Scientists Identify Woolly Mammoth Genes | Prehistoric News

First comprehensive analysis of the woolly mammoth genome completed! Enjoy!

Reference: First comprehensive analysis of the woolly mammoth genome completed

By: The Prehistoric Master.

Why the case against designer babies falls apart

See on - The future of medicine and health

When it comes to technological advances that could reduce human suffering, improve health and reduce disease, we are generally all in favour. But recent advances in procedures that tinker with reproductive cells are often seen as an exception. They attract fierce opposition from people who believe they are unethical and should be treated as serious criminal offences – which in some jurisdictions they are already. I don’t think these arguments are decisive, however. Indeed some of them are not convincing at all.

Ethical debates about changing the human genome make a distinction between two different types of cells. All cells except those involved in reproduction are known as somatic. These have been the subject of less controversial research for a number of years now – for example editing a type of white blood cell known as T-cells has become a major area of enquiry in cancer research.

Cells involved in reproduction are called germ cells. Changing them, which is sometimes described as germline editing, can have effects that can be inherited by the offspring of the people whose bodies are amended. In other words, the changes can enter the gene pool.

See on The main objections to such procedures fall into four categories: they are unpredictable and dangerous; they are the slippery slope to eugenics and designer babies; they interfere with nature and involve playing God; and they will exacerbate social inequality and cause a division between the genetically enhanced and the rest of us. First among equals To begin with, not everything that leads to social inequality is unethical. And even in instances when such practices are unethical, it doesn’t automatically follow that they should be illegal. For instance, it is clearly arguable that any advanced system of higher education might perpetuate social inequality. Those who succeed in their studies might tend to get better jobs than people who are less educated. And the children of parents who are highly educated are more likely to become highly educated than other children. But very few would argue that this makes higher education or indeed family units unethical. Neither do we normally say that scientific research should be undertaken only if won’t lead to social inequality and divisiveness. It is whimsical to attach such a requirement in the case of genome editing.

Oliver Nova

Founder and former owner of Lightwell Pharma, youngest son of Cole and Ember Nova. He and his twin sister Liv inherited their father’s Kasari genome after Cole failed to recognize his efforts to suppress those traits had not succeeded. Liv later asked her father to re-sequence her dna so she could properly die in peace, which Cole mercifully agreed to, upsetting Oliver greatly. He wouldn’t allow himself to get attached to anyone else again until his son Zach was born. Unfortunately Zach was not immortal and eventually died but left five children behind, including Harlow’s grandfather Daniel

Oliver is a calm and calculating man who due to his extraordinary lifespan has a hard time feigning interest in much of anything. Like his father Cole, the full extent of his magical abilities are largely a mystery as he rarely makes use of them finding that it gives him too great of an advantage in most situations which in turns further bores him. Despite his rougher edges he does have a softer side thanks to his mother’s gentle upbringing and loves to cook for anyone who comes to call. Cole is the only one that refuses to eat his cooking, mostly because it reminds him of Ember, and since his mate died so long ago it kind of sends him into a depression. Since Harlow descends from his beloved son he took pity on her when her parents died and has put in a great deal of effort to ensure she has a long and happy life. 


Oliver is nearly a full blooded Kasari (gamplay wise: alien/witch) but has trace amounts of his mother’s power in him (she’s basically a fire elemental).   

anonymous asked:

You've probably already been asked this or it was explained in the show and I somehow forgot, but why is Cosima the only clone who wears glasses? It's never mentioned that any other clones wear contacts.

Cosima’s need for glasses stems from her environment and not her genetics. She read a lot of books and studied a lot for school growing up, so her vision deteriorated unlike that of the other clones. So you could say that a propensity toward vision deterioration is in the clone genome, but it requires certain environmental factors to play out, and so far Cosima is the only clone who had those factors.


1A/3a: A human being shall be defined as a person recognized and accepted by a reasonable layperson as being human on the basis of form, behavior, or external appearance, and no authority shall be permitted to use any element of a genetic profile to exclude a person from that definition.

