Ancient Ancestors Had More DNA Than We Do Now: Have we Devolved?

Adding to the number of unsolved mysteries regarding the ancient origins of humanity and the biology of our species, scientists have discovered that we have less DNA now than our ancient ancestors possessed. Are we de-evolving?

A study published this week in the journal Science has found that modern humans lost DNA as we evolved after our split from apes. Our ancient ancestors, early humans, possessed substantially more amounts of genetic data than we do now. This surprising discovery raises many questions, the most obvious one being: why did we lose all that genetic information? Also, what difference has the loss made?

The short answer is: we don’t know yet.

According to news website Gizmodo, the team of researchers led by Professor Evan Eichler, geneticist at the Department of Genome Sciences, University of Washington, sequenced the genomes of 236 individuals from 125 distinct populations. They found that Homo sapiens have shed approximately 40.7 million base pairs of DNA after breaking from our closest living relatives, chimpanzees, around 13 million years ago.

Map of the 125 populations sampled in the study and their relation to each other. (P. Sudmandt et al 2015)

The genome of modern humans now contains 3 billion base pairs of DNA (complex molecules which contain all of the information necessary to build and maintain an organism, the building blocks of life), and even then scientists are unsure how much of that number is so-called “junk DNA”—genomic data whose function, if it has any, is not understood—but they do assert that at least 27.96 million of the base pairs lost were unique.

Common relationships were traced via DNA deletions among groups of humans. The longer lines show groups with more missing DNA. (P. Sudmandt et al 2015)

Have modern humans beneficially shed superfluous DNA, or have we lost something important over the generations?

Eichler proposes that a migration out of Africa reduced the human population in new areas and played a role in the loss of DNA.

Study authors write, “the breadth of the dataset allowed us to reconstruct the structure and content of the ancestral human genome prior to human migration and subsequent gene loss.’

‘As expected, Africans were more likely to show evidence of these ancestral sequences compared to non-African populations, as the latter have experienced more population bottlenecks and thus retained less of the ancestral human diversity.” Meaning that those individuals who were more connected with Africa had retained more DNA than those who had descended from migrated populations.

MailOnline reports, “The human genome has around three billion base pairs, which reside in 23 chromosomes in the heart of almost every cell in our body. The average gene in the human genome is around 765 base pairs long, meaning humans could have lost the equivalent of up to 37,000 genes since splitting from our ape cousins.”

Adding to this mix is the historic breeding of modern humans with the now extinct Denisovans and Neanderthals. Segments of Denisovan and Neanderthal DNA can be identified now in modern populations. But Neanderthals and Denisovans had around 104,000 base pairs in their genomes that are not found in modern humans. Researchers found that Neanderthals and Denisovans were missing some ancient DNA as well, suggesting these extinct species had lost significant portions of genetic code.

“Their results showed that our ancestors shed about 15.8 million base pairs of DNA before leaving Africa. As populations spread across Earth’s continents, they jettisoned additional chunks of DNA here and there. But certain populations have also been gaining DNA, mostly through duplication events where portions of the genetic code were accidentally copied and passed on,” reports Gizmodo.

While modern humans may presume that the shedding of DNA has honed us to the peak of evolutionary perfection, science can show that not all of our changes have been beneficial. In one example, research suggests that our hands are actually more primitive than those of our chimp ancestors, despite our adaptations for the use of tools.

Chimpanzee hand, at left, and human hand, right.

This is the first time scientists have documented the loss (and gain) of large chunks of DNA in ancient populations. This genetic research may shed light on the enduring questions of how modern humans evolved and survived while other hominin died out.

Scientists still can only speculate as to what these results indicate, but as more research is done we can fill in the missing gaps of our understanding of the ancient story of humanity.

Featured Image: A DNA molecule that is methylated on both strands on the center cytosine. DNA methylation plays an important role for epigenetic gene regulation in development and cancer. (C. Bock/Wikimedia Commons)

By Liz Leafloor    

First Complete Mapping Of Human Proteome Discovers 193 New Proteins

May 29, 2014 | by Janet Fang

Photo credit: Catalog of human proteins / H. Hahne, TUM

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In separate papers published this week, two independent teams have drafted the first maps of the human proteome -- which charts all of the proteins that make up a person. And both teams discovered that proteins do come from “noncoding” DNA sequences. 

