All four newly-elected directors will serve six-year terms from April 2017 to March 2023.

1.Anthony R. Gregg, MD, MBA, FACOG, FACMG: President-Elect

As ACMG's President-elect, Dr. Gregg is currently the Professor and Chief of Maternal-Fetal Medicine (MFM) at the University of Florida (UF). He is also the Director of Obstetrics at UF Health and Program Director of the Maternal-Fetal Medicine Fellowship. He completed his clinical genetics fellowship at Baylor College of Medicine and remained on the faculty with appointments in OB/GYN and Molecular and Human Genetics. He later became Associate Professor and Director of MFM as well as Medical Director (Division of Genetics) and Medical Director of the Genetics Counseling Program at the University of South Carolina.

In his dual role as a geneticist and MFM specialist, Dr. Gregg provides care to women with complicated pregnancies who experience maternal medical and obstetric complications and fetal complications such as birth defects, genetic conditions and physiologic perturbations. Dr. Gregg has held several research collaborations and with his colleagues has published numerous works addressing the clinical application of genetics and genomics technologies in prenatal care. To learn more about his pub med citations, click here.

Specializing in women's health, he is board certified in OB/GYN, MFM and Clinical Genetics.

From 2009-2015 he served on the ACMG Board of Directors and was Clinical Vice President from 2013-2015. During his Board member term, he served on numerous committees that produced policy statements and points to consider documents on topics intersecting OB/GYN and MFM, including expanded carrier screening and noninvasive prenatal screening. In December 2015 he represented ACMG's position on noninvasive prenatal screening before a congressional sub-committee. Dr. Gregg is currently a member of the ACMG Foundation Board where he is Chair of the Development Committee.

Dr. Gregg received his biology degree, MD, and residency in OB/GYN from Loyola University (Chicago). Afterwards, he went on to complete his fellowship training in maternal fetal medicine at the University of Iowa then in clinical genetics at Baylor. Most recently, he completed his MBA at the University of Florida.

2.Laurie A. Demmer, MD, FACMG: Clinical Genetics Director

Clinical genetics, medical education and clinical research are important to Dr. Demmer, the incoming Clinical Genetics Director on the ACMG Board. She is an author of more than 75 peer-reviewed works including publications, reviews and book chapters. Based in Charlotte, North Carolina, Dr. Demmer currently works as a Clinical Geneticist and Associate Pediatric Residency Program Director at Levine Children's Hospital/Carolinas Health Care. From medical education, dysmorphology, applications of genetic and genomic testing in clinical practice, and ethics she will bring multifaceted knowledge to the ACMG Board. As an active ACMG member and leader, she has worked on numerous ACMG committees. Currently, she serves on the Membership Committee (2013-present) and prior to that she served on the Program Committee (2007-2013), the Maintenance of Certification Committee (2009-2014) and the Genetics Education Task Force (2011-2013).

In addition to serving on ACMG committees, Dr. Demmer is a dedicated proponent of medical genetics education, training and recruitment. Throughout her leadership, she has been president of three organizations: the American Board of Medical Genetics and Genomics (ABMGG) (2015), the Association of Professors of Human and Medical Genetics (APHMG) (2013-2015), and the Medical Genetics Residency Program Directors Group (2010-2012). She is one of the original members of the organizing committees which founded the Residency Program Directors and the Medical Student Course Directors Special Interest Groups of the Association of Professors of Human and Medical Genetics (APHMG). She also participated in the creation of the Medical Genetics Milestones, the ACMG Competencies for Physician Medical Geneticist Project, and the Intraining Exam for Genetics Trainees. Furthermore, she is the Past Chair of the American Board of Medical Genetics and Genomics (ABMGG) MOC committee, and is a current member of the American Board of Medical Specialties (ABMS) Committee on Continuing Certification. Her most recent projects include advocating for improvements in the Maintenance of Certification process, and serving as Chair of the Accreditation Council for Graduate Medical Education (ACGME) RRC for Medical Genetics (2016-2019).

