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GENTAUR Europe

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    The polymerase chain reaction (PCR) is a common technique used to amplify, or copy, pieces of DNA. Amplified DNA is then used in genetic analyses for everything from medicine to forensics. In plant research, PCR is a vital step in detecting and sequencing genes, and its applications are endless. However, compounds found in plants often inhibit PCR. Researchers at the University of Southern Mississippi discovered that the use of an additive allows PCR to successfully amplify DNA from once problematic plants.

    PCR is widely used in plant sciences but is not 100 percent reliable. Many plant researchers encounter roadblocks when implementing PCR. For example, many plant species contain phenolic compounds that deter herbivores. These compounds are often extracted along with plant DNA and can stop PCR from working.

    Graduate student Tharangamala Samarakoon and colleagues have found a technique to overcome many of these inhibitory plant compounds. They added a reagent to the PCR mixture that contains three ingredients: trehalose, bovine serum albumin, and polysorbate-20 (all three abbreviated TBT-PAR). "Unlike several other studies, TBT-PAR works at the PCR stage instead of at the DNA extraction stage, so it has promise for pigeon-holed and half-forgotten extractions that previously failed to be amplified using PCR," says Samarakoon. The authors published their research in the January issue of Applications in Plant Sciences.

    Samarakoon tested the TBT-PAR reagent on DNA extracted from tropical and temperate species across four plant families, including Achariaceae, Asteraceae, Lacistemataceae, and Samydaceae. PCR with TBT-PAR successfully amplified DNA for all species, whereas standard DNA extraction and PCR techniques consistently failed.

    TBT-PAR enhanced PCR for DNA extracted from fresh, silica-dried, and herbarium plant material. "Since we study tropical plants, many of which are geographically restricted or rare," explains Samarakoon, "herbarium material is sometimes all that we have available for DNA extraction, and curators are gracious to allow even a small destructive sampling for a single extraction attempt. We want that one attempt, of course, to be successful." Samarakoon predicts that inhibitory plant compounds could be the underlying cause of many PCR failures in herbarium specimens and hopes TBT-PAR will have widespread benefits in herbarium specimen DNA amplification. 

    TBT-PAR was first used in the PCR detection of a shrimp virus by co-author Shiao Wang and his colleagues. "The additive has also been helpful in a colleague's lab where they had trouble amplifying DNA from gopher tortoise ticks, so its utility extends beyond plants," comments Samarakoon. TBT-PAR has the potential for broad use in PCR techniques across DNA samples, species, and taxa.

    The article will be published in the first issue of Applications in Plant Sciences (APPS), a new journal released by the Botanical Society of America. Theresa Culley, Editor-in-Chief of APPS, describes the new journal as a venue to "expedite the dissemination of innovative information encompassing all areas of the plant sciences, including but not limited to genetics, structure, development, evolution, systematics, and ecology."APPS publishes new methods in plant sciences -- an important niche to fill in an age of rapid technological advances.

    Published in News

    genome-breast-cancer-gentaur-antibodiesTwo recent studies by CRG researchers delve into the role of chromatin modifying enzymes and transcription factors in tumour cells.

    In one, published on September 9 in Genes & Development, it was found that the PARP1 enzyme activated by kinase CDK2 is necessary to induce the genes responsible for the proliferation of breast cancer cells in response to progesterone. In addition, extensive work has been undertaken to identify those genes activated by the administration of progesterone in breast cancer, the sequences that can be recognised and how these genes are induced. This work will be published on November 21 in the journal Molecular Cell.

    Cancer is a complex set of diseases and only thanks to advances in genomic techniques have researchers begun to understand, at a cellular and molecular level, the mechanisms which are disrupted in cancer cells, a prerequisite for developing effective strategies to treat these diseases.

    One clear example of this is breast cancer. It has long been known that hormones such as estrogen and progesterone encourage the proliferation of cancer cells. Because of this, one of the most common treatments is the administration of hormone receptor blockers. The block, however, affects all the cells of the body not only the cancer cells, and causes a number of side effects in patients. Additionally, most cancers develop resistance after a time and continue to grow despite anti-hormone therapy. To treat these patients it is necessary to understand the mechanisms that trigger the proliferation, which will allow their direct inhibition.