The proteome is an important complement to the genome and transcriptome, and together they create a more complete resource for researching health and diseases. While genes determine many of our characteristics, they’re able to do that by providing instructions for making proteins. So these draft maps -- which you can think of as the Human Genome Project for proteins -- consist of profiles of proteins expressed in all sorts of different human cell types. Both drafts were generated using mass spectrometry. 

One of the teams, led by Akhilesh Pandey from Johns Hopkins University, identified and annotated proteins encoded by 17,294 genes – that accounts for around 84 percent of all the genes in the human genome that are predicted to encode proteins (that number is estimated at 19,629, if you’re curious). The team extracted proteins from samples of 30 different tissues, then used enzymes to cut them into small pieces called peptides. They ran the peptides through a series of instruments to identify and measure their relative abundance. 

They also discovered 193 novel proteins that come from regions of the genome that haven't been predicted to code for proteins. Within the genome, there are stretches of DNA whose sequences don’t follow a conventional protein-coding gene pattern – these have been labeled as noncoding. “The fact that 193 of the proteins came from DNA sequences predicted to be noncoding means that we don’t fully understand how cells read DNA, because clearly those sequences do code for proteins,” Pandey explains in a news release. 

The other team, led by Bernhard Kuster of Technische Universität München (TUM) in Germany, assembled protein evidence for over 18,000 genes (or 92 percent of the entire proteome) by compiling raw mass spec data from databases and other analyses that were already available. These include a core of 10,000–12,000 proteins expressed in several different tissues, and to fill in the gaps, they generated their own mass spec data by analyzing 60 human tissues, 13 body fluids, and 147 cancer cell lines. 

Like the Hopkins team, they also found evidence of translation from DNA regions that were not thought to be translated. This includes more than 400 translated long, intergenic non-coding RNAs (lincRNAs). "While we have a good idea of what the genome looks like, we didn't know how many of those potentially 20,000 protein-coding genes would actually make protein," Kuster tells BBC. The team also identified protein markers that may pre

dict an individual’s resistance or sensitivity to drugs for diseases like cancer.

“You can think of the human body as a huge library where each protein is a book,” Pandey says. “The difficulty is that we don’t have a comprehensive catalog that gives us the titles of the available books and where to find them.” Now it looks like we’ve got two first drafts of that comprehensive catalog. Each group has built a publicly accessible, interactive database of their datasets: Human Proteome Map and ProteomicsDB. 

Although they had seen each other's work at conferences, both Pandey and Kuster tell BBC they had "no idea" they were headed towards publishing simultaneously. And now they share a Nature cover. "We never saw this as a race to be first," Kuster says. "My interpretation is that when the time is right, somebody's going to just do it. And perhaps two people are going to do it!" Here's the human body map of protein expression. 

The findings [here and here] were published in Nature this week. 

[Johns Hopkins, TUM via The Scientist, BBC]

Images: H. Hahne, TUM

Semi-Synthetic Organism Uses New DNA Bases

 by Lisa Winter

Photo credit: schulergd

Life, on the most basic level, is incredibly simple in theory yet vastly complex in practice.

DNA is made out of only four nucleic acids: adenine which pairs with thymine, and cytosine which pairs with guanine. For simplicity’s sake, these molecules are typically referred to by just their first letter. A set of three ‘letters’ is known as a codon, which is how DNA is read.

There are 64 possible codons that code for one of 20 standard amino acids (though three are used for punctuation purposes) for eukaryotes. The order in which the amino acids are put in the chain will determine the shape, structure, and function of all the different proteins created.

If all of that diversity can stem from only 4 nucleic acids, what would happen if new ‘letters’ were introduced to the genetic alphabet?

Recent research led by Floyd Romesberg of The Scripps Research Institute leads us one step closer as his team has created a plasmid with a novel pair of nucleic acids known as d5SICS and dNaM in the sequence and introduced it into E. coli bacteria.

Though this has been shown possible in a test tube, this is the first time it has been accomplished in an organism. The details of the research have been described in Nature.

