal DNA methylation status such as cancer and aging.


...different cells of a population can have different chromatin marks at the same genomic region, and such marks are dynamically changed through the enzymatic activity of methylases and demethylases. Therefore, we use the term “seesaw” rather than “mutual exclusion” to define such mechanism, which includes a balanced state with both marks enriched at lower levels."

My comment: 
DNA methylation regulates discrimination of enhancers from promoters through two different histone marker sets. Enhancers and promoters are widely used by the cell in a mechanism called alternative splicing, which makes it possible for the cell to produce thousands of different proteins based just on one multifunctional gene. DNA methylation patterns are typically affected by diet type, climate, stress etc. which means that these clever mechanisms help organisms go through their ecological adaptation processes. The seesaw mechanism provides a balanced state between two analog type regulatory functions. The interaction between several genomic elements points to Design and Creation. There are no mechanisms for evolution because any change in organisms is based on epigenetic regulation of existing biological information OR loss of it. Don't get lost.


Evolutionary biologists are surprised - Mice are able to see colors

Evolutionary biologists are surprised - Mice are able to see colors


Excerpt from abstract:"

The M5 Cell: A Color-Opponent Intrinsically Photosensitive Retinal Ganglion Cell


•M5 cells are a morphologically and functionally distinct unique ipRGC type
•They have both melanopsin responses and chromatically opponent cone-based signals
•They receive color-opponent signal (UV-ON, green-OFF) via Types 6–9 bipolar cells
•M5 cells innervate the dorsal lateral geniculate nucleus (dLGN)


Intrinsically photosensitive retinal ganglion cells (ipRGCs) combine direct photosensitivity through melanopsin with synaptically mediated drive from classical photoreceptors through bipolar-cell input. Here, we sought to provide a fuller description of the least understood ipRGC type, the M5 cell, and discovered a distinctive functional characteristic—chromatic opponency (ultraviolet excitatory, green inhibitory). Serial electron microscopic reconstructions revealed that M5 cells receive selective UV-opsin drive from Type 9 cone bipolar cells but also mixed cone signals from bipolar Types 6, 7, and 8. Recordings suggest that both excitation and inhibition are driven by the ON channel and that chromatic opponency results from M-cone-driven surround inhibition mediated by wide-field spiking GABAergic amacrine cells. We show that M5 cells send axons to the dLGN and are thus positioned to provide chromatic signals to visual cortex. These findings underscore that melanopsin’s influence extends beyond unconscious reflex functions to encompass cortical vision, perhaps including the perception of color." 

My comment: Several mammals have been thought to be color blind or at least limited with color vision. Evolutionary biologists have believed that only the so-called "more evolved" mammals have the ability to see the colors. A typical argument of evolutionists has also been that the color vision would have evolved due to couple of random, lucky mutations. A recent study shows that evolutionists have once again been wrong. Mice are able to see the colors and the mechanism for seeing the colors is much more complicated than has hitherto been understood. 

The claims of development of color vision are pseudoscientific nonsense, like any other claim that genetic mutations and selection would result in the growth of structural or functional complexity. The Evolutionary theory is the most serious heresy of our time.


lncRNAs might function as barcodes for identifying genomic addresses for maintaining cellular states

lncRNAs might function as barcodes for identifying genomic addresses for maintaining cellular states


Excerpt:"Long noncoding RNAs (lncRNAs) have been implicated in diverse biological processes, including embryonic stem cell (ESC) maintenance. However, their functional mechanisms remain largely undefined. Here, researchers from TU Dresden show that the lncRNA Panct1 regulates the transient recruitment of a putative X-chromosome-encoded protein transient octamer binding factor 1 (TOBF1), to genomic sites resembling the canonical Oct-Sox motif. TOBF1 physically interacts with Panct1 and exhibits a cell-cycle-specific punctate localization in ESCs. At the chromatin level, this correlates with its recruitment to promoters of pluripotency genes. Strikingly, mutating an octamer-like motif in Panct1 RNA abrogates the strength of TOBF1 localization and recruitment to its targets. Taken together, these data reveal a tightly controlled spatial and temporal pattern of lncRNA-mediated gene regulation in a cell-cycle-dependent manner and suggest that lncRNAs might function as barcodes for identifying genomic addresses for maintaining cellular states."