    The scientists from the Cromatin and Gene Expression lab at the CRG, led by Miguel Beato, are dedicated to understanding how hormones activate cell division in breast cancer, focusing on regulating the expression of the genes that control the cell cycle.

    Hormone receptors are transcription factors that bind to DNA sequences in the vicinity of the genes they regulate. But the DNA of the genes is packed into a dense structure known as "chromatin," which is considered a barrier preventing the access of transcription factors to genes. Therefore the chromatin must be decompacted for the transcription factors to activate the target genes expressed in RNA and subsequently translate them into proteins that stimulate cell proliferation. This is where the progesterone, via its receptor, activates various enzymes initiating chromatin opening.

    In the study published on September 1 in the journal Genes & Development, the researchers looked at the role of an enzyme, PARP-1, which is primarily responsible for the repair of cuts in DNA. "It was not known how PARP-1 is activated and we found that it happens via the activation of another enzyme, CDK2, which phosphorylates and activates PARP-1, which in turn modifies the histone H1 and the chromatin displacement. And if PARP1 does not do this, many of the progesterone's target genes are not regulated," explains Roni Wright, first author of the study. Wright is a postdoctoral researcher in Beato's lab. She believes that much remains to be discovered in this area of research. "This experiment was conducted on cell lines, but now we have to do it on real, patient cells to see if their behaviour is the same," adds the researcher.

    How do we know how the proliferation of cancer cells is controlled?

    Gene regulation (how genes activate and deactivate) is the key to the overall understanding of how our genome works and when this function is altered. "It is important to discover the mechanism by which genes are activated around chromatin," explains Miguel Beato, head of the Chromatin and Gene Expression group. The chromatin packs the DNA at several levels, the first being the "nucleosomes," which help stabilise the DNA chain. "It was thought that the chromatin structure was not relevant to explaining how genes turn on and off, but we have discovered that it is crucial," adds Beato.

    The second study, published online on November 21, 2012 in the journal Molecular Cell, addresses this issue. Firstly, all the genes that progesterone activates or represses in breast cancer cells were identified. Then the researchers identified which DNA sequences recognise the progesterone receptor in the genome. They found that these represented only a small proportion of the possibilities, making them think that interaction with DNA was not sufficient. It was necessary for the sequences which bind to the receptor to be incorporated into nucleosomes, which also provide interaction sites. "It seems that chromatin has a lot to do with determining which genes are activated and which are not," says Cecilia Ballaré, first author of this second paper.

    The researchers believe that the only way to create increasingly specific and effective cancer treatments is by studying the role of all the elements that regulate gene expression and cell proliferation in response to hormones. "Knowing the exact way progesterone affects the proliferation of cancer cells may help develop more specific treatments that fight only cancer cells and thus produces fewer side effects," adds Ballaré.

    Published in News
    Thursday, 04 July 2013 11:22

    Phoretix Array Pro

    Phoretix Array has a simple and easy to use interface, designed to be quick to learn

    It can analyse high-densityDNA and protein arrays. Each array layout can be a regular grid of sub-arrays(pictured) or fully-customisable composite grids.

    Simple User Interface High Density Array 

    Two Channel Analysis

    Phoretix Array can analyse two-channel arrays, giving measurements as ratios between the two channels. Reporting and measurement are configurable with results available

    • Per channel
    • Ratios between channels
    • Difference between channels
    • Fold-change between channels
    • Per replicate group
    Red and green channel arrays Results window 

    Easy Editing and Visualisation of Results

    Phoretix Array provides a scatter plot for visualising results and checking quality control of your experiments

    You can edit individual spots, or the grid as a whole and it can easily handle different grid layouts such asinterleaved array grids.

    Multi-channel scatter plot Adjusting spot size Inter-leaved array

     

    Order it NOW and get 10% discount

    Price: 1688 1520 Euro

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    Published in Promos
    Thursday, 04 July 2013 10:31

    Stem-cell transplants may purge HIV

    Daniel-KuritzkeTwo men with HIV may have been cured after they received stem-cell transplants to treat the blood cancer lymphoma, their doctors announced today at the International AIDS Society Conference in Kuala Lumpur.