Before anyone gets worried that this new DNA data is going to take over the world or some such nonsense, don’t get too ahead of yourself. Since these molecules aren’t found in natural cells, the ingredients to make them aren’t readily available in cells either.

The researchers were able to make this breakthrough by utilizing a triphosphate transporter found in microalgae that was capable of dealing with these new additions.

"When we stopped the flow of the unnatural triphosphate building blocks into the cells, the replacement of d5SICS-dNaM with natural base pairs was very nicely correlated with the cell replication itself—there didn't seem to be other factors excising the unnatural base pairs from the DNA," lead author Denis Malyshev said in a press release. "An important thing to note is that these two breakthroughs also provide control over the system. Our new bases can only get into the cell if we turn on the 'base transporter' protein. Without this transporter or when new bases are not provided, the cell will revert back to A, T, G, C, and the d5SICS and dNaM will disappear from the genome."

While these new molecules work well during DNA replication, the next steps in the research will be to manipulate RNA so they can be integrated into the synthesis of new unnatural proteins. This could be used for information storage as well as a new family of nanomaterials

Scientists Believe They Have Explained The Great Flu Outbreak Of 1918

by Stephen Luntz

Photo credit: US Naval Centre. This scene of mass hospitalization in Dartmouth from the 1918 flu epidemic was repeated all around the world

A paper claims to have solved on of the most important puzzles in infectious disease research: what made the 1918 influenza pandemic so lethal?

“Ever since the great flu pandemic of 1918 it has been a mystery where that virus came from and why it was so severe,” says Professor Michael Worobey of the University of Arizona. Between 50 and 100 million people died from the outbreak dubbed “the Spanish flu”, several times more than World War I, yet history books generally relegate it to a footnote.

While most of those who die from normal flu outbreaks are the very young or the elderly the 1918 outbreak was different – the heaviest death toll was among young adults, including those that had been in good health beforehand.

Interest is more than historical. There is little reason to doubt that a similar strain could return, and while modern medical technology would limit the death toll, no healthcare system in the world could cope with the volume of patients struck down in such a short period. Moreover, airtravel would likely see the disease cross the globe far faster than in an era when circumnavigating the world in 80 days was still the benchmark for speed.

The reason we still lack a universal flu vaccine is that the virus is always scrambling the hemagglutinin and neuraminidase proteins on its surface. "Imagine a soccer ball studded with lollipops," said Worobey. "The candy part of the lollipop is the globular part of the HA protein, and that is by far the most potent part of the flu virus against which our immune system can make antibodies. If antibodies cover all the lollipop heads, the virus can't even infect you." A different sort of lollipop, but with the same type of stick, will still attract antibodies that won't prevent infection but may slow the development of the virus “which protects you from severe disease and death," Worobey said.

Once infected or inoculated our body produces defenses against a particular combination, but these are of little or no use against a different form. The 1918 version has been labeled H1N1. Other versions of H1N1 have appeared since – the so called “swine flu” epidemic of 2009 was treated with such alarm because it was also H1N1 - but none have been so lethal.

Worobey compared samples from different H1N1 outbreaks to try to find the origins of the 1918 catastrophe. He thought this might settle debate between the two competing theories – a jump from birds or the reshuffling of genes between existing human and swine varieties. Instead in the Proceedings of the National Academy of Sciences he proposes a third option in which a human flu virus with the H1 protein in circulation for 10-15 years gained the N1 genes from a version infecting birds. He believes previous researchers have missed this because after 1922 a slightly different form of H1 displaced the one responsible for the 1918 outbreak, and scientists have been examining the wrong one until samples taken during the original outbreak were found.

"It sounds like a modest little detail, but it may be the missing piece of the puzzle," Worobey said. "Once you have that clue, many other lines of evidence that have been around since 1918 fall into place." 

It has previously been suggested that the reason people over 35 were less likely to die in the 1918 epidemic might be because they had been exposed to a form of flu with some similarity to the epidemic of that year; the same lollipop stick in Worobey's analogy. While the common features might not have been enough to stop them getting sick the immune system would have had just enough recognition to save their lives. Worobey endorses this, suggesting widespread exposure to either H1 or N1 in childhood would explain the relatively low death rate among the elderly from the pandemic.

