Category Archives: DNA

A cloned human embryo is seen in this file photo. Centre for Life File

Right now, such genetic manipulation of human embryos isn't known to be possible, and no one could do it in the U.S. The Food and Drug Administration would have to approve it and is barred by Congress from using its funding to consider anything that involved changing a human embryo.

It might be possible down the road, and labs in other countries might do it, the committee said in its

And if someone finds a way to prevent disease using these techniques, there would be a clamor for it to be made available.

"However, genome editing to enhance traits or abilities beyond ordinary health raises concerns about whether the benefits can outweigh the risks, and about fairness if available only to some people," said Alta Charo, a bioethicist at the University of Wisconsin who helped chair the panel.

Gene therapy is still experimental. The idea is to treat genetic disease by replacing faulty genes with healthy ones. But the technique is imprecise.

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Gene editing is a big step up from simple gene therapy. New techniques, such as one called CRISPR, allow scientists to precisely alter genes in a much more controlled way than before, offering the possibility that embryos could be changed not only to prevent the development of genetic diseases, but to prevent any resulting children from passing harmful traits to their own offspring.

In 2015, Chinese scientists

One obvious question is whether labs might try to offer parents babies that are prettier, smarter or stronger than the genetic lottery would otherwise allow them to be. It's not so easy: even eye color is not controlled by a single gene or even a few genes, and there are no known genes for intelligence.

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But a genetic disease such as muscular dystrophy is caused by easily measured genetic mutations, and it's possible that finding a genetic cure for MD might lead to ways to make healthy babies more muscular, the panel said.

"And using the technology to increase someone's muscle strength to the extreme end of human capacity (or beyond) would almost certainly be considered enhancement," the report reads.

That's when people might need to start thinking about how far is too far to go in improving children.

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Tests for so-called germline editing for people would be ethically acceptable if there were no reasonable alternatives; if it was being done to prevent a serious disease or condition and if the genes being changed were clearly shown to cause the condition, the panel recommended.

Any change should resemble naturally occurring genetic sequences, not introduce some exotic change to DNA, the panel added. Data should be openly shared and there should be oversight, it added.

Some of the better known genetic diseases include muscular dystrophy, cystic fibrosis and the premature aging disease progeria, but there are dozens more.

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Edited DNA OK for Health, But Not Designer Babies, Panel Says - NBCNews.com

The researchers' findings suggest that DNA variations linked to Type 2 diabetes interfere with the ability of Regulatory Factor X to bind to a "runway" of DNA before the start of various genes, and therefore with its ability to do its job in the reading of those genes.ANN ARBORWhy do some people get type 2 diabetes, while others who live the same lifestyle never do?

For decades, scientists have tried to solve this mysteryand have found more than 80 tiny DNA differences that seem to raise the risk of the disease in some people, or protect others from the damagingly high levels of blood sugar that are its hallmark.

But no one "type 2 diabetes signature" has emerged from this search.

Now, a team of scientists has reported a discovery that might explain how multiple genetic flaws can lead to the same disease. They've identified something that some of those diabetes-linked genetic defects have in common: they seem to change the way certain cells in the pancreas "read" their genes.

The discovery could eventually help lead to more personalized treatments for diabetes. But for now, it's the first demonstration that many type 2 diabetes-linked DNA changes have to do with the same DNA-reading molecule. Called Regulatory Factor X, or RFX, it's a master regulator for a number of genes.

The team reporting the findings in a new paper in the Proceedings of the National Academy of Sciences comes from the University of Michigan, National Institutes of Health, Jackson Laboratory for Genomic Medicine, University of North Carolina and University of Southern California.

They report that many diabetes-linked DNA changes affect the ability of RFX to bind to specific locations in the genomes of pancreas cell clusters called islets. And that in turn changes the cells' ability to carry out important functions.

Islets contain the cells that make hormones, including insulin and glucagon, which keep blood sugar balanced in healthy people. In people with diabetes, that regulation goes awryleading to a range of health problems that can develop over many years.

"We have found that many of the subtle DNA spelling differences that increase risk of type 2 diabetes appear to disrupt a common regulatory grammar in islet cells," said Stephen Parker, assistant professor of computational medicine and bioinformatics, and of human genetics, at the U-M Medical School. "RFX is probably unable to read the misspelled words, and this disruption of regulatory grammar plays a significant role in the genetic risk of type 2 diabetes."