    One of the men received stem-cell transplants to replace his blood-cell-producing bone marrow about three years ago, and the other five years ago. Their regimens were similar to one used on Timothy Ray Brown, the 'Berlin patient' who has been living HIV-free for six years and is the only adult to have been declared cured of HIV. Last July, doctors announced that the two men — the ‘Boston patients’ — appeared to be living without detectable levels of HIV in their blood, but they were still taking antiretroviral medications at that time.

    Timothy Henrich, an HIV specialist at Brigham and Women’s Hospital in Boston, Massachusetts, who helped to treat the men, says that they have now stopped their antiretroviral treatments with no ill effects. One has been off medication for 15 weeks and the other for seven. Neither has any trace of HIV DNA or RNA in his blood, Henrich says.

    If the men stay healthy, they would be the third and fourth patients ever to be cured of HIV, after Brown and a baby in Mississippi who received antiretroviral therapy soon after birth.

    But Henrich and Daniel Kuritzkes, a colleague at Brigham who also worked with the men, caution that it is still too early know whether or not the Boston patients have been cured. For that, doctors will need to follow the men closely for at least a year, because the virus may be hiding out in 'reservoirs' — parts of the men’s bodies, such as their brain or gut, that can harbour the virus for decades.

    “We’re being very careful not to say that these patients are cured,” Kuritzkes says. “But the findings to date are very encouraging.”

    HIV researcher Steven Deeks of the University of California, San Francisco, says that doctors might need to wait at least two years before declaring that a cure has been achieved. “Any evidence that we might be able to cure HIV infection remains a major advance,” Deeks says. But, he adds, “there have been cases of patients who took many weeks off therapy before the virus took off”.

    Exciting news

    Still, researchers and doctors are excited about the news, especially because the Boston patients’ treatment differed from the Berlin patient’s regimen in one key way. Brown was given stem cells that were predisposed to resist HIV infection, because the donor happened to have a mutated version of a key protein — CCR5 — that is needed for HIV to infect cells. So Brown’s transplant was akin to gene therapy with HIV-resistant cells.

    But the Boston patients received stem cells without the protective mutation. The transplanted cells must therefore have been protected from infection by the antiretroviral drugs taken during cancer treatment. Their doctors think that an immune response called graft-versus-host disease — a post-transplant reaction in which donated cells kill off a patient’s own cells — may have then wiped out the patients’ HIV reservoirs, potentially curing the men.

    Transplant specialist Christine Durand of Johns Hopkins University School of Medicine in Baltimore, Maryland, says that the case of the Boston patients may show that current antiretroviral drugs are powerful enough, on their own, to protect the transplanted cells. “If cure has been achieved in the Boston patients, then it was the antiretroviral therapy, not gene therapy, that protected the donor cells,” she says.

    The finding is very important for people with HIV who also need blood-cell transplants, but the treatment is unlikely to be used more generally because the risks from transplants are high. Durand says that Johns Hopkins is now revising its transplant procedures to keep people with both cancer and HIV on antiretroviral drugs during the transplant regimen.

    Separately, the International Maternal Pediatric Adolescent AIDS Clinical Trials (IMPAACT) Group, based in Silver Spring, Maryland, is trying to replicate the Berlin patient’s cure by giving CCR5-mutated HIV-resistant blood from umbilical cords to children and adults with HIV and cancer. 

    Everyone with HIV could benefit from this work, researchers say, because it could yield valuable information about how to eliminate the HIV reservoir.

    “We are still a long way off from a viable cure option for most patients,” Durand says. “But every step counts, and these cases can teach us important lessons.”