However, Worobey also turns the idea on its head by proposing exposure to a very different version of the flu virus primed the immune system to misread epidemic version. The finger of suspicion is pointed at an H3N8 virus common between 1889 and 1900. Tens of millions of people would have been exposed to this virus in childhood and recovered, but Worobey said, “A person with an antibody arsenal directed against the H3 protein would not have fared well when faced with flu viruses studded with H1 protein. And we believe that that mismatch may have resulted in the heightened mortality in the age group that happened to be in their late 20s during the 1918 pandemic." 

Of course people could have been infected by both the H3 and the H1 versions at different times, but essential to Worobey's thesis is the idea that the first infection has the most impact in terms of the antibodies produced, what some researchers have called “original antigenic sin”. Even if they were infected by an H1 version in the early years of the century, those whose first exposure was to H3N8 were vulnerable.

Whether prior infection by the H3N8 virus was better than nothing remains unclear. On the one hand, island populations that may never have encountered flu at all experienced death rates higher than anything seen in urban areas. On the other,in places with good health records there is an extraordinary match in the death rates between those people who would have been exposed to H3N8 as their first dose of flu and the proportion who died (see chart below),

Worobey found support from recent outbreaks to back his theory up. In recent years The H5N1 virus has been much more likely to kill people born after 1968 than before. On the other hand, H7N9 is lethal to those born earlier, particularly in the late 1940s. He attributes this to each group having been exposed to a particular virus when young that offered some protection against one of the recent strains, but not against the other.

The good news here is that much of the population has now been immunized against numerous strains of flu. While these might not be enough to stop people getting sick from a novel version, it should keep the death rates down if we experience something as potentially devastating as the 1918 outbreak again. Further research on the way specific hemagglutinin and neuraminidase match up might help us design vaccines that would offer widespread partial protection to cover all options for future pandemics.

Confirmation of Human Neanderthal Interbreeding

 by Stephen Luntz

Photo credit: ICHTO. Come on, isn't it clear why humans interbred with Neanderthals like this one

A new study claims to have settled one of the great debates of human evolution, concluding that modern humans interbred with Neanderthals.

It is known that people whose recent ancestry is in Africa have fewer genes in common with Neanderthals than those whose origins lie in Europe or Asia.

However, there are two explanations for this. The more obvious one is that humans and Neanderthals occasionally got frisky, and that the genetic relationship was close enough that some of the offspring survived to pass on their genes to us. Call it the Clan of the Cave Bear scenario.

The alternative is that Neanderthals split off from a sub-population of our common ancestors, and that this sub-population also provided most or all of the people who subsequently left Africa. 

The debate between these two has gone back and forth. Like most matters in the field of early human origins it has become rather heated at times. Previous methods of genome analysis have struggled to distinguish between the two.

Now a paper in Genetics may have found a way through the issue. “Our approach can distinguish between two subtly different scenarios that could explain the genetic similarities shared by Neanderthals and modern humans from Europe and Asia," said co-author Dr Konrad Lohse of the University of Edinburgh. 

The technique was originally developed for comparing related insect species and subspecies, as well as isolated island populations of pigs in South East Asia."Because the method makes maximum use of the information contained in individual genomes, it is particularly exciting for revealing the history of species that are rare or extinct," said Lohse.

Lohse compared four genomes, those of an African, someone from outside Africa, a chimpanzee and Neanderthal fossil. He split the genome into short blocks and created estimates of the likelihood of the two scenarios for each given the similarities of the two modern humans compared to the other species. The method proved robust for different block lengths. The paper states, “Our analysis allows us to conclusively reject a model of ancestral structure in Africa and instead reveals strong support for Neanderthal admixture in Eurasia.”

The study also found a higher proportion of Neanderthal genes in non-African humans than previous research (3.4-7.3%, rather than 1.5-2.1%). However, Lohse says different methods will produce somewhat different results on this question.

Lohse estimates the time for the divergence between humans and Neanderthals as 329-349 thousand years ago, and between those who left Africa and those who stayed behind at 122-141 thousand years. His work is consistent with recent studies suggesting there was also interbreeding amongst humans and Neanderthals with Denisovans and another mystery relative as well, although many estimates of the dates for leaving Africa are substantially later.