1A/3d: A human being shall not be subject to any commercial claim, patent, or restriction on the basis of any part of the genome or genetic profile, whether altered or unaltered. 

1A/3e: A human being, regardless of any engineering of their genome or introduction of non-human or artificial DNA, shall not cease to be classed as human under any circumstances.

1A/3g: A human being or part of thereof may not be owned by any individual or organization.

( Head-cannon!!  WARNING; This will lead to spoilers for the series Tengen Toppa Gurren Lagann.  READ AT YOUR OWN RISK!!!  Thank you!

Beastmen..  In the TTGL fandom, the beastmen have always been a very mysterious culture that no one really knows a whole lot about, or better yet how the beastmen functioned in the the series.

What was their military like?  How did they learn to read?  Were they genetically bred only for fighting?  What about their life spans?

These questions never got a definitive answer… well, most of them anyways.  So, I am going to try and write up a few theories based on what I have gathered through friends and Real World.

First off; Life Spans.

We know for a fact that a beastman’s life span is quite short.  Through some sources and friends they last for about 30 years.  On top of that some have to recuperate every so many hours otherwise they will degrade, degradation, a term Lord Genome had mention before.

When you think about it that’s a pretty short life compared to a human’s 100 year lifespan. 

But, remember.  The beastmen are genetically modified.  They have both animal AND human genes.  So, a few years in beastmen years is a couple of decades in human years.

Confused?  Well, let’s start with what we know about animals.  For example; cats and dogs.

On average a dog and/or cat can live to about 15 to 20 years when domesticated.  The reason for this is because they mature more quickly, and that’s just in animal years.  In human years that’s nearly 90 to 100 years.

If beastmen can live up to 30 years including their genes, and depending on what kind of animal they are; Fish, Whale, Monkeys, etc…

That’s nearly 200 in human years!! (Now that I think about that, that would mean Cytomander, who is believed to be a little over 200 years, he would be 30 years old?!)

This is important to me because I think this for Viral and as well as for my character, Tsuuma.

For my head-cannon; Tsuuma and Viral were raised together, born and raise to fight in the military.  They would just be little babies, kittens really.

By the end of the first year, they are a grown adult.  Which would mean that they 18 years old in human years.

Tsuuma’s life span is preserved when she gets trapped inside of her pod.  Though, I think it might just add a few more years onto her lifespan.

… Hmmm.  What about Viral?

In the TTGL series I like to think Viral is a year, or 2 years old.  That would make him 18 or 24.  Viral has the genetics of a cat and shark, and sharks are said live to about… 30 to 40 years.

Yes, Viral becomes immortal but let’s pretend for a moment that fact isn’t there.

The series skips 7 years, so that makes Viral 45.  That would explain him looking a tad bit older.. facial features and longer hair, taller.

The very last episode skips to 20 years.  In 27 years, Viral is now…


… Well, s***!!

Despite being immortal, Viral lived up to 100 years that would mean he would be over 400 years old!!  WITHOUT AGING!!!

Above: A resolved Tree of Life with eukaryotes colored red, archaea green and bacteria blue

Defining the tap roots to the tree of life

It was way back in 1977 that American microbiologist Carl Woese applied phylogenetic taxonomy 16s ribosomal RNA to discover the third Domain of Life, the Archaea, depicted in green in the phylogenetic tree above. Phylogenetics based on the comparison of the slow-evolving ribosomal genes thus replaced those solely based on the subjectivity of organism morphology. Prior to Woese, all prokaryotes were lumped together. Ever since Woese, there has been increasing acceptance of the three-domain tree of life with taps roots of the Bacteria, the Archaea and the Eukarya. Moreover, it has been increasingly accepted that the Eukarya are descended from the Archaea, and not Bacteria. Next Generation Sequencing (NGS, also called deep sequencing) is now enabling science to apply ever more rigorous tests of the three-domain hypothesis; no small feat given that events in question likely occurred well more than a billion years ago. Technological advances have brought the cost of sequencing down to less than $1000/per full genome.