     

    Published in News
    Monday, 24 June 2013 15:06

    New Purified Genomic DNA Products

    Vibrio cholerae Z132, DNA (10 µg)

    PRODUCT DESCRIPTION: Each aliquot contains 10 µg of DNA extracted from a pure culture of Vibrio cholerae. The identification of this organism was confirmed by 16S sequencing. The purity of the culture was monitored by Gram staining and by additional culturing. The DNA was extracted from the cells following the bacterial protocol from the Qiagen®Genomic DNA Handbook using Qiagen®Genomic DNA Buffers with a 500/G genomic tip.DNA concentration and A260/280 ratios are determined using a NanoDrop ND-1000®. The extracted DNA also tested positive on an inhouse real time PCR assay.

    INTENDED USE: Purified Genomic DNA is designed for use as an amplification and/or detection control for nucleic acid testing of Vibrio cholerae. It can also be used to determine a limit of detection (LOD), in diagnostic assay development, cross-reactivity studies or genomic sequencing. When used as a control for nucleic acid tests, the same protocols as those used to amplify extracted clinical specimens should be employed.

    PRECAUTIONS:
    - Use Universal Precautions when handling Genomic DNA.
    - The material may be re-frozen after thawing. Repetitive freezing and thawing is not recommended (aliquot material if necessary).
    - To avoid cross-contamination, use separate pipette tips for all reagents.

    RECOMMENDED STORAGE: This control is supplied in TE Buffer and should be frozen at -20°C or below.

    DO NOT USE IN HUMANS: These products are intended for research, product development or manufacturing use only. These products are NOT intended for use in the manufacture or processing of injectable products subject to licensure under section 351 of the Public Health Service Act or for any other product intended for administration to humans.

    Escherichia coli O111:NM, DNA (10 µg)

    PRODUCT DESCRIPTION: Each aliquot contains 10 µg of DNA extracted from a pure culture of Escherichia coli. The identification of this organism was confirmed by 16S sequencing. The purity of the culture was monitored by Gram staining and by additional culturing. he DNA was extracted from the cells following the bacterial protocol from the Qiagen®Genomic DNA Handbook using Qiagen®Genomic DNA Buffers with a 500/G genomic tip.DNA concentration and A260/280 ratios are determined using a NanoDrop ND-1000®. The extracted DNA also tested positive on an inhouse real time PCR assay.

    INTENDED USE: Purified Genomic DNA is designed for use as an amplification and/or detection control for nucleic acid testing of Escherichia coli. It can also be used to determine a limit of detection (LOD), in diagnostic assay development, cross-reactivity studies or enomic sequencing. When used as a control for nucleic acid tests, the same protocols as those used to amplify extracted clinical specimens should be employed.

    PRECAUTIONS:
    - Use Universal Precautions when handling Genomic DNA.
    - The material may be re-frozen after thawing. Repetitive freezing and thawing is not recommended (aliquot material if necessary).
    - To avoid cross-contamination, use separate pipette tips for all reagents.

    RECOMMENDED STORAGE: This control is supplied in TE Buffer and should be frozen at -20°C or below.

    Plesiomonas shigelloides Z130, DNA (10 µg)

    PRODUCT DESCRIPTION: Each aliquot contains 10 µg of DNA extracted from a pure culture of Plesiomonas shigelloides. The identification of this organism was confirmed by 16S sequencing. The purity of the culture was monitored by Gram staining and by dditional culturing. The DNA was extracted from the cells following the bacterial protocol from the Qiagen® Genomic DNA Handbook using Qiagen® Genomic DNA Buffers with a 500/G genomic tip. DNA concentration and A260/280 ratios are determined using a NanoDrop ND-1000®. The extracted DNA also tested positive on an inhouse real time PCR assay.

    INTENDED USE: Purified Genomic DNA is designed for use as an amplification and/or detection control for nucleic acid testing of Plesiomonas shigelloides. It can also be used to determine a limit of detection (LOD), in diagnostic assay development, crossreactivity tudies or genomic sequencing. When used as a control for nucleic acid tests, the same protocols as those used to amplify extracted clinical specimens should be employed.

    PRECAUTIONS:
    - Use Universal Precautions when handling Genomic DNA.
    - The material may be re-frozen after thawing. Repetitive freezing and thawing is not recommended (aliquot material if necessary).
    - To avoid cross-contamination, use separate pipette tips for all reagents.