Genetics Editor-in-chief Mark Johnston praised the work for not only putting the controversial question to rest, but opening a path to understanding other species' evolutionary history. 

Settling the question is important for our understanding of our own history. It also arguably tells us something philosophically significant about or place in nature and our capacity to relate to those different from ourselves.

Copied by S.M. Anderson

 

Summery:

Adopted off the black market, Alexander Mitchell, has no idea his DNA is copyrighted and property of military weapons giant Texacom Defense. Nor that his DNA is being used to develop an army of clones. When the company discovers he was not properly disposed of 17 years ago, they send an assassin copy, BETA23, to terminate Xan and cover it up.

After he narrowly escapes BETA23’s first attempt, Xan teams up with Lacey, a genetically engineered genius he’s surprised to find common ground with— only they’re awkward together. Half of the time she stares at Xan like the science project he is and the other half…let’s just say Xan can’t keep his eyes off her lips.

When they manage to capture a company copy by luck and sheer stupidity on Xan’s part, Lacey is determined to see the good in their prisoner to the point she believes BETA23 can be persuade to give them the intelligence they need to keep the company forever off Xan’s back. Xan’s not sure if he can trust the darker version of himself, not when it means gambling with the lives of his family and the possibility of losing Lacey.

My review:

It amazing that I have to write review on 2 books at the same time that deal in the subject of genetics. This one - Copied that deal with human genetics and the other one "A cure to die for" which deal with plant genetics. Both of them also deal with heavy ethical issues. In both of them I intend to divide my review to 2 - one part which will deal with the plot and the other with some technical subjects ( I can't prevent this Biology is in my blood).

 For the plot of Copied - The book is a fast reading it is really enchanting and I couldn't stop reading it. The story makes you think a lot  about the ethics of cloning and gratitude for individualism. It is presented in the voice of two main characters - Xan (Alexander Mitchell) and Betha - 23 . While Xan raised with a normal family Betha is a Texacomdefense's company property;

Betha-23 was raised with other many clones like him from the same DNA template from one donor (this donor isn't alive anymore) in artificial womb. All the clones get the same treatment from their first day as embryo till the day they will sent so the recycling tank. As a company property they are not allowed to independent thought, they have to obey to their superior without any questions, some of them trained to be a perfect war machines, some will sent to study.Their life span program short from the beginning and to extend it they have to get a treatment of enzyme that will prevent the quick process of aging (In a way it ensure the dependency of the clones in the company, and their returned). In his training wasn't any place for emotions , farther then emotions and empathy considered as weakness. They had to analyzed, coldly, the situations and seek the most efficient benefits out of them.... This time Betha mission was to get rid from Xan. He orchestrate a very complex situation with burning of a building in this situation Xan had to die and also Miels his best friend which wasn't in the right place and the right time. To his advantage he use his face which were identical to Xan to lead the blame on Xan head (and now you already understand that Betha and Xan share the same DNA).

Xan (Alexander Mitchell) -  after this "accident" everybody, include Xan parents and his best friend Miles and his  girlfriend Malinda were sure that Xan is guilty. Till this moment Xan didn't now about cloning and the other clones which has identical DNA to his. He also puzzled about his mysterious rescuer, who saved him from the fire.  Xan was desperate and the only friend face was belong to Lacy (which considered as a genius nerd and never went around Xan's fellows). Lacy came with friend of her own - Jamal and Allen very smart and brilliant - Jamal has a very successful blog about conspiracy theories and he will be the one of these two who will help the most.

Meanwhile Betha put a surveillance at Xan and Lacy's home and could follow each move of them. When he in his calculation he reached to conclusion that Lacy is a  big risk factor he put a sophisticated bomb under the sink in her privet lab at home. It was a sheer luck that she found it with one of her old nanny camera's. Xan was amazed to find a similar face on the assassin. At the same time he discovered that he was adopted by his parents. He wanted to know about his real parent and after many inquiries , his father admitted that they know nothing about them.

Xan sent to himself a message to meet with  Betha knowing that Betha will track it. Lacy followed him and together they caught him, because alone he didn't has a chance against his trained clone. Now they both hoped to get some information.