Parker is one of four co-senior authors on the study, which also includes Michael Boehnke of the U-M School of Public Health's Department of Biostatistics; Francis Collins, director of the National Institutes of Health; and Michael Stitzel of the Jackson Laboratory.

Prior to their current faculty positions Parker and Stitzel worked in Collins' lab at the National Human Genome Research Institute. Parker's graduate student, Arushi Varshney, is one of the study's co-first authors with Laura Scott and Ryan Welch of the U-M School of Public Health's Department of Biostatistics and Michael Erdos of the National Human Genome Research Institute.

They performed an extensive examination of DNA from islet samples isolated from 112 people. They characterized differences not just in DNA sequences, but also in the way DNA was packaged and modified by epigenetic factors, and the levels of gene expression products that indicated how often the genes had been read and transcribed.

This allowed them to track the "footprints" that RFX and other transcription factors leave on packaged DNA after they have done their job.

RFX and other factors don't bind directly to the part of a gene that encodes a protein that does a cellular job. Rather, they bind to a stretch of DNA near the genea runway of sorts. But when genetic changes linked to type 2 diabetes are present, that runway gets disrupted, and RFX can't bind as it should.

Each DNA change might alter this binding in a different way, leading to a slightly different effect on type 2 diabetes risk or blood sugar regulation. But the common factor for many of these changes was its effect on the area where RFX is predicted to bind, in the cells of pancreatic islets.

So, says Parker, this shows how the genomethe actual sequence of DNAcan influence the epigenome, or the factors that influence gene expression.

The researchers note that a deadly form of diabetes seen in a handful of babies born each year may be related to RFX mutations. That condition, called Mitchell-Riley syndrome, involves neonatal diabetes and malformed pancreas, and is known to be caused by a rare autosomal recessive mutation of one form of RFX.

In addition to co-senior and co-first authors listed above, the study's authors include a range of researchers from several institutions. The study was funded by the National Institutes of Health.

Parker is a 2014 recipient of the American Diabetes Association's Pathway to Stop Diabetes grant, a type of grant awarded annually by the American Diabetes Association to provide up to $1.625 million to each scientist over a five- to seven-year grant term to spur breakthroughs in clinical science, technology, diabetes care and potential cures. Since launching in 2013, Pathway has awarded more than $36 million to 23 leading scientists.

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Diabetes in your DNA? Scientists zero in on the genetic signature of risk - U of M News Service

We have all seen those advertisements on television. Spit here, scrape there and send the samples in to have your DNA analyzed.

But what really happens? What can you really learn?

There are a variety of tests available and each company has its merits. The company you choose will probably be determined by what you want to learn.

It may sound unfair but only men can have their yDNA studied, which will follow their male line from their father through his father through his father and so forth. Simply put, fathers pass the yDNA only to their sons, which makes them boys. This can follow family name, but not always.

People changed last names more often in past human history than they do now in this computer age. They changed spellings because they couldnt spell or they wanted to seem more English to blend in. There were adoptions, rapes, plagues, invasions and affairs. Children were orphaned, abandoned, kidnapped and rescued. There were indentures, slavery and people running away from their past. This was life then and our history. Dont be upset if you cannot follow a name very far. Just assume it was for a good purpose and move on.

In the yDNA test you can opt to have a 12, 25, 37, 64, or 111 marker test. Yep, each tiny yDNA has that many unique parts. Since 12 wasnt as specific as most people need, we opted to order the 37 marker test, which I recommend. We knew we could always upgrade if we wanted to later on.

If women want to follow their fathers yDNA, they will need to ask their brother, father, uncle or cousin with the same grandpa to take the test for them.

Men or women can have the mitochondrial DNA test which follows the line of their mothers mothers mother, etc. This changes family name every generation and is very difficult to follow, but you will learn regional origin for your motherly line.

One company will tell you if you are a carrier of genetic variances or of other health related issues. This group also claims to be able to predict things like lactose intolerance or baldness.

Most companies offer a general DNA study that gives an overall view. It is technically called autosomal DNA. This test determines your ancestors origins by percentage. Some of the tests divide this up by countries. Others are more general. If you want to know your Irish or Scots percentage see how these areas are reported by a company. Sometimes it just comes out as British Isles. You also need to remember that the borders of today are most likely not the borders of 300 years ago.

Research which test company is best for your needs. There are some great comparison sites online. Just do an online search or ask at the library for some articles on the subject.

My husband was the perfect test subject for the yDNA test. His father to son line had been in Ohio since 1836, and was solidly documented. We knew nothing of his paternal line before that.