    RECOMMENDED STORAGE: This control is supplied in TE Buffer and should be frozen at -20°C or below.

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    Published in Promos

    Ready-to-use cocktail containing all components,except primer, for the amplification and detection of DNA in real-time quantitative PCR(qPCR).

    The AccuPower® 2X Greenstar qPCR Master Mix is a ready-to-use cocktail containing all components,except primer, for the amplification and detection of DNA in real-time quantitative PCR(qPCR). It combines the automatic "Hotstart" technology of Top DNA polymerase and SYBR Green I fluorescent dye to deliver excellent sensitivity in the quantification of target sequences, with a linear dose response over a wide range of target concentration. Volumes are provided for 100 or 200 amplification reactions of 50ul each.

    accupower-greenstarmaster product f01

    Features and Benefits

    High Specificity : AccuPower® 2X Greenstar qPCR Master Mix provides more accurate Real-time PCR result by application of Hot-start method.
    Stability: The chemical stabilizer maintains enzyme activity for 2 years at -20°C
    Simplicity: Ready to use, AccuPower® 2X Greenstar qPCR Master Mix contains everything of Real-time PCR excluding primer and template.
    Reproducibility: Gentaur's strict quality controlled production system ensures that your results will be reproducible experiment after experiment

     

    Applications

    - Real-time quantification of DNA and cDNA targets
    - Gene expression profiling
    - Microbial & Viral pathogen detection

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    Published in Promos
    Monday, 27 May 2013 09:04

    Vampire Moth Discovered

    vampire-moth-evolution-gentaurA previously unknown population of vampire moths has been found in Siberia. And in a twist worthy of a Halloween horror movie, entomologists say the bloodsuckers may have evolved from a purely fruit-eating species.

    Only slight variations in wing patterns distinguish the Russian population from a widely distributed moth species, Calyptra thalictri, in central and southern Europe known to feed only on fruit.

    When the Russian moths were experimentally offered human hands this summer, the insects drilled their hook-and-barb-lined tongues under the skin and sucked blood.

    Entomologist Jennifer Zaspel at the University of Florida in Gainesville said the discovery suggests the moth population could be on an "evolutionary trajectory" away from other C. thalictri populations. This is the second population of vampire moths Zaspel and her team have found. They discovered the first in Russia in 2006.

    Next January, she will compare the Russian population's DNA to that of other populations and other species to confirm her suspicions.

    "Based on geography, based on behavior, and based on a phenotypic variation we saw in the wing pattern, we can speculate that this represents something different, something new," Zaspel said.

    "But it is really difficult to say without knowing genetic differences between individuals in that population, and among individuals from other populations, how different this group is going to be."

    Blood Feeding

    If it turns out that Zaspel has indeed caught a fruit-eating moth evolving blood-feeding behavior, it could provide clues as to how some moths develop a taste for blood.

    Published in News

    The Tibetan antelope lives at dizzying altitudes of 4000-5000mHow can the Tibetan antelope live at elevations of 4,000-5,000m on the Qinghai-Tibetan Plateau? Investigators rom Qinghai University, BGI, and other institutes now provide evidence of genetic factors that may be associated with the species' adaption to harsh highland environments. The data in this work will also provide implications for studying specific genetic mechanisms and the biology of other ruminant species.

    The Tibetan antelope (Pantholops hodgsonii) is a native of the high mountain steppes and semi-desert areas of the Tibetan plateau. Interestingly, it is the only member of the genus Pantholops. Tibetan antelope is a medium sized antelope with the unique adaptations to against the harsh high-altitude climate. For non-native mammals such as humans, they may experience life-threatening acute mountain sickness when visiting high-altitude regions.

    In this study, researchers suggest that Tibetan antelopes must have evolved exceptional mechanisms to adapt to this extremely inhospitable habitat. Using next-gen sequencing technology, they have decoded the genome of Tibetan antelope and studied the underlying genetic mechanism of high-altitude adaptations.