Love and relationship -  Xan find himself feeling toward Lacy. His girlfriend, Malinda, didn't lose hope that they will return to each other. His relationship with his Best friend Miles reached to an end. Xan shaw to his adopted parents that he still love and care for them and vica versa. Betha surprised to find a soft emoticons toward Lacy. But Lacy don't know which she prefer more Betha or Xan. The staying so long out side the company compound cause a big change in Betha toward what it is important.

I can't say more without taking the reader trill of finding thing all by himself so now I'll pass to the second part of my review.

In terms of a relationship between cloning and genetic engineering, there is obvious overlap between the two fields- Specifically, in relation to human germ line genetic modification, cloning provides a powerful set of tools that, if certain technical improvements are forthcoming, could enable gene targeting [that disrupts or mutates a gene sequence]. A second breakthrough has been the ability to make artificial eggs or sperm from stem cells, either embryonic or adult stem cells that can develop into different cell types in the human body. The third breakthrough involves "designer" recombinant molecules that have the ability to break apart and reassemble DNA strands. Each technology could eventually help scientists make genetic modifications to a living organism's genome.

The cloning idea -  or why clone human embryos at all?
 The answer is stem cells. Stem cells are primitive, unspecialized cells.  Scientists classify the natural stem cells in mammals into two broad categories: adult stem cells and embryonic stem cells. Adult stem cells are found in various tissues and replenish the cells found in those specific tissues, such as skin or blood. Embryonic stem cells are from the embryonic stage of development, and can differentiate into all the varied cells found in a complex organism, from the brain down to the toes. A 5-day-old human embryo, called a blastocyst, contains an inner cell mass composed of about 12 embryonic stem cells. Doctors have hoped to use embryonic stem cells to essentially repair damaged tissue - injecting them into a spinal cord, for example, to grow new nerve cells after paralysis.  This talent that could make them the stars of regenerative medicine, the goal of which is to grow fresh cells and tissues from patients suffering from various diseases. Most of the scientist will say: "We think that it is wrong to attack some innocent human lives here and now to help others down the road,"(which is one of the subjects that Copied is dealing with). Fortunately, the great advances we are seeing in the use of adult and iPS stem cells provide promising alternative ways to heal illnesses without raising people’s temptations to engage in such attacks" - Based on this I was sundries to find the idea of recycling tank at the story, knowing that there is no need to all body to replace an organ. Also on based that even attaching the person organ itself is still problematic and given to a very narrow time window .

The cloning procedure works by combining a patient's body cell with an unfertilized egg cell from a donor. Since the 1950s when researchers cloned a frog, scientists have cloned dozens of animal species, including mice, cats, sheep, pigs and cows. When  it published that researchers have used cloning to make human embryos for the purpose of producing stem cells may have some people wondering if it would ever be possible to clone a person. Although it would be unethical, experts say it is likely biologically possible to clone a human being. But even putting ethics aside, the sheer amount of resources needed to do it is a significant barrier. Also, in each case, researchers encountered problems that were needed to be overcome with trial and error.

With mice, researchers were able to use thousands of eggs, and conduct many experiments, to work out these problems. But with primates, eggs are a very precious resource, and it is not easy to acquire them to conduct experiments. For instance, cloning an animal requires that researchers first remove the nucleus of an egg cell. When researchers do this, they also remove proteins that are essential to help cells divide. What's more, cloned animals often have different kinds of genetic abnormalities that can prevent embryo implantation in a uterus, or cause the fetus to spontaneously abort, or the animal to die shortly after birth. These abnormalities are common because cloned embryos have just one parent rather than two, which means that a molecular process known as "imprinting" (Differentiation of cells to target tissues) the  does not occur properly in cloned embryos.

Growing in artificial wombs -  The idea of genetically modified humans living healthier lives may not appease those who fear the "Cloud Atlas" vision of mass-manufactured clone workers. Luckily for them, the science fiction idea of growing humans in artificial wombs may take far longer to realize than human genetic modification. One of the biggest challenges comes from recreating the placenta that helps transmit nutrients and oxygen from the mother to the growing human fetus.