We sent in his DNA sample with the name of the oldest man on his fathers male line, Gershom Cottrell, and waited.

First thing we learned is that the processing never goes as fast as you wish it would. In fact that month or six weeks or two month wait does not begin until they receive it and log the sample into their laboratory.

We have a good friend, a retired pathologist, who says the clinical crime shows on television drive him crazy. He blames these shows for misleading the public to believe that DNA can be analyzed instantaneously. Trust me, it takes awhile. Be patient. And if the lab is busy, it might take even longer.

Meanwhile, all the companies have either information-filled websites or literature you can request. Do yourself a favor. Read the basic stuff. Read the commonly asked questions. Look at the examples. Get familiar with the terms while you wait.

Then finally one day we got a message that the results were in and logged into the website.

Wow. We were amazed at how many relatives there were and, as predicted, how few had the same last name. There was obviously a lot of life going on in the family history way back then.

Since the company we chose included contact information for emails we planned on reaching out to the Cottrels on the list. However before we could, we got an email from New Jersey. It was Cousin Bob.

Turns out the Cottrells in New Jersey have an extra L at the end of their names and a very nice complicated tree with one dead end written in pencil. Gershom moved to Ohio 1836. For them my husband was the missing link.

Bob mailed us a copy of the tree. It covered our dining room table. We looked at the spot where we fit in and followed it up to Newport, Rhode Island, where my hubbys ancestor Nicholas Cottrell was one of the original settlers not long after the Pilgrims arrived.

Of course we had to take a trip to visit with our New Jersey cousins, Bob and Pat, and they showed us where the Cottrells had lived since 1700. Funny thing was they had the same canister set on their kitchen counter as we did. What were the odds of that? We hope to visit the family historical sites in Newport someday.

Now this is the dream come true for genetic genealogists, but it is the rare acorn. My husbands yDNA test results were like finding the golden ticket in a Willy Wonka bar. Most people just get the chocolate.

When the results get in you dont get a carefully designed scrap book like in some of those family history television programs. The test results are just the beginning of the process. Sometimes it sheds light, sometimes you connect with other researchers, and sometimes it is just downright frustrating like my Dads yDNA study, which I will tell you about later.

Next week, Ill let you know how some of our western Clark County neighbors have done with this new form of family research. Cannot wait to write more on this subject.

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Cottrel: DNA test results a golden ticket for family history - Springfield News Sun

Finding our way around DNA -- ScienceDaily Science Daily A new tool has been developed that maps functional areas of the genome to better understand disease. and more »

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Finding our way around DNA -- ScienceDaily - Science Daily

February 14, 2017 9:21am NASDAQ:IBB

From Jon Markman: It really is a brave new world. Not long ago, a group of prominent scientists announced plans for a project to create synthetic human DNA from scratch.

That seems appropriate for Valentines Day. If you dont like your lover, one day you might just be able to design a new one.

The project will be led by synthetic biologists Jef Boeke, of the Langone Medical Center at New York University, and George Church, of Harvard Medical School. And it will take up where the previous project to read the human genome ended.

In 2003, the Human Genome Project (HGP) was completed. It was supposed to open the door to countless new treatments and cures for illnesses that had plagued humans for centuries. It didnt quite work out that way. It seems understanding the relationship between genes and illness is more complex than scientists originally thought.

The Human Genome Project-write (HGP-write), as the name implies, will attempt to synthetically write human DNA code. The idea is that writing and understanding genetic code made from scratch will help scientists learn more about those complex gene relationships.

And while creating the building blocks for human life in a lab may seem like science fiction, there is some precedent.

In 2010, scientists at the J. Craig Venter Institute created bacteria controlled by a synthetic genome, effectively turning code back into life. HGP-write will be like that experiment, only on a much bigger scale.

Writing DNA is tedious and expensive work. It involves precisely manipulating tiny amounts of chemicals and a DNA molecule.

These chemicals are sugary building blocks designated A, T, C and G and they must be added in the correct amounts and the proper order hundreds of times to change the structure of DNA.

Boeke and Church believe completing HGP-write will shrink development costs for DNA fabrication by a factor of one thousand. If true, that could actually lead to all of the revolutionary treatments promised by the original Human Genome Project. Yet, pesky ethical questions remain.