Dr. Demmer graduated from Dartmouth College, Hanover, NH with degrees in Biology and French. She received her MD and MA (Biochemistry) from Washington University in St. Louis. Subsequently, she completed her Pediatrics Residency at St. Louis Children's Hospital and Medical Genetics Fellowship at Washington University in St. Louis. Afterwards, she joined the University of Massachusetts Medical School where she was the Division Chief in Genetics from 1995-2002. Dr. Demmer then moved to Tufts University School of Medicine where she served as Professor of Pediatrics, Division Chief of Genetics and Metabolism, Program Director for the Genetics Residency and Director for the Medical Student Genetics Course until 2012.

3. Elaine Lyon, PhD, FACMG: Laboratory Molecular Genetics Director

Dr. Elaine Lyon will serve as a new ACMG Laboratory Molecular Genetics Director. After completing two fellowships at the University of Utah in Clinical Molecular Genetics and Molecular Pathology she joined the faculty in the Pathology department as a Medical Director of Clinical Molecular Genetics at ARUP Laboratories, a not-for-profit reference laboratory owned by the University of Utah. Currently, she is a tenured Professor of Pathology. For nine years she was the program co-director for the Clinical Molecular Genetics Fellowship program and is now chair of the departmental academic committee responsible for the department's faculty appointment, review and advancement.

Certified in Clinical Molecular Genetics by the American Board of Medical Genetics and Genomics (ABMGG), Dr. Lyon has served on numerous ACMG committees: the Program Committee (2006-2010), the Quality Assurance Committee (2007-2011) and the ACMG/College of American Pathologists (CAP)Biochemical/Molecular Resource Committee (2007-2012). She has also been active with other professional organizations. She served as President for the Association for Molecular Pathology (AMP), Chairman of the Board, and Chair of the Executive Committee (2013-2014), and was on the Executive Committee and AMP Board of Directors (2012-2015). She was also chair of the Clinical Practice (2005-2007), Professional Relations (2009-2011), and Strategic Opportunities (2012-2013) committees and is a member of the Professional Relations and Economic Affairs committees (2008-present). Additionally, she serves on the Molecular Pathology Advisory Group for the American Medical Association (2012-present), and CSER advisory panel for the National Human Genome Research Institute (NHGRI).

Dr. Lyon oversees clinical molecular testing for inherited diseases, applying methods for variant detection, deletion/duplication and sequence analysis (Sanger and massively parallel sequencing). Furthermore, she develops/validates assays for clinical application under CLIA and (recently) ISO requirements, and reviews/interprets cases. As an author of more than 100 publications, including book chapters, review articles, she has contributed to the following ACMG guidelines: CYP2C9/VKORC1 testing (2008), interpretation of sequence variants (2008, 2015), CYP2D6 testing (2012), next generation sequencing quality standards (2012), and Fragile X testing (2013).

To ensure regulation protocol, she has been a collaborative site investigator for three recent grants: Improving the time to diagnosis in infants detected by newborn screening (CF Foundation), Newborn screening for identification and follow-up of infants with SMA for the National Institute of Child Health and Human Development (NICHHD), and A unified clinical genomics database for the National Human Genome Research Institute (NHGRI). Furthermore, she has been a co-investigator for an Exploratory Centers of Excellence in an ELSI Research grant (NIH) focusing on molecular-based screening (carrier, newborn or non-invasive prenatal screening). Her most recent effort is demonstrating clinical utility for molecular testing.

She graduated from Brigham Young University in Provo, UT, and received a BS and MS degree in Microbiology. She subsequently received her PhD in Medical Genetics from the University of Alabama at Birmingham.

4. Catherine W. Rehder, PhD, FACMG: Laboratory Cytogenetics Director

Dr. Catherine Rehder will serve as an ACMG Laboratory Cytogenetics Director. After the completion of her Cytogenetics and Molecular Genetics fellowships at Duke University in 2007, she accepted a position there as Assistant Professor of Pathology.Currently, she is the Director of the Duke Cytogenetics Laboratory and Associate Director of the Duke Molecular Diagnostics Laboratory. She is also the training co-director of the Duke ABMGG Laboratory Genetics and Genomics fellowship, and is board certified in both Cytogenetics and Molecular Genetics. Dr. Rehder also served briefly as the interim director of the Fullerton Genetics Laboratory in Asheville, NC in 2014.