 As for genetic Enhancement: In the story we meet Lacy - she is very very smart actually she is genius. Her father is rich nan who work in analyzing economic opportunities for pharmaceutical company. In the story we had been told that her cleverness is a result of "gentle intervention" in her genes. The only problem is that genius is a result of many many genes that of them contribute in its own way to this ability. I just can't see hoe it was a "gentle intervention". The other problem is how to direct the intervention to the right places. If her indeed came from her parents it was enough that she inherit her cleverness from at list one parent.

Lacy's mother has a sever Muscular dystrophy . Muscular dystrophy -  characterized by progressive skeletal muscle weakness, defects in muscle proteins, and the death of muscle cells and tissue.  There are more than 30 types of MD.  Duchenne and Becker muscular dystrophies, being caused by a mutation of a gene located on the X chromosome, predominantly affect males, although females can sometimes have severe symptoms as well. Most types of MD are multi-system disorders with manifestations in body systems including the heart, gastrointestinal system, nervous system, endocrine glands, eyes and brain. Antisense therapy is a form of treatment for genetic disorders or infections. When the genetic sequence of a particular gene is known to be causative of a particular disease, it is possible to synthesize a strand of nucleic acid (DNA, RNA or a chemical analogue) that will bind to the messenger RNA (mRNA) produced by that gene and inactivate it, effectively turning that gene "off". Alternatively, the strand might be targeted to bind a splicing site on pre-mRNA and modify the exon content of an mRNA.

According the story Lacy don't have the disease and don't even carry it. also according to the story her father is a carrier. So how come? One possibility is that she is not her parents daughter at list not her mother which carry two defected genes. But if her father is a carrier she had at list to carry his mutation on her chromosome X. There is  other possibility is that somehow somebody fixed the mutation in the her embryo cells. To this day it is very hard to direct the right "fixing" to it's place on the DNA strand.

OK enough with technical things  - the bottom line is that the story stand for itself it very fast going and very interesting and I recommend it with all my heart !!!

About S.M. Anderson

S. M. Anderson (Sarah Anderson) was born in Lima, Peru. She has lived in seven different countries, on five continents, and speaks a smattering of languages. As a child and even young adult, writing and reading were difficult for her, so difficult that she received extra help outside the classroom and was diagnosed with a learning disability. However, she always loved stories, especially ethnic folktales from the countries she lived in. It was the desire to create stories of her own that fueled her determination to overcome the challenges that came with writing. She has a BA in Art Education from BYU, with a minor in Russian, and a love of power tools. She has a growing family of three kids and currently lives in Springville, Utah.

Interview:

What inspired Copied?

I had sort of a Doc. Brown flux-capacitor moment. I was sitting in the passenger seat of my car on that open stretch of highway between Las Vegas and LA, when I had this scene play out in my mind of a scientist saying his last farewells to his cloned son, before representatives from a company arrived to exploit the scientist’s creation.
This scene was the premise behind Copied and at one point was part of a prologue. The prologue was eventually axed, but I hope reconstruct it as a novella length prequel sometime in the future.

What was your favorite scene to write?

The awkward kissing scene. This is a little embarrassing to admit, but some of it was based off of personal experience. I also enjoyed the final fight scene after I took the time to act it out. Before then it was just a headache.

If you could have lunch with any author or character, who would it be and where would you go?

Hmm this is a rather difficult one. I think I would prefer a character over an author, just because I’d be afraid of falling into total fan mode, my normal self is awkward enough. I’d probably want to meet Harimad sol from the Blue Sword, eat traditional Damarian food at the palace, and go for a ride on a bridle-less horse. And for course since this is fantasy, I’d be awesome at it.

What book most influenced your life?

My intention is not to go into religion here, but the book that has most influenced my life is the Book of Mormon.  I struggle with dyslexia and when I was in elementary school reading was very difficult for me—almost physically painful. Now I want to pause and thank all my elementary teachers who took the time to read to me. I was so starved for stories that I savored every minute they read out loud. I would even borrow my mom’s audio books and listen to them alone in my room just to satisfy my need for stories.
In Junior high I decided to read the Book of Mormon, a severe undertaking for a kid who had never finished a book (aside from the picture ones) on her own. I was probably at a 3^rd grade reading level when I started, maybe a 4^th.  I was that kid who would refuse to read aloud because if I did the other kids would make fun of me as I stumbled over every other word.
Anyway, it took two years and when I was finished I could read anything. Even adult books. I was like a person who hikes a hill after climbing a mountain. The first book I read after that was the Blue Sword. I went on to read books by; Robert Heinlein, Anne McCaffrey, Louis L’amour, and many more. 