These are heightened by Churchs own colorful and controversial history. In his 2012 book, Regenesis: How Synthetic Biology Will Reinvent Nature and Ourselves, he wrote about a world where humans with genomes made in the lab become immune to all viruses. According to Church this could be done simply by removing the host material from our genes that viruses need to replicate. And thats just a start. Hes been vocal about his efforts to resurrect the wooly mammoth now that perfectly preserved DNA material from the prehistoric beast has been recovered. Church is also using CRISPR, a gene editing tool he helped develop, to alter pig genes so that their organs can be transplanted into humans. As for humans, hes not shy about his cradle-to-grave outlook.

Hes aggressively in favor of gene editing to avoid potential birth defects and hes working with gene therapies to reverse the aging process. It doesnt help that when hes pressed about ethics, he demurs to comparisons to the industrial revolution. This type of talk often lands scientists in hot water. And Church has been cooked so many times that he should have developed a rubbery exterior by now. Hell need it.

It should take $100 million and ten years to create the human genome from scratch. If the project is successful, scientists say theyll restrict potential use cases to the petri dish to avoid ethical considerations. Thats not exactly Mary Shelleys Frankenstein but it is one giant step closer to Aldous Huxleys Brave New World.

As is often the case in biotech, the most reliable investment for investors in this space will be the proverbial picks and shovels: The makers of lab equipment and disposables, like Becton Dickinson and Co. (BDX), Teleflex Inc. (TFX) and Cantel Medical Corp. (CMD).

Of course, the members of my services Tech Trend Trader receive both more numerous stock recommendations and more detailed analyses of the companies behind them.

The iShares NASDAQ Biotechnology Index ETF (NASDAQ:IBB) rose $0.50 (+0.17%) in premarket trading Tuesday. Year-to-date, IBB has gained 8.07%, versus a 4.10% rise in the benchmark S&P 500 index during the same period.

IBB currently has an ETF Daily News SMART Grade of A (Strong Buy), and is ranked #2 of 36 ETFs in the Health & Biotech ETFs category.

This article is brought to you courtesy of Money And Markets.

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Biotech's Next Big Catalyst Could Be Synthetic DNA - ETF Daily News (blog)

New twin-splitting technology is being put to the test for the first time ever in a Hub courtroom this week, and Suffolk prosecutors hope the new-age science can finally help solve a pair of rapes that occurred nearly 15 years ago.

An old DNA test couldnt separate the chief suspect in the case, Dwayne McNair, from his identical twin brother, Dwight McNair. That issue put Suffolk District Attorney Daniel F. Conley in a tight spot, and in 2014 he temporarily dropped charges stemming from a pair of 2004 rapes so he could see if a new test developed in Germany would work.

Prosecutors say it did, and that it conclusively shows that Dwayne McNairs DNA was in a condom he allegedly used during the crime. That potentially damning piece of evidence only exists because a quick-thinking woman McNair is accused of raping kept the condom and brought it to authorities.

Dwayne McNair was eventually re-indicted, and now Conleys office must prove that the test is worthy of being used in a Massachusetts court.

After going through the extensive methodology used by Germany-based Eurofins Scientific to differentiate the McNair twins yesterday, Suffolk prosecutor David Deakin asked his expert how likely it is that Dwights DNA was found.

The scenario is extremely unlikely, said Dr. Burkhard Rolf, head of DNA services Eurofins.

But Robert Tobin, Dwayne McNairs defense attorney, went on the offensive, arguing that the science is relatively new, completely untested by other scientists and has never been considered in any courtroom anywhere.

This has never been entered into evidence in any court in the whole world, right? Tobin asked.

Not yet, Rolf said.

The $120,000 test is vital to the rape case, and if Superior Court Judge Linda Giles allows a jury to consider its results, it would be akin to an admission. Thats why a line of experts are expected to testify about the merits and faults of the test in the coming days.

It has not been accepted in the forensic community, has it? Tobin asked Rolf.

What does accepted mean? Rolf responded. It has not been performed very often, but that doesnt mean it hasnt been accepted.

The test has been published in one peer-reviewed journal, and according to Rolf no one has debunked the science.

But there is no clear answer as to whether Massachusetts will break the mold and allow this science into court.

Its an interesting experiment, Tobin said, his arms full of files as he left the courtroom. Its just not ready for prime time.

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McGovern: DA fighting for twin's DNA test to be accepted in trial - Boston Herald

February 13, 2017 DNA double helix. Credit: public domain

Sardinia sits at a crossroads in the Mediterranean Sea, the second largest island next to Sicily. Surrounded by sparkling turquoise waters, this Mediterranean jewel lies northwest of the toe of the Italian peninsula boot, about 350 kilometers due west of Rome.

For evolutionary biologists, islands are often intriguing, geographically isolated pockets with unique populations that can be ripe for exploration.