My comment: Barcoding and addressing system together point to Intelligent design and Creation. The role of lncRNAs is very important especially during embryonic development, when lncRNAs transmit the necessary information for the cellular differentiation procedure. There are over a hundred of different types of epigenetic markers that these long non coding RNA molecules carry for establishing the histone coding system, a biological database which determines almost all traits of an organism.
For the theory of evolution these lncRNAs are very truth revealing molecules. For example, the similarity of human/pig lncRNA transcripts is 57% as the corresponding number between humans and chimps is only 29.8%.


"Finally, a large number of pig lncRNAs appeared to have human homologs (57% of total identified lncRNAs) illustrating the similarities between humans and pigs at the genome level."


"The learned transcript similarity threshold for each pair of comparing species varied as a function of distance between species: the empirical threshold for calling a significant human-chimp alignment was 29.8 % sequence similarity."


Cellular programming by 3D folding of the DNA

Cellular programming by 3D folding of the DNA - Incredibly complex mechanism behind the cell differentiation


Excerpt: "During differentiation of pluripotent stem cells to cardiomyocytes, the three-dimensional folding of the DNA reorganizes itself. This reorganization of the DNA architecture precedes and defines important epigenetic patterns. A team lead by private lecturer Dr. Ralf Gilsbach and Stephan Nothjunge, who both conduct research at the University of Freiburg in the Department of Experimental and Clinical Pharmacology and Toxicology headed by Prof. Dr. Lutz Hein, have come to this conclusion. The results suggest that the genome's spatial organization is an important switch for defining cell types, thereby representing a very promising starting point for future reprogramming strategies. The team recently published its results in the scientific journal Nature Communications.

The genome stores information about an organisms development. Each cell carries this information tightly packed on a two-meter long DNA strand in the cell nucleus and specific epigenetic mechanisms control access to the 'blueprint of life'. Because every cell type in a mammalian organism requires access to genomic areas in a tempo-spatial specific manner, the epigenome is crucial for determining cellular identity. It is already known that various epigenetic mechanisms are associated with cell differentiation. Particularly indispensable is the methylation of DNA, in which methyl groups are attached to specific nucleotides of double-stranded DNA. Recent studies also show that differentiation processes are accompanied by a reorganization of the three-dimensional folding of the DNA. Up until now, however, it has been unclear what comes first during cardiomyocyte differentiation: the reorganization of the DNA's folding in the cellular nucleus or the DNA's methylation - and whether these mechanisms are dependent on one another.

In order to address this question, the team lead by the Freiburg pharmacologists used modern sequencing methods. These made it possible to map the three-dimensional genome organization as well as epigenetic mechanisms during the differentiation of cardiomyocytes across the entire genome. For this purpose, the researchers established methods for isolating cardiomyocytes in various developmental stages from healthy mouse hearts. This cell-type-specific analysis was essential to demonstrate that there is a close interplay between epigenetic mechanisms and the spatial folding of the DNA in the cardiomyocytes' nucleus. The comparison of different stages of development showed that the type of spatial folding of DNA defines which methylation patterns are formed and which genes are activated. The researchers proved that the spatial arrangement of the DNA is not dependent on the DNA methylation with cells, among other things, that have no DNA methylation at all. The three-dimensional genome organization is thus a central switchboard for determining cellular identity. In the future, the researchers want to use this switch to control cellular functions."

My comment: Are human programmers able to use 3D folding as a regulator of sub-program activity? I have not heard about such intelligent way of coding. Can you see how perfectly controlled the epigenetic programming for the cellular differentiation is? It has nothing to do with random mutations or selection. These sophisticated mechanisms point to Design and Creation. Don't get lost.


Due to Rapid Human DNA Degradation Rare Diseases Are Increasing in Frequency

Due to Rapid Human DNA Degradation Rare Diseases Are Increasing in Frequency


Human DNA is rapidly degrading. The article below puts quite a bit of figures on the table. As a result of genetic deterioration, there is a huge spectrum of rare genetic diseases. These are not weeded out from the population by any kind of selection, but as the article says, the number of rare diseases is rapidly growing.