Have you always wanted to be a writer?

Ha, no way. In college I actually avoided English like it was the plague and if I found out that professor tested via essays and another via multiple choice, I would drop the first class and switch to the second.
Plus, my first draft of Copied looks like it was written by an eighth grader and that’s being generous.

How long did it take to write Copied?
Four years to contract.

What does it take to become an author?

Work.

Excerpt:

Beta opened his swollen eyes. Craning his neck sideways, he took a good look at his surroundings. Pain throbbed through his skull and down his spine. Everything blurred, but the outline of the shelves confirmed he was still in the storeroom. His mouth omitted a soft groan. The screech of a heavy wooden chair sliding across the tile floor resonated in his ears, and Beta winced. The slight flex of his facial muscles shot needles of pain through the bruises on his face.

A blurry figure appeared above him. “How are you feeling?”

He waited a moment for his vision to clear and ignored the burning itch of his skin as his cells started the process of regeneration.

Lacey hovered over him, brow furrowed and lips pursed as she examined him. When he didn’t respond, she rested a hand on his shoulder and gave it a little shake.

“Beta?”

The light touch of her palm sent a wave of energy through him. He jolted upright. “Ouch!”

Pain so severe that he felt like the walls of his head would collapse in on themselves riveted through his body.

She winced. “Sorry. I didn’t mean to startle you. Please don’t move if it hurts.”

Beta scooted to the top of the bed and leaned his back against the brass headboard.

“You didn’t startle me. I just…” His voice trailed off. He couldn’t think of a way of saying what he meant without sounding weak.

“Never mind.” She gingerly touched the edge of his swollen eye with the tips of her fingers. “Are you in pain?”

He stiffened like the reflex of a beaten animal the first time it knows the touch of a gentle hand. Why should she care? “It’s fine. We heal quickly.”

Her gaze slid across his face. She probed every bruised nook and cranny. There was a hunger in her eyes as if she was the question and he the answer. He felt something else too; an emotion or feeling that he couldn’t put a name to. Something he'd never, in his short life, experienced. Beta stared past her, his eyes focused on the faint brush strokes of the wall’s dried white paint. If he could just ignore the strange new animal that had awakened inside him, he’d rally again and escape.

He cleared his throat.

“Sorry.” Lacey pulled back. “You must be hungry.”

She disappeared from the room and returned with a tray of food in her hands. Then she unfolded two short legs from the bottom of the tray and laid it across his lap. A loose strand of her ebony hair brushed against his cheek. Beta’s fingers twitched, knocking his wrists against the handcuffs. He wanted to tangle his hands in that silky-looking hair, just to know what it felt like.

She dipped a spoon into a bowl full of watery soup and pressed a mouthful to his lips. Beta slurped down soft noodles with bits of chicken. Warmth spread from his belly to the rest of his body. He glanced up at Lacey’s face, inches away from his. Large red marks ran along the side of her jaw and neck. His throat tightened, remembering he had been responsible for those bruises. The little air he could suck in with bruised ribs tasted stale and stagnant. Another new sensation breached the impenetrable hold of his heart, this one unbearable. Beta swallowed hard. He had never regretted hurting someone before.

Praised for Copied:

“A chilling tale of nature vs. nurture, the power of trusting, and the belief in the transformative power of kindness to change who we are. The underlying theme that we can choose to be whoever we want to be, despite what we’ve been taught, screams from the pages of Copied.” -Cindy M. Hogan, author of the Watched trilogy.

Copied by S. M. Anderson was a fresh, exciting novel that seamlessly wove together elements of science fiction with our everyday world. Not only was it a great read, but it got me thinking–what makes a person truly unique, and what would happen if that uniqueness was challenged? I definitely recommend it.”  - Tristi Pinkston, freelance editor and author

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Copied

by S.M. Anderson

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