Now, in a new study appearing in the advanced online edition of Molecular Biology and Evolution an international team led by geneticist Anna Olivieri from the University of Pavia tackles a highly interesting question: what were the origins of the Sardinian population in the context of European prehistory and ancient human migrations?

The authors analyzed 3,491 modern, whole mitochondrial DNA genomes from Sardinia (which are only passed down maternally). These were compared with 21 samples of ancient mitogenomes from the island, a large panel of non-Sardinian mitogenomes -and even tzi (the nickname of Europe's oldest natural mummy, the 3,300 BCE-year old "Tyrolean Iceman") -to better understand their origins.

Their findings show Sardinia as an outlier in the general European genetic landscape. Almost 80 percent of modern Sardinian mitogenomes belong to branches that cannot be found anywhere else outside the island. Thus, they were defined as Sardinian-Specific Haplogroups (SSHs) that most likely arose in the island after its initial occupation. Almost all SSHs coalesce in the post-Nuragic, Nuragic and Neolithic-Copper Age periods. However, some rare SSHs display age estimates older than 7,800 years ago, the postulated archeologically-based starting time of the Neolithic in Sardinia.

"Our analyses raise the possibility that several SSHs may have already been present on the island prior to the Neolithic," said prof. Francesco Cucca, from the Institute of Genetic and Biomedical Research (IRGB), at the CNR in Cagliari (Sardinia).

The most plausible candidates would include haplogroups K1a2d and U5b1i1, which together comprise almost 3 percent of modern Sardinians, and possibly others. Such a scenario would not only support archaeological evidence of a Mesolithic occupation of Sardinia, but could also suggest a dual ancestral origin of its first inhabitants. K1a2d is of Late Paleolithic Near Eastern ancestry, whereas U5b1i1 harbours deep ancestral roots in Paleolithic Western Europe.

This work provides evidence that contemporary Sardinians harbour a unique genetic heritage, as a result of their distinct history and relative isolation from the demographic upheavals of continental Europe. Anna Olivieri stresses: "It now seems plausible that human mobility, inter-communication and gene flow around the Mediterranean from Late Glacial times onwards may well have left signatures that survive to this day. Some of these signals are still retained in modern Sardinians."

"Although in the past the stress has often been on the spread of the Neolithic, genetic studies too are beginning to emphasize the complexity and mosaic nature of human ancestry in the Mediterranean, and indeed in Europe more widely," concludes prof. Antonio Torroni, from the University of Pavia. "Future work on ancient DNA should be able to test directly to what extent this more complex model is supported by genetic evidence, and whether our predictions of Mesolithic ancestry in contemporary Sardinians can be sustained."

Explore further: Hair from mummy's clothes provides insights into red deer lineage

More information: Anna Olivieri, et al, Mitogenome Diversity in Sardinians: a Genetic Window onto an Island's Past, Molecular Biology and Evolution (2017). DOI: 10.1093/molbev/msx082

Genetic analysis of Neolithic deer hair from Italian Alps mummy's clothes ties deer population to modern day western European lineage, in contrast to the eastern lineage found in the Italian alps today, according to a study ...

A genomic analysis of 28 dog breeds has traced the genetic history of the remarkable Fonni's Dog, a herd guardian endemic to the Mediterranean island of Sardinia. The results, published in the journal Genetics, reveal that ...

A study was published last week on the DNA of Helicobacter pylori, the pathogen extracted from the stomach of tzi, the ice mummy who has provided valuable information on the life of Homo Sapiens.

The Iceman mummy, also known as Otzi, is about 5,300 years old. Scientists studying his body since his discovery in the Italian Alps in 1991 have learned many things, including the cause of his death (an arrow to the back) ...

One look at Sardinia's white-sand beaches and turquoise water would lead you to assume that this part of the world is devoted entirely to idyllic getaways and sun-filled vacations. You'd never guess that the island's population ...

The first ancient human genome from Africa to be sequenced has revealed that a wave of migration back into Africa from Western Eurasia around 3,000 years ago was up to twice as significant as previously thought, and affected ...

(Phys.org)A team of researchers at the Shanghai Institutes for Biological Sciences has found that rhesus monkeys can pass the mirror self-awareness test if they are first taught how mirrors work. In their paper published ...

University of Georgia researchers have confirmed that becoming a parent brings about more than just the obvious offspringit also rewires the parents' brain.

Male guppies pay a high cost for their sexual harassment of female guppies including much higher mortality rates a new study from Macquarie University has found.