    Through the comparison between Tibetan antelope and other plain-dwelling mammals, researchers found the Tibetan antelope had the signals of adaptive evolution and gene-family expansion in genes associated with energy metabolism and oxygen transmission, indicating that gene categories involved in energy metabolism appear to have an important role for Tibetan antelope via efficiently providing energy in conditions of low partial pressure of oxygen (PO2).

    Further research revealed that both the Tibetan antelope and the highland American pika have signals of positive selection for genes involved in DNA repair and the production of ATPase. Considering the exposure to high levels of ultraviolet radiation, positive selective genes related to DNA repair may be vital to protect the Tibetan antelope from it.

    Qingle Cai, Project manager from BGI, said, "The completed genome sequence of the Tibetan antelope provides a more complete blueprint for researchers to study the genetic mechanisms of highland adaptation. This work may also open a new way to understand the adaptation of the low partial pressure of oxygen in human activities."

    Published in News
    Sunday, 03 February 2013 00:00

    Mutant Gene Gives Pigeons Fancy Hairdos

    DECODED GENOME REVEALS SECRETS OF PIGEON TRAITS AND ORIGINS

    Old Dutch capuchine manecrest2University of Utah researchers decoded the genetic blueprint of the rock pigeon, unlocking secrets about pigeons’ Middle East origins, feral pigeons’ kinship with escaped racing birds, and how mutations give pigeons traits like a fancy feather hairdo known as a head crest.

    “Birds are a huge part of life on Earth, and we know surprisingly little about their genetics,” especially compared with mammals and fish, says Michael D. Shapiro, one of the study’s two principal authors and an assistant professor of biology at the University of Utah. “There are more than 10,000 species of birds, yet we know very little about what makes them so diverse genetically and developmentally.”

    He adds that in the new study, “we’ve shown a way forward to find the genetic basis of traits – the molecular mechanisms controlling animal diversity in pigeons. Using this approach, we expect to be able to do this for other traits in pigeons, and it can be applied to other birds and many other animals as well.”

    The study appears Jan. 31 on Science Express, the website of the journal Science. Shapiro led the research with Jun Wang of China’s BGI-Shenzhen (formerly Beijing Genomics Institute) and other scientists from BGI, the University of Utah, Denmark’s University of Copenhagen and the University of Texas M.D. Anderson Cancer Center in Houston.

    Key findings of the study of pigeons, which first were domesticated some 5,000 years ago in the Mediterranean region:

    – The researchers sequenced the genome, or genetic blueprint, of the rock pigeon, Columba livia, among the most common and varied bird species on Earth. There are some 350 breeds with different sizes, shapes, colors, color patterns, beaks, bone structure, vocalizations and arrangements of feathers on the feet and head – including head crests that come in shapes known as hoods, manes, shells and peaks.

    The pigeon is among the few bird genomes sequenced so far, along with those of the chicken, turkey, zebra finch and a common parakeet known as a budgerigar or budgie, so “this will give us new insights into bird evolution,” Shapiro says.

    – Using innovative software developed by study co-author Mark Yandell, a University of Utah professor of human genetics, the scientists revealed that a single mutation in a gene named EphB2 causes head and neck feathers to grow upward instead of downward, creating head crests.

    “This same gene in humans has been implicated as a contributor to Alzheimer’s disease as well as prostate cancer and possibly other cancers,” Shapiro says, noting that more than 80 of the 350 pigeon breeds have head crests, which play a role in attracting mates in many bird species.

    – The researchers compared the pigeon genome to those of chickens, turkeys and zebra finches. “Despite 100 million years of evolution since these bird species diverged, their genomes are very similar,” Shapiro says.

    – The study turned up more conclusive evidence that major pigeon breed groups originated in the Middle East, and that North American feral pigeons – which are free-living but not wild – are close relatives of racing pigeons, named racing homers.

    A Genome for the Birds, a Gene for Head Crests

    The study assembled 1.1 billion base pairs of DNA in the rock pigeon genome, and the researchers believe there are about 1.3 billion total, compared with 3 billion base pairs in the human genome. The rock pigeon’s 17,300 genes compare with about 21,000 genes in people.

