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Showing posts from March, 2017

Rapid degradation of the human DNA forces science to use gene editing architectures

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Gene editing of human embryos yields early results https://www.sciencenews.org/article/gene-editing-human-embryos-yields-early-results Excerpt: "Scientists have long sought a strategy for curing genetic diseases, but — with just a few notable exceptions — have succeeded only in their dreams. Now, though, researchers in China and Texas have taken a step toward making the fantasies a reality for all inherited diseases. Using the gene-editing tool known as CRISPR/Cas9, the researchers have successfully edited disease-causing mutations out of viable human embryos. Other Chinese groups had previously reported editing human embryos that could not develop into a baby because they carried extra chromosomes, but this is the first report involving viable embryos. In the new work, reported March 1 in Molecular Genetics and Genomics, Jianqiao Liu of Guangzhou Medical University in China and colleagues used embryos with a normal number of chromosomes. The embryos were created using eggs and sp

Goodbye junk-dna!

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'Jumping genes' and transposons are cut or silenced by clever mechanisms Eukaryotic cells are able to produce even thousands of different proteins from one gene. This is why there are even two millions of different proteins in a human body, although there are only about 19,600 protein coding genes used for human cells to produce the huge number of different proteins. This clever mechanism is called alternative splicing. RNA-mediated mechanism uses a gene like a library; it makes a template and modifies it by several ways. Cutting, pasting, recombining, moving, removing etc. Sometimes some strands (rna-like retrotransposos) needed for the alternative splicing mechanism are inserted into the genome by mistake. These genomic parasites can be harmful for genomic stability and integrity. Especially in germline cells they can cause serious troubles, even cell death. That's why there are mechanisms designed in the cell, that silence or remove those erroneous genetic sequences. The

Human traits and Epigenetics

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Human traits are determined by epigenetic control of gene expression 1. Height https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4208652/ Excerpt: "Genome‐wide SNP analyses have identified genomic variants associated with adult human height. However, these only explain a fraction of human height variation, suggesting that significant information might have been systematically missed by SNP sequencing analysis . A candidate for such non‐SNP‐linked information is DNA methylation. Regulation by DNA methylation requires the presence of CpG islands in the promoter region of candidate genes. Seventy two of 87 (82.8%), height‐associated genes were indeed found to contain CpG islands upstream of the transcription start site (USC CpG island searcher; validation: UCSC Genome Browser), which were shown to correlate with gene regulation. Consistent with this, DNA hypermethylation modules were detected in 42 height‐associated genes, versus 1.5% of control genes (P = 8.0199e−17), as were dynamic met

The DNA methylation revealed a much stronger link to survival than point mutations

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The DNA methylation revealed a much stronger link to survival than point mutations http://www.news-medical.net/news/20170320/Methylation-status-of-ten-positions-in-genome-correlates-with-all-cause-mortality.aspx Excerpt: "Various chemical modifications in the genome determine whether genes are read or deactivated. Methyl labels in the DNA play a key role in this "epigenetic" regulation of gene activity. Life style and environmental factors influence the methylation in the genome. Scientists have already well documented links between the methylation status of specific positions in the genome and cancer as well as other diseases. ...The DNA methylation revealed a much stronger link to survival than all other previously studied alterations in individual DNA building blocks (SNPs, single nucleotide polymorphisms). The epigenetic risk profile thus proved to be a more accurate indicator for lifespan than all other previously established genetic risk profiles that are based on

How diet impacts our genome

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Dietary anti-cancer compound may work by influence on cellular genetics https://medicalxpress.com/news/2017-03-dietary-anti-cancer-compound-cellular-genetics.html Excerpt: "Researchers have discovered one of the reasons why broccoli may be good for your health. They found that sulforaphane, a dietary compound from broccoli that's known to help prevent prostate cancer, may work through its influence on long, non-coding RNAs. This is another step forward in a compelling new area of study on the underlying genetics of cancer development and progression. The findings were published by researchers from Oregon State University in the Journal of Nutritional Biochemistry. The research provides more evidence for how these lncRNAs, which were once thought to be a type of "junk DNA" of no particular value or function, may instead play a critical role in triggering cells to become malignant and spread. Growing evidence shows that lncRNAs, which number in the thousands, have a ma

Protein coding genes are just raw data

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An astonishing similarity of protein coding genes in humans, pigs, mice, dolphins, kangaroos, spiders etc. https://proteomics.cancer.gov/whatisproteomics Excerpt: "The human genome contains about 21,000 protein-encoding genes, but the total number of proteins in human cells is estimated to be between 250,000 to one MILLION." My comment: Newest studies have confirmed the number of human protein coding genes to be about 19,000. RNA-directed cellular mechanisms are able to build thousands of different proteins by using raw data of one gene, without changing the gene's sequence. Mechanism is called alternative mRNA splicing. Based on DSCAM gene in Drosophila Melanogaster, the fruit fly's cell is able to build even 38,016 different proteins, without changing the sequence. The way of how the cell uses protein coding genes tells us that genes are not drivers. Instead, they are just raw data, libraries for RNA-directed mechanisms. http://www.sciencedirect.com/science/article/