By 2020, about 10% of people will carry at least one disease-causing genetic mutation. In Europe, this is about 42 million people, over 400 million in Asia and some 52 million in North America. There are so many diseases caused by genetic mutations that the medical industry is not able to handle them all. When a certain genetic disease is affected by a relatively small proportion of the population, pharmaceutical companies are not economically viable to develop treatment for rare illness. This causes problems for society.

The total number of disease-causing genetic mutations in the human DNA at population level is 214,158. Annual increase was more than 20,000.


According to the Nature's study, about 73% of mutations in human DNA have occurred during the last 5,000 years. All these scientific facts confirm that evolutionary theory is the most serious heresy of our time and that man has not been wandering for many thousands of years on this planet.



Mechanisms behind the cell differentiation

The sophisticated mechanisms behind the cell differentiation reveal the fallacies of the evolutionary theory

There are at least 37 trillion cells in a human body. They can roughly be classified into two hundred cell types that our body needs for different tissue types to produce the necessary proteins and to handle several, e.g. metabolism related tasks. All of our cells have exactly the same DNA sequences (only brain neurons and T cells controlled by the immune defense system make an exception). How does the cell differentiation occur? Why does the skin cell have a completely different identity than a bone cell? Both have exactly the same DNA, so it is clear that the DNA sequences do not determine the task or function of the cell.

Differentiation of the cells begins already during embryonic development. The process is called epigenetic reprogramming. If all of the epigenetic markers on the DNA are wiped out of the cell, it becomes a pluripotent stem cell capable of differentiating into any task. During the embryonic development, cells may have to be re-programmed up to two or three times. Only cells programmed by the immune system will not be reprogrammed, which is, of course, a brilliant solution. The most important epigenetic markers affecting cell differentiation are DNA methylation and epigenetic markings of histone, i.e. DNA packaging proteins (including methylation, acetylation, ubiquitination, phosphorylation etc.).

These epigenetic information layers determining cell differentiation are set in epigenetic reprogramming by non-coding RNA molecules. The information transmitted by the MicroRNAs and lncRNAs will be stored in histone epigenetic markers that act as a biological database and an address system. Thus, all information related to the cell function is stored outside of the DNA sequences. In practice, this means activating or suppressing genes and transcriptional regions and bending chromatin to contact certain regions of DNA. As the organism adapts, it experiences the changes in epigenetic information structures. This often results in deleterious DNA sequence changes because methylation acts as a DNA stabilizer. When the methylation profiles change, the cell is exposed to oxidative stress that causes deamination of DNA bases, whereby the base may change. This is where a genetic mutation occurs. This is the most significant mechanism of DNA degradation.


When the organism adapts to, for example, a new nutritional type or a cooler climate, it is primarily necessary to investigate the changes in epigenetic profiles. DNA sequence changes may also occur, but they are also results of changed epigenetic profiles. Random mutations and natural selection have no role in the ecological adaptation of organisms. If we want to compare the genomic similarity between the two organisms, it should be done between the mechanisms affecting the cell differentiation. Thus, if we compare the human and chimpanzee lncRNA molecules, which set up the biological address database in the embryonic development, are the fallacies of the evolutionary theory revealed: The similarity of human and chimpanzee lncRNA molecules is only 29.8% !! So we're not related to apes. The evolutionary theory is the most serious heresy of our time. Don't get lost, good people.


Rapid ecological adaptation points to Design and Creation

Rapid ecological adaptation points to Design and Creation

If the emergence of a new species of birds does not take more than a couple of generations, there is evidence for Design and Biblical creation, the flood and the subsequent rapid formation of biodiversity.


Excerpt: "Researchers previously assumed that the formation of a new species takes a very long time, but in the Big Bird lineage it happened in just two generations, according to observations made by the Grants in the field in combination with the genetic studies."

We can observe everywhere the rapid ecological adaptation of organisms, based primarily on epigenetic gene regulation caused by diet type, climate and various stressors, which also causes genetic changes. However, most DNA sequence modifications result in genetic errors that lead to DNA degradation. The change is therefore not about mutations and natural selection, but due to mechanism-based ecological adaptation. Those mechanisms also cause changes to the pheromone production of the organism, which in turn controls its mating behavior. This is why scientists use the term 'species', although rather it should be said about race, for example.

There's no mechanism for evolution because any change in organisms is caused by epigenetic regulation of existing biological information OR loss of it. Don't be deceived.