Scientists at the University of Wrzburg have generated new insights into the intricate molecular underpinnings of ubiquitin signaling. Their results may provide new avenues for cancer therapy.

The protein that helps the sperm and egg fuse together in sexual reproduction can also fuse regular cells together. Recent findings by a team of biomedical researchers from the Technion-Israel Institute of Technology, Argentina, ...

Sardinia sits at a crossroads in the Mediterranean Sea, the second largest island next to Sicily. Surrounded by sparkling turquoise waters, this Mediterranean jewel lies northwest of the toe of the Italian peninsula boot, ...

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An ancient people of Sardinia were once called the Shardana...... as in Shar-DAN-a. They were one of the 'Sea Peoples' that plyed the Mediterranean during the Greek Dark Ages, as were the Danoi or DAN-oi of Mycenea and the Dan-nan-oi or DAN-nan-oi of Thutmose's Egypt and the Israeli Tribe of Dan from Tel-Dor in Israel. All were of the 'Danites' and emanated from Israel about the time of the Exodus in the Torah, about 1500 BCE. There is physical archaeology indicating all of this. For further distant antecedants, one need look at pre-Exodus Hebrews working as slaves in Egypt's 'Valley of Terror'. Cave inscriptions there bear some of first uses of modern alphabet.

Pronunciations in southern Europe and the Levant seem all relative to varying forms of pronunciation of alphabetic or abjadic letters. Russia, as remote as it seems, got much of its culture from ancient Dacia which is where also later on the Kievan' Rus.......Ukraine, got started. The French suffix 'in' has its vowel sounding almost like a flat 'aanh'. These differing vowel pronunciations spread all across cultures from ancient Iberia to Capodoccia to Assyria to Ur across not only distance but also time measured in millennia. The Hebrew's ancient alphabet or 'alef-bet' came from Linear-A script copied into Heiratic in Egypt with its 600 letters whose' difficulty in learning was a purposeful act to prevent the common folk from educating themselves. That those secretive fuedal societies like the Hittites and Egyptian Pharoanics left so little behind seems a tribute to their shared interest in looting their present, uncaring of future progress.

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Looking at Sardinian DNA for genetic clues to an island'sand ... - Phys.Org

February 13, 2017 by Dr. Maren Berghoff A complex tag for DNA-repair: 3D cartoon showing the linkage of ADP-ribose to the amino acid serine in a protein (turquoise). Credit: Max Planck Institute for Biology of Ageing

Cells need to repair damaged DNA in our genes to prevent the development of cancer and other diseases. Our cells therefore activate and send "repair-proteins" to the damaged parts within the DNA. To do this, an elaborate protein language has evolved. Now scientists from the Max Planck Institute for Biology of Ageing in Cologne have discovered the way a new letter of this alphabet is used in cells. This novel protein modification, called serine ADP-ribosylation, has been overlooked by scientists for decades. This finding reveals how important discoveries may be hidden in scientific "blind spots."

In basic science, one often starts a new research project by trying to reproduce, confirm and build upon what others have shown before. This was exactly what a young team of scientists did, led by Ivan Matic, research group leader at the Max Planck Institute for Biology of Ageing, in collaboration with the group of Ivan Ahel at the University of Oxford. The end result was that the team found a new mechanism, turning some old discoveries upside down.

The research group investigates how the cell determines the fate of specific proteins using tags, so called "post-translational modifications." These are small chemical flags, added to proteins in order to activate them and make them functional. They function as letters of a coding alphabet that the cell can use to determine what to do with a specific protein, for instance sending it off to the cell nucleus to repair damage to our genes. "We were investigating one of the most complex tags, which is known as adenosine diphosphate ribosylation (ADPr). Researchers in the field have thought for many years that this tag is added to particular parts of proteins - the amino acids glutamate, aspartate, arginine and lysine. However, when we looked deeply into the data, we always saw the amino acid serine very close by, which made us very suspicious. After a long time of struggling we could show, that actually the amino acid serine is tagged," explains Matic.