Plant Epigenetics points to Design

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Plant diversity and epigenetic mechanisms http://www.the-scientist.com/?articles.view/articleNo/48120/title/Infographic--Plant-Methylation-Basics/ Excerpt from Jef Akst | February 1, 2017 "There are three different types of DNA methylation in plants: CG, CHH (where H is any base except G), and CHG. In Arabidopsis, CG methylation is found on some genes, but primarily on repeat sequences that make up transposons, as well as other repeat sequences in the genome. CHH methylation is found only where there is CG methylation and often near transposable elements, though some evidence points to CHH methylation on some silenced genes as well. CHG methylation is typically found with the CHH variety. METHYLATION MAINTENANCE Every time a cell divides, it must replicate its genome and its epigenome. Plants have diverse pathways overseeing the faithful passage of the methylome to daughter cells. CG methylation Copying CG methylation patterns to the two daughter strands is relatively straightforw

Muntjacs fight pseudoscience

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Rapid 'speciation' and chromosome loss don't support the theory of evolution http://eol.org/pages/38814/details Excerpt: "The Red Muntjac has the lowest diploid chromosomal number in mammals (2n = 6 for females and 7 for males) whereas Reeves' Muntjac has 2n = 46 in both sexes (remarkably, these two species can produce viable F1 hybrids in captivity)." My comment: Despite the huge difference in chromosome count (2n=6 and 2n=46), those two breeds of Muntjac are able to get viable offspring. Such interesting cases of hybridization can be observed in captivity, for example in zoos. Chromosomes of the Red Muntjacs are tightly packaged because of huge areas of heterochromatin. Telomeres are also very strong indicating large areas of faulty genes.   I also found an interesting phenomenon regarding the number of chromosomes. Because shifting diet causes genetic mutations, the heavy loss of chromosomes has driven the Red Muntjac into omnivory. This finding needs a lot

GMO corn causes genetic mutations

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Genetically modified corn leads to oxidative stress and genetic mutations http://sustainablepulse.com/2016/12/19/new-study-shows-major-molecular-differences-between-gmo-and-non-gmo-corn/#.WMTtttLyios Excerpt: "In-depth analysis of types of proteins (“proteomics”) and small biochemical molecules (“metabolomics”) revealed major compositional differences between NK603 and its non-GMO parent. The results obtained show not only disturbances in energy utilisation and oxidative stress (damage to cells and tissues by reactive oxygen), but worryingly large increases in certain substances (polyamines). Polyamines found to be present in increased amounts in GMO NK603 corn include putrescine and cadaverine, which can produce various toxic effects. For example, they enhance the effects of histamine, thus heightening allergic reactions, and both have been implicated in the formation of carcinogenic substances called nitrosamines. Overall, the findings of this study disprove industry and regulat

How the cell uses cytokines as knobs instead of switches

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Epigenetic layers function as analog information regulators http://news.harvard.edu/gazette/story/2017/03/how-a-child-made-scientists-think-of-cytokines-as-knobs-instead-of-switches/ Excerpt: "Conventional wisdom has held that cytokines are “digital,” in that they either bind to a cellular receptor — triggering a cascade of signals within the cell — or they don’t. If a mutation prevents perfect binding, no cascade. There is no middle ground. But maybe there is. A rare case of a rare disease has led an international research team headed by Broad Institute of Harvard and MIT associate member Vijay Sankaran of Dana-Farber/Boston Children’s Cancer and Blood Disorders Center, postdoctoral fellow Ah Ram Kim, and Yale University’s Daryl Klein to propose an “analog” view of cytokine function. It may be, as they show in Cell, that cytokine mutations that affect not whether a protein and receptor interact, but the quality of that interaction, can tune a cell’s biochemical response, triggeri

A lack of methyl groups in the gene body may develop cancer

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A lack of methyl groups in the gene body may develop cancer https://www.sciencedaily.com/releases/2017/02/170223101841.htm Excerpt: "Every cell in our body contains the complete DNA library. So-called methyl groups regulate that in body tissues only the genetic information is expressed that is indeed needed in this tissue. Now, for the first time, researchers from the Leibniz Institute on Aging in Jena, Germany, verified that a lack of methyl groups in the gene body leads to an incorrect gene activation and, as a consequence, may lead to the emergence of cancer. The stunning results were published in the journal Nature on February 22, 2017. Each cell in the body contains the basic building plan of our entire organism. It is written in the "DNA" and comprises single genes which determine specific individual attributes. Gene expression is strictly regulated in order to build tissue-specific cells with tissue-specific attributes. For example in an intestinal cell, the genet