For the past six years, Dr. Rehder has been a member of the ACMG Laboratory Quality Assurance Committee and has served as Chair for the past two years. She is currently a member of the American Cytogenetics Conference Board of Directors, and has served on the Program Committee for that organization's biennial meeting (2012-2016) including the position of Program Chair for the 2014 meeting. From 2013-2016 she served on the organizing committee of the Cancer Genomics Consortium's Annual Meeting.Additionally, Dr. Rehder is a member of the NC Physician Advisory Group Task Force on Emerging Issues in Coverage of Genetic Screening Tests and is part of the North Carolina newborn screening expansion committee.

Dr. Rehder is an author on more than 30 peer-reviewed publications, review articles, and laboratory guidelines, which cover a wide variety of cytogenetics and molecular genetics topics, most notably the ACMG standards and guidelines for documenting suspected consanguinity as an incidental finding of genomic testing. In addition to her various roles as laboratory director, lecturer, training program director, and active participant on several intramural and extramural committees, her other primary areas of interest and publication include the reporting practices of genomic testing, Pompe disease and other glycogen storage diseases, as well as newborn screening and cancer cytogenetics.

A graduate from North Carolina State University in Raleigh, she earned her BS degree in Biochemistry, a BA degree in Multidisciplinary Studies (self-designed curriculum entitled Genetics and Human Affairs) and a minor in Genetics. She completed her PhD in Human Genetics at Virginia Commonwealth University in Richmond, VA.

Four ACMG Directors completed their terms on the ACMG Board and are thanked for their service: Soma Das, PhD, FACMG; Gail E. Herman, MD, PhD, FACMG; Mira Bjelotomich Irons, MD, FACMG; and Christa L. Martin, PhD, FACMG. A complete list of the ACMG Board of Directors is available at http://www.acmg.net.

About the American College of Medical Genetics and Genomics (ACMG) and ACMG Foundation

Founded in 1991, ACMG is the only nationally recognized medical society dedicated to improving health through the clinical practice of medical genetics and genomics. The American College of Medical Genetics and Genomics (www.acmg.net) provides education, resources and a voice for nearly 2000 biochemical, clinical, cytogenetic, medical and molecular geneticists, genetic counselors and other healthcare professionals, nearly 80% of whom are board certified in the medical genetics specialties. The College's mission is to develop and sustain genetic initiatives in clinical and laboratory practice, education and advocacy. Three guiding pillars underpin ACMG's work: 1) Clinical and Laboratory Practice: Establish the paradigm of genomic medicine by issuing statements and evidence-based or expert clinical and laboratory practice guidelines and through descriptions of best practices for the delivery of genomic medicine. 2) Education: Provide education and tools for medical geneticists, other health professionals and the public and grow the genetics workforce. 3) Advocacy: Work with policymakers and payers to support the responsible application of genomics in medical practice. Genetics in Medicine, published monthly, is the official ACMG peer-reviewed journal. ACMG's website (www.acmg.net) offers a variety of resources including Policy Statements, Practice Guidelines, Educational Resources, and a Find a Geneticist tool. The educational and public health programs of the American College of Medical Genetics and Genomics are dependent upon charitable gifts from corporations, foundations, and individuals through the ACMG Foundation for Genetic and Genomic Medicine (www.acmgfoundation.org).

Kathy Beal, MBA kbeal@acmg.net

To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/the-american-college-of-medical-genetics-and-genomics-acmg-announces-new-board-members-and-president-elect-300423332.html

SOURCE American College of Medical Genetics and Genomics

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The American College of Medical Genetics and Genomics (ACMG) Announces New Board Members and President-elect - PR Newswire (press release)

NEW YORK (GenomeWeb) Cancer Genetics reported today that its fourth quarter revenues grew 32 percent year over year.