In the 6 May issue of Nature, Sprang et al. present research using NGS with impressive bioinformatics to define a new group of Archaea named Lokiarchaeota, and present strong evidence that places it as the closest known prokaryotic relative of the eukaryotes. Moreover, Lokiarchaeota’s genetic machinery are consistent with requirements for carrying out endocytosis or phagocytosis, as would have been required for a prokaryote to engulf a cyanobacterium as prescribed in the theory of endosymbiosis, leading to the mitochondrial powerhouses of eukaryote cells. This work portends that technology has reached a stage that many hypotheses about evolution in deep geologic time well be tested in the years ahead.

First comprehensive atlas of human gene activity released

A large international consortium of researchers has produced the first comprehensive, detailed map of the way genes work across the major cells and tissues of the human body. The findings describe the complex networks that govern gene activity, and the new information could play a crucial role in identifying the genes involved with disease.

“Now, for the first time, we are able to pinpoint the regions of the genome that can be active in a disease and in normal activity, whether it’s in a brain cell, the skin, in blood stem cells or in hair follicles,” said Winston Hide, associate professor of bioinformatics and computational biology at Harvard School of Public Health (HSPH) and one of the core authors of the main paper in Nature. “This is a major advance that will greatly increase our ability to understand the causes of disease across the body.”

The research is outlined in a series of papers published March 27, 2014, two in the journal Nature and 16 in other scholarly journals. The work is the result of years of concerted effort among 250 experts from more than 20 countries as part of FANTOM 5 (Functional Annotation of the Mammalian Genome). The FANTOM project, led by the Japanese institution RIKEN, is aimed at building a complete library of human genes.

Researchers studied human and mouse cells using a new technology called Cap Analysis of Gene Expression (CAGE), developed at RIKEN, to discover how 95% of all human genes are switched on and off. These “switches”—called “promoters” and “enhancers”—are the regions of DNA that manage gene activity. The researchers mapped the activity of 180,000 promoters and 44,000 enhancers across a wide range of human cell types and tissues and, in most cases, found they were linked with specific cell types.

“We now have the ability to narrow down the genes involved in particular diseases based on the tissue cell or organ in which they work,” said Hide. “This new atlas points us to the exact locations to look for the key genetic variants that might map to a disease.”

DNA: Celebrate the unknowns | Philip Ball

On the 60th anniversary of the double helix, we should admit that we don’t fully understand how evolution works at the molecular level, suggests Philip Ball.

This week’s diamond jubilee of the discovery of DNA’s molecular structure rightly celebrates how Francis Crick, James Watson and their collaborators launched the ‘genomic age’ by revealing how hereditary information is encoded in the double helix. Yet the conventional narrative — in which their 1953 Nature paper led inexorably to the Human Genome Project and the dawn of personalized medicine — is as misleading as the popular narrative of gene function itself, in which the DNA sequence is translated into proteins and ultimately into an organism’s observable characteristics, or phenotype.

Sixty years on, the very definition of 'gene’ is hotly debated. We do not know what most of our DNA does, nor how, or to what extent it governs traits. In other words, we do not fully understand how evolution works at the molecular level.

That sounds to me like an extraordinarily exciting state of affairs, comparable perhaps to the disruptive discovery in cosmology in 1998 that the expansion of the Universe is accelerating rather than decelerating, as astronomers had believed since the late 1920s. Yet, while specialists debate what the latest findings mean, the rhetoric of popular discussions of DNA, genomics and evolution remains largely unchanged, and the public continues to be fed assurances that DNA is as solipsistic a blueprint as ever.

[Read more]


If you haven’t heard by now - their ‘Real Vegan Cheese’ Indiegogo campaign is nearly fully funded - a team of Biohackers from Oakland, CA are currently developing cruelty-free vegan cheese by studying animal genomes to source natural milk-protein genetic sequences, which are then optimized for yeast to produce a yeast milk protein, synthesize, then, once placed in yeast cells, real milk-protein is produced from the DNA “blueprint” procured by the team.