The devil is in the details

For non-scientists this may seem like a small detail. But in the cell "factory" this is an important mechanism. It is like discovering a new letter to an alphabet you thought you knew namely the alphabet the cell uses for sending internal messages. The research team could show that this modification plays a crucial role for repairing DNA damage a process that they can now start to decode. Damage in our DNA can cause mutations that lead to a variety of diseases, such as cancer or neurodegeneration. This damage is inevitable, and repairing it is essential for any organism, including humans. Having discovered this new letter in the cell's alphabet, the research team has now also described its molecular mechanism and shown that its usage is widespread. "We found that this modification is particularly utilized by processes important for genome stability. This research opens up new possibilities to improve and increase the efficiency of the DNA repair machinery," comments Juan Jos Bonfiglio, a researcher in the group of Ivan Matic

The blind spot

But how can it happen that this modification has been overlooked for so many years? Tom Colby, a scientist working in the Matic group tries to explain: "Scientists today are supposed to produce and analyse large amounts of data. That means that you rely on pre-developed tools and apply them to biological systems. But the problem is that these tools are sometimes built on assumptions that can cause blind spots. The most interesting results are sometimes hidden in the blind spots nobody thinks of." Matic adds to this: "I am old-fashioned. I like to step back and look at the original data in detail. Without this we would have overlooked this new modification as people did in the years before."

Explore further: Plant regulatory proteins 'tagged' with sugar

More information: Juan Jos Bonfiglio et al. Serine ADP-Ribosylation Depends on HPF1, Molecular Cell (2017). DOI: 10.1016/j.molcel.2017.01.003

Orsolya Leidecker et al. Serine is a new target residue for endogenous ADP-ribosylation on histones, Nature Chemical Biology (2016). DOI: 10.1038/nchembio.2180

New work from Carnegie's Shouling Xu and Zhiyong Wang reveals that the process of synthesizing many important master proteins in plants involves extensive modification, or "tagging" by sugars after the protein is assembled. ...

A team of scientists under the lead of Ivan Dikic, Director of the Institute of Biochemistry II at Goethe University Frankfurt, has now discovered a novel mechanism of ubiquitination, by which Legionella bacteria can seize ...

Scientists on the Florida campus of The Scripps Research Institute (TSRI) have developed a new tool for studying the molecular details of protein structure.

DNA can be damaged by different environmental insults, such as ultraviolet light, ionizing radiation, oxidative stress or certain drugs. If the DNA is not repaired, cells may begin growing uncontrollably, leading to the development ...

Researchers at the Institute of Molecular Biology (IMB) and Johannes Gutenberg University Mainz (JGU) have shown that a new way of regulating genes is vital for the activity of the nervous system. They found that this form ...

When the pharmaceutical industry develops new medicines for example for cancer treatment it is important to have detailed knowledge of the body's molecular response to the medicine.

Biological invasions pose major threats to biodiversity, but little is known about how evolution might alter their impacts over time.

From eyes the size of basketballs to appendages that blink and glow, deep-sea dwellers have developed some strange features to help them survive their cold, dark habitat.

Growing up in tough conditions can make wild animals live longer, new research suggests.

Cells need to repair damaged DNA in our genes to prevent the development of cancer and other diseases. Our cells therefore activate and send "repair-proteins" to the damaged parts within the DNA. To do this, an elaborate ...

Previous studies of flocks, swarms, and schools suggest that animal societies may verge on a "critical" pointin other words, they are extremely sensitive and can be easily tipped into a new social regime. But exactly how ...

A team at the Wellcome Trust Sanger Institute has discovered how a promising malarial vaccine target - the protein RH5 - helps parasites to invade human red blood cells. Published today in Nature Communications, the study ...

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DNA repaira new letter in the cell alphabet - Phys.Org

Chinese biomed ApolloBio negotiated exclusive rights to develop Inovios lead DNA immunotherapeutic for human papillomavirus (HPV), VGX-3100, within China, Hong Kong, Macao and Taiwan. The collaboration and licence agreement covers development of VGX-3100 for treating and/or preventing pre-cancerous HPV infections and HPV-driven dysplasias, and excludes HPV-driven cancers and all combinations of VGX-3100 with other immunostimulants.

Under terms of the deal ApolloBio will fund all clinical development costs for VGX-3100 within its licensed geographies. Inovio will earn $15 million in up front and near term payments, and could receive another $20 million in regulatory milestones, plus double digit sales royalties.

$12 million of near-term payments will be made to Inovio when FDA lifts the existing VGX-3100 Phase III pre-initiation clinical hold, which has been in place since October 2016. The agency refused to allow the start of the proposed Phase III VGX-3100 trial because it wanted additional data on the shelf-life of disposable parts of the CELLECTRA 5PSP immunotherapy delivery device.

ApolloBio has separately agreed to invest up to $35 million in Inovio, after the clinical hold has been lifted. The firms said that the aggregate investment may be kept below an amount that would make ApolloBio the largest shareholder in Inovio.