Signs of human chromosome loss

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Mutations are leading to heavy loss of biological information https://phys.org/news/2016-01-quirky-chromosome-human-species.html • A 1984 report describes a family with 3 adult siblings who had 44 chromosomes, #s 13 and 14 combined. • A 1988 report tells of 3 distantly-related families in Finland, also involving #s 13 and 14, whose Rob chromosome passed in carriers through at least 9 generations, appearing in at least one homozygote. • A 1989 paper describes a Rob between #s 14 and 21 in a homozygote whose carrier parents were related. Trickling into the headlines was a case report from 2013 of a 25-year-old healthy Chinese man who has 44 chromosomes because each 14 joins a 15 – a combo not seen before. http://genetics.thetech.org/original_news/news124 " In a recent article , a doctor in China has identified a man who has 44 chromosomes instead of the usual 46. Except for his different number of chromosomes, this man is perfectly normal in every measurable way." My comment: G

Three basic tenets of the Evolutionary theory refuted by a single study

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In addition to mutations in genes, aberrant enhancer element activity at non-coding regions of the genome is a key driver of tumorigenesis http://www.nature.com/articles/ncomms14400 Excerpt from abstract: "In addition to mutations in genes, aberrant enhancer element activity at non-coding regions of the genome is a key driver of tumorigenesis. Here, we perform epigenomic enhancer profiling of a cohort of more than forty genetically diverse human colorectal cancer (CRC) specimens. Using normal colonic crypt epithelium as a comparator, we identify enhancers with recurrently gained or lost activity across CRC specimens. Of the enhancers highly recurrently activated in CRC, most are constituents of super enhancers, are occupied by AP-1 and cohesin complex members, and originate from primed chromatin. Many activate known oncogenes, and CRC growth can be mitigated through pharmacologic inhibition or genome editing of these loci. Nearly half of all GWAS CRC risk loci co-localize to recur

Cells are guiding each other

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Why cloning using a DNA sample will not be successful? Why genetically identical twins might have different colors of eys, hair and skin? http://www.bionews.org.uk/page_787519.asp Excerpt: "Stem cells from an adult mouse have been used to grow a structure resembling a mouse embryo in vitro for the first time. The ability to study the early stages of embryo development outside the womb may one day help explain why a significant number of human pregnancies fail. This breakthrough in developmental research originated from the same team at University of Cambridge which recently developed a technique that allows human embryos to develop in the lab up to the legal limit of 14 days in the UK. 'We are very optimistic that this will allow us to study key events of this critical stage of human development without actually having to work on (IVF) embryos,' said lead researcher Professor Magdalena Zernicka-Goetz of the University of Cambridge. The development of a fertilised egg into

Salt flats are remnants of a mega-flood in Mars

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Every salt flat on Earth is located close to a volcano https://phys.org/news/2017-03-remnants-mega-flood-mars.html Excerpt: "A combination of volcanism, tectonics, collapse and subsidence in the Tharsis region led to several massive groundwater releases from Echus Chasma, which subsequently flooded the Kasei Valles region around 3.6–3.4 billion years ago. These ancient mega-floods have left their mark on the features seen today." http://www.dailymail.co.uk/sciencetech/article-3189834/Is-life-finally-died-Mars-Salt-flats-place-water-survived-red-planet-study-finds.html Excerpt: "The 18-square-mile chloride salt deposit is similar to Utah's Bonneville Salt Flats, they say." My comment: It's obvious that the Earth's salt flats are also remnants of a mega-flood. It's not a coincidence that every salt flat or saline lake of the Earth is located close to a volcano, a caldera or a tectonic crossroad. The origin of salt is under the crust. Other planets and

Why Humanity’s DNA May be in Trouble in the Future

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Rapidly weakening gene pool is a hard evidence against evolution http://genetics.thetech.org/weakened-gene-pool Excerpt: "A new review in GENETICS explains this potential problem pretty well. It has to do with DNA changes or mutations that pop up in each generation. And the loss of the ability to weed out the ones with minor, negative effects. Over time, these minor mutations might build up and have serious consequences. Left unchecked, our DNA might decline in quality, generation after generation. Now that isn’t to say that this article says that DNA quality is only going to go downhill. With screening and maybe even fixing broken genes (gene editing), we may eventually lose really bad mutations from the gene pool. So future generations may not get as many deadly genetic diseases as we do today. But it is the mutations that just cause minor problems that are, well, potentially the problem. We will not be able to easily find and screen for these. And combined they may have real co