Why do this? From the campaign site:

Indiegogo || Facebook || Twitter || Wiki || YouTube || Website

Read the article over at Motherboard to learn more, because this is as cool as it sounds.

Support this!

New Reprogramming Method Makes Better Stem Cells

A team of researchers from the University of California, San Diego School of Medicine, Oregon Health & Science University (OHSU) and Salk Institute for Biological Studies has shown for the first time that stem cells created using different methods produce differing cells. The findings, published in the July 2, 2014 online issue of Nature, provide new insights into the basic biology of stem cells and could ultimately lead to improved stem cell therapies.

Capable of developing into any cell type, pluripotent stem cells offer great promise as the basis for emerging cell transplantation therapies that address a wide array of diseases and conditions, from diabetes and Alzheimer’s disease to cancer and spinal cord injuries. In theory, stem cells could be created and programmed to replace ailing or absent cells for every organ in the human body.

The gold standard is human embryonic stem cells (ES cells) cultured from discarded embryos generated by in vitro fertilization, but their use has long been limited by ethical and logistical considerations. Scientists have instead turned to two other methods to create stem cells: Somatic cell nuclear transfer (SCNT), in which genetic material from an adult cell is transferred into an empty egg cell, and induced pluripotent stem cells (iPS cells), in which adult cells are reverted back to a stem cell state by artificially turning on targeted genes.

Until now, no one had directly and closely compared the stem cells acquired using these two methods. The scientists found they produced measurably different results. “The nuclear transfer ES cells are much more similar to real ES cells than the iPS cells,” said co-senior author Louise Laurent, PhD, assistant professor in the Department of Reproductive Medicine at UC San Diego. “They are more completely reprogrammed and have fewer alterations in gene expression and DNA methylation levels that are attributable to the reprogramming process itself.”

Read more here

Pictured: Scanning electron micrograph of cultured human neuron from induced pluripotent stem cell. Image courtesy of Mark Ellisman and Thomas Deerinck, National Center for Microscopy and Imaging Research, UC San Diego

Schizophrenia not a single disease but multiple genetically distinct disorders

New research shows that schizophrenia isn’t a single disease but a group of eight genetically distinct disorders, each with its own set of symptoms. The finding could be a first step toward improved diagnosis and treatment for the debilitating psychiatric illness.

The research at Washington University School of Medicine in St. Louis is reported online Sept. 15 in The American Journal of Psychiatry.

About 80 percent of the risk for schizophrenia is known to be inherited, but scientists have struggled to identify specific genes for the condition. Now, in a novel approach analyzing genetic influences on more than 4,000 people with schizophrenia, the research team has identified distinct gene clusters that contribute to eight different classes of schizophrenia.

“Genes don’t operate by themselves,” said C. Robert Cloninger, MD, PhD, one of the study’s senior investigators. “They function in concert much like an orchestra, and to understand how they’re working, you have to know not just who the members of the orchestra are but how they interact.”

Cloninger, the Wallace Renard Professor of Psychiatry and Genetics, and his colleagues matched precise DNA variations in people with and without schizophrenia to symptoms in individual patients. In all, the researchers analyzed nearly 700,000 sites within the genome where a single unit of DNA is changed, often referred to as a single nucleotide polymorphism (SNP). They looked at SNPs in 4,200 people with schizophrenia and 3,800 healthy controls, learning how individual genetic variations interacted with each other to produce the illness.

In some patients with hallucinations or delusions, for example, the researchers matched distinct genetic features to patients’ symptoms, demonstrating that specific genetic variations interacted to create a 95 percent certainty of schizophrenia. In another group, they found that disorganized speech and behavior were specifically associated with a set of DNA variations that carried a 100 percent risk of schizophrenia.

“What we’ve done here, after a decade of frustration in the field of psychiatric genetics, is identify the way genes interact with each other, how the ‘orchestra’ is either harmonious and leads to health, or disorganized in ways that lead to distinct classes of schizophrenia,” Cloninger said. 