The firms claim that there are currently no approved non-surgical treatments for persistent HPV infection or cervical dysplasia. Commenting on the deal with Inovio, Dr. Weiping Yang, ApolloBios CEO, said, We are delighted to begin 2017 with a strategic collaboration with Inovio. VGX-3100 is the worlds first therapeutic vaccine being developed for HPV pre-cancers. This collaboration, license and equity investment marks our determination to introduce late stage innovative new drugs to meet severely unmet medical needs within the Greater China region.

Inovio is exploiting its SynCon DNA plasmid technology and electroporation delivery platform to develop DNA immunotherapeutics against multiple cancers and infectious diseases, including HIV and hepatitis. VGX-3100 is designed to activate functional, antigen-specific CD8 T-cells to clear persistent HPV 16/18 infection, and to reverse the development of precancerous cervical dysplasia.

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ApolloBio Licenses Inovio's Late-Stage HPV DNA Immunotherapeutic for China - Genetic Engineering & Biotechnology News

The age old adage asserts What doesnt kill you makes you stronger. However, this might not be the case for people who suffer from more viral infections.

A new joint study led by UW assistant professor of anthropology Dan Eisenberg indicates that peoples protective stretches of DNA, which cap the ends of their chromosomes, appear shorter if they experience more infections during infancy.

Understanding humans from evolution

The study is part of human biology research, which aims to understand humans from an evolutionary perspective.

[We are] looking at [what] our roots say as mammals, and primates, Eisenberg said. And how that may influence our biology as it is today.

Eisenberg looks across different places around the world where culture, ecology, and evolution may affect different populations in various ways. In this recent study, he used health data from the Cebu Longitudinal Health and Nutrition Survey, which keeps health records of over 3,000 infants born between 1983-84 in Cebu City in the Philippines.

Detailed health data and feeding habits were collected every two months from these infants up to age 2. Researchers recorded the frequencies of diarrhea in particular, since they most likely indicated infections due to environmental and public health concerns in Cebu City at the time. Researchers kept collecting data over the next 20 years. Of these babies, 1,776 provided their blood samples once again as young adults in 2005.

Eisenberg found that adults with more diarrhea infections as infants showed shorter protective stretches of DNA, which may bring them a higher burden of diseases later in their lives.

Telomeres, the protective stretches of our DNA

Telomeres, which cap the ends of chromosomes, play an important role in cellular aging. They protect genes from damage and improper regulation.

The analogy is that telomeres are like little plastic tips at the ends of our shoelaces, Eisenberg said. When these fray, you shoelaces dont work as well.

The telomeres get a bit shorter each time a cell in our body replicates. Eventually, the cell stops replicating when the telomeres become too short. Thus telomeres in peoples cells become shorter and shorter as they become older, making them more vulnerable to health and environmental issues.

Short telomeres are part of the reason why our bodies do not work well as we get older, Eisenberg said. For example, if you accidentally cut yourself, your skin has to make new cells to heal the wound. When your telomeres are shorter, you are less likely able to regrow skin as quickly.

Similar processes happen everywhere in our bodies while cells are being replaced. Shorter telomeres appear to predict increased sickness and earlier death.

Cells of the immune system, such as white blood cells in the bloodstream, have to replicate and create an army of cells to fight off pathogens. If telomeres in these cells are too short, the immune system may take more effort. On the other hand, overcoming infections also shortens telomeres.

There are good reasons to predict [how] early-life infections might be associated with telomeres in later life, Eisenberg said.

Research findings and further questions

While one could quickly draw the conclusion that more infections in infancy results in shorter telomeres and shorter lives, interpreting current research findings turned out to be more complicated.

This was only an association that we found, but we had to consider whether there could be other reasons why we saw this, Eisenberg said. Part of the ways that longer telomeres help to protect our health is [that] they actually can promote better immune function. So another possible explanation for our findings is that infants born with longer telomeres were better able to fight off the infections.

In the midst of receiving more samples from the Philippines as the study continues, Eisenberg is looking into ways to improve the study.

If you manage to get samples very early in peoples life, maybe right after they were born or within the first few months, you can look to see whether kids with longer telomeres have decreased infections, Eisenberg said. When they do get infections, we can get samples later on to see if their telomeres become shorter. That will be an ideal way to study.

Reach reporter Zezhou Jing at science@dailyuw.com. Twitter: @Zz_Jing

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Research finds association between infancy infection and length of protective DNA stretches - Dailyuw