    The researchers first constructed a “reference genome” – a full genetic blueprint – from a male of the pigeon breed named the Danish tumbler. They did less complete sequencing of two feral pigeons and 38 other pigeons from 36 breeds.

    Shapiro says his team’s study is the first to pinpoint a gene mutation responsible for a pigeon trait, in this case, head crests.

    “A head crest is a series of feathers on the back of the head and neck that point up instead of down,” Shapiro says. “Some are small and pointed. Others look like a shell behind the head; some people think they look like mullets. They can be as extreme as an Elizabethan collar.”

    The study found strong evidence that the EphB2 (Ephrin receptor B2) gene acts like an on-off switch to create a head crest when mutant, and no head crest when normal. It also showed the mutation and related changes in nearby DNA are shared by all crested pigeons, so the trait evolved just once and was spread to numerous pigeon breeds by breeders. They ruled out the alternate possibility the mutation arose several times independently in different breeds.

    The researchers analyzed full or partial genetic sequences for 69 crested birds from 22 breeds, and 95 uncrested birds from 57 breeds. They found a perfect association between the mutant gene and the presence of head crests.

    “The way we tracked this trait was innovative,” Shapiro says. “We used gene-finding software from Mark Yandell’s group that was developed to find mutations that control human diseases. We adapted this software to find mutations that control interesting traits in pigeons. This should be extendable to other animals as well.”

    The scientists also showed that while the head crest trait becomes apparent in juvenile pigeons, the mutant gene affects pigeon embryos by reversing the direction of feather buds – from which feathers later grow – at a molecular level.

    Other genetic factors – not identified in the new study – determine what kind of head crest east pigeon develops: shell, peak, mane or hood, according to Shapiro.

    Tracking the Origins of Pigeons

    A 2012 by Shapiro study provided limited evidence of pigeons’ origins in the Middle East and some breeds’ origins in India, and indicated kinship between common feral or free-living city pigeons and escaped racing pigeons.

    In the new study, “we included some different breeds that we didn’t include in the last analysis,” Shapiro says. “Some of those breeds only left the Middle East in the last few decades. They’ve probably been there for hundreds if not thousands of years. If we find that other breeds are closely related to them, then we can infer those other breeds probably also came from the Middle East. That’s what we did.”

    “We found that the owl breeds – which are pigeon breeds with very short beaks and that are very popular with breeders – likely came from the Middle East,” he says. “They are very closely related to breeds we know came from Syria, Lebanon and Egypt.”

    Shapiro says the study also “found a lot of shared genetic heritage between breeds from Iran and breeds we suspect are from India, consistent with historical records of trade routes between those regions. People were not only trading goods along those routes, but probably also interbreeding their pigeons.”

    As for the idea that free-living pigeons descended from escaped racing pigeons, Shapiro says his 2012 study was based on “relatively few genetic markers scattered throughout the genome. We now have stronger evidence based on 1.5 million markers, confirming the previous result with much better data.”

    The scientists analyzed partial genomes of two feral pigeons: one from a U.S. Interstate-15 overpass in the Salt Lake Valley, and the other from Lake Anna in Virginia.

    “Despite being separated by 1,000 miles, they are genetically very similar to each other and to the racing homer breed,” Shapiro says.

    He notes that pigeons were one of evolutionist Charles Darwin’s “favorite examples of how selection works. He used this striking example of artificial selection [by breeding] to communicate how natural selection works. Now we can get to the DNA-level changes that are responsible for some of the diversity that intrigued Darwin 150 years ago.”

    The study’s University of Utah co-authors were Yandell; Eric Domyan, biology postdoctoral fellow; Zev Kronenberg and Michael Campbell, Ph.D. students in human genetics; Anna Vickery, biology undergraduate student; Sydney Stringham, Ph.D. student in biology; and Chad Huff, a former postdoctoral fellow in human genetics now at the University of Texas.

    The study was funded by the Burroughs Wellcome Fund, the National Science Foundation, the University of Utah Research Foundation, the National Institutes of Health and the Danish National Research Foundation.

    Published in News
    Wednesday, 15 May 2013 14:19

    NATtrol CT.NG Panel

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    Published in Promos
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