Although individual genes have only weak and inconsistent associations with schizophrenia, groups of interacting gene clusters create an extremely high and consistent risk of illness, on the order of 70 to 100 percent. That makes it almost impossible for people with those genetic variations to avoid the condition. In all, the researchers identified 42 clusters of genetic variations that dramatically increased the risk of schizophrenia.

“In the past, scientists had been looking for associations between individual genes and schizophrenia,” explained Dragan Svrakic, PhD, MD, a co-investigator and a professor of psychiatry at Washington University. “When one study would identify an association, no one else could replicate it. What was missing was the idea that these genes don’t act independently. They work in concert to disrupt the brain’s structure and function, and that results in the illness.”

Svrakic said it was only when the research team was able to organize the genetic variations and the patients’ symptoms into groups that they could see that particular clusters of DNA variations acted together to cause specific types of symptoms.

Then they divided patients according to the type and severity of their symptoms, such as different types of hallucinations or delusions, and other symptoms, such as lack of initiative, problems organizing thoughts or a lack of connection between emotions and thoughts. The results indicated that those symptom profiles describe eight qualitatively distinct disorders based on underlying genetic conditions.

The investigators also replicated their findings in two additional DNA databases of people with schizophrenia, an indicator that identifying the gene variations that are working together is a valid avenue to explore for improving diagnosis and treatment.

By identifying groups of genetic variations and matching them to symptoms in individual patients, it soon may be possible to target treatments to specific pathways that cause problems, according to co-investigator Igor Zwir, PhD, research associate in psychiatry at Washington University and associate professor in the Department of Computer Science and Artificial Intelligence at the University of Granada, Spain.

And Cloninger added it may be possible to use the same approach to better understand how genes work together to cause other common but complex disorders.

“People have been looking at genes to get a better handle on heart disease, hypertension and diabetes, and it’s been a real disappointment,” he said. “Most of the variability in the severity of disease has not been explained, but we were able to find that different sets of genetic variations were leading to distinct clinical syndromes. So I think this really could change the way people approach understanding the causes of complex diseases.”


Leave me your DNA … and I’ll 3D-print your face | The Guardian

Your DNA is as personal as you can get. It has information about you, your family and your future. Now, imagine it is used – without your consent – to create a mask of your face. Working with the DNA bits left behind by strangers, a Brooklyn artist makes us think about issues of privacy and genetic surveillance.

Heather Dewey-Hagborg, a 30-year-old PhD student studying electronic arts at Rensselaer Polytechnic Institute has the weird habit of gathering the DNA people leave behind, from cigarette butts and fingernails to used coffee cups and chewing gum. She goes to Genspace (New York City’s Community Biolab) to extract DNA from the detritus she collects and sequence specific genomic regions from her samples. The data are then fed into a computer program, which churns out a facial model of the person who left the hair, fingernail, cigarette or gum behind. Using a 3D printer, she creates life-sized masks – some of which are coming to a gallery wall near you.

[Read more]

3D Sculpture pictured is by: Sophie Kahn


A Mitogenomic Phylogeny of Living Primates

  • by Knut Finstermeier, Dietmar Zinner, Markus Brameier, Matthias Meyer, Eva Kreuz, Michael Hofreiter and Christian Roos

“Primates, the mammalian order including our own species, comprise 480 species in 78 genera. Thus, they represent the third largest of the 18 orders of eutherian mammals. Although recent phylogenetic studies on primates are increasingly built on molecular datasets, most of these studies have focused on taxonomic subgroups within the order. Complete mitochondrial (mt) genomes have proven to be extremely useful in deciphering within-order relationships even up to deep nodes. Using 454 sequencing, we sequenced 32 new complete mt genomes adding 20 previously not represented genera to the phylogenetic reconstruction of the primate tree. With 13 new sequences, the number of complete mt genomes within the parvorder Platyrrhini was widely extended, resulting in a largely resolved branching pattern among New World monkey families. We added 10 new Strepsirrhini mt genomes to the 15 previously available ones, thus almost doubling the number of mt genomes within this clade. Our data allow precise date estimates of all nodes and offer new insights into primate evolution. One major result is a relatively young date for the most recent common ancestor of all living primates which was estimated to 66-69 million years ago, suggesting that the divergence of extant primates started close to the K/T-boundary. Although some relationships remain unclear, the large number of mt genomes used allowed us to reconstruct a robust primate phylogeny which is largely in agreement with previous publications. Finally, we show that mt genomes are a useful tool for resolving primate phylogenetic relationships on various taxonomic levels” (read more/open access).

(Open access sourcePLoS ONE 8(7): e69504, 2013; top image: Petter and Desbordes. 2013. Primates of the World: and Illustrated Guide. Princeton University Press)
Scientists develop a self-destruct button for DNA
Christopher Voigt dreams of programming living cells the same way engineers program robots.

CRISPR could protect genetic intellectual property by self-destructing synthetic sequences:

“A lot of efforts have been made around creating [biological] kill switches. We’re building on that, so that [a bacterium] wouldn’t just kill itself, but delete its synthetic DNA before doing that.” It’s like the biological version of hitting CTRL-Z.”

Wondering if it’s working with DNA Storage.

Detecting Fetal Chromosomal Defects Without Risk
Noninvasive sequencing is faster, cheaper and safer for mother and fetus, say researchers

Chromosomal abnormalities that result in birth defects and genetic disorders like Down syndrome remain a significant health burden in the United States and throughout the world, with some current prenatal screening procedures invasive and a potential risk to mother and unborn child.

In a paper published online this week in the Early Edition of PNAS, a team of scientists at the University of California, San Diego School of Medicine and in China describe a new benchtop semiconductor sequencing procedure and newly developed bioinformatics software tools that are fast, accurate, portable, less expensive and can be completed without harm to mother or fetus.  

“We believe this approach could become the standard of care for screening of prenatal chromosomal abnormalities,” said Kang Zhang, MD, PhD, professor of ophthalmology, founding director of the Institute for Genomic Medicine at UC San Diego and a staff physician at the San Diego VA Healthcare System.

The incidence of chromosomal abnormalities – in numbers or structure – is one in 160 live births in the United States, higher in other countries. In China, for example, the rate is one in 60 live births. The effects of these abnormalities, known as aneuploidies, can be severe, from developmental delays and neurological disorders to infertility and death. The incidence rate rises with maternal age, most notably after age 35.

Current diagnoses of fetal aneuploidies often rely upon invasive tests that sample amniotic fluid or placental tissues for fetal DNA that can then be analyzed using a variety of complex and expensive methods, including full karyotyping in which the entire set of chromosomes is viewed microscopically. While highly reliable, these invasive tests may cause infections in the pregnant woman and pose as much as a 1 percent risk of miscarriage and fetal loss. Results are not available for one to two weeks, extending anxiety for families waiting for information.

The new method relies upon massively parallel sequencing of cell-free fetal DNA using a benchtop semiconductor sequencing platform (SSP) called an Ion Torrent sequencer developed by Life Technologies. Cell-free fetal DNA is genetic material from the fetus that circulates naturally and freely in the mother’s bloodstream. It can be obtained through an ordinary blood draw, with SSP analysis achieved in less than four days.

To assess the SSP method, researchers tested 2,275 pregnant women. More than 500 participated in a retrospective analysis, undergoing full karyotyping to establish known chromosomal abnormalities followed by SSP testing. The remainder participated in a prospective study without prior karyotyping, and SSP testing results were then compared to karyotyping results. The sequencing and automated bioinformatics analyses were performed at iGenomics in Guangzhou, China.

“We used the retrospective study to establish the method and the prospective study to validate it,” said Zhang.

In the retrospective study, the researchers found that SSP detected multiple types of chromosomal abnormality with virtually 100 percent sensitivity and specificity compared to full karyotyping.

“To our knowledge, this is the first large-scale clinical study to systematically identify chromosomal aneuploidies based on cell-free fetal DNA using SSP,” said Zhang. “It provides an effective strategy for large-scale, noninvasive screenings in a clinical setting. It can be done in hospitals and outpatient clinics, more quickly and cheaply.”