For the three months ended Dec. 31, 2016, the company reported revenues of $7.2 million up from $5.5 million in Q4 2015.

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Cancer Genetics Q4 Revenues Up 32 Percent - GenomeWeb

Toward the end of trading Thursday, the Dow traded up 0.29 percent to 20,721.07 while the NASDAQ rose 0.17 percent to 5,831.32. The S&P also rose, gaining 0.22 percent to 2,353.52.

Leading and Lagging Sectors

Thursday afternoon, the financial sector proved to be a source of strength for the market. Leading the sector was strength from New England Realty Associates LP (NYSE: NEN) and Ladenburg Thalmann Financial Services (NYSE: LTS).

In trading on Thursday, telecommunications services shares fell 0.12 percent. Meanwhile, top losers in the sector included China Mobile Ltd. (ADR) (NYSE: CHL), down 3 percent, and Partner Communications Company Ltd (ADR) (NASDAQ: PTNR), down 1.5 percent.

Top Headline

Conagra Brands Inc (NYSE: CAG) reported stronger-than-expected earnings for its third quarter.

Conagra reported Q3 earnings of $0.48 per share on revenue of $1.98 billion. Analysts were expecting earnings of $0.44 per share on revenue of $1.98 billion.

Equities Trading UP

HTG Molecular Diagnostics Inc (NASDAQ: HTGM) shares shot up 106 percent to $4.40 after the molecular profiling company confirmed regulatory approval for its products in Europe. HTG Molecular announced that it has obtained CE marking in the European Union for its HTG EdgeSeqALKPlus Assay EU, an in vitro diagnostic assay which is intended to measure and analyze mRNA ALK gene rearrangements in formalin-fixed, paraffin-embedded lung tumor specimens from patients previously diagnosed with non-small cell lung cancer.

Shares of Cancer Genetics Inc (NASDAQ: CGIX) got a boost, shooting up 17 percent to $3.39 after the company posted a narrower-than-expected quarterly loss.

Flexion Therapeutics Inc (NASDAQ: FLXN) shares were also up, gaining 36 percent to $26.75. Fierce Pharma reported that Sanofi is on verge of $1 billion-plus deal for Flexion, according to sources.

Equities Trading DOWN

Tandem Diabetes Care Inc (NASDAQ: TNDM) shares dropped 19 percent to $1.25. Tandem Diabetes Care priced its 18 million share offering at $1.25 per share.

Shares of Alphatec Holdings Inc (NASDAQ: ATEC) were down around 25 percent to $2.00 as the company reported an $18.9 million private placement.

Heat Biologics Inc (NASDAQ: HTBX) was down, falling around 15 percent to $0.872. Heat Biologics priced its 5 million share offering at $0.80 per share.

Commodities

In commodity news, oil traded down 0.54 percent to $47.78 while gold traded down 0.31 percent to $1,248.90.

Silver traded up 0.18 percent Thursday to $17.61, while copper rose 0.82 percent to $2.65.

Eurozone

European shares closed higher today. The eurozones STOXX 600 rose 0.85 percent, the Spanish Ibex Index rose 0.93 percent, while Italys FTSE MIB Index rose 1.07 percent. Meanwhile the German DAX gained 1.14 percent, and the French CAC 40 rose 0.75 percent while U.K. shares rose 0.22 percent.

Economics

Initial jobless claims rose 15,000 to 258,000 in the latest week. Economists projected jobless claims to reach 240,000 in the week.

New-home sales rose 6.1 percent to an annual rate of 592,000 in February. Economists were expecting a 571,000 annual pace.

Supplies of natural gas dropped 150 billion cubic feet for the week ended March 17, the U.S. Energy Information Administration reported. Analysts projected a fall of 153 billion cubic feet.

Data on money supply for the recent week will be released at 4:30 p.m. ET.

Dallas Federal Reserve Bank President Robert Kaplan will speak in Chicago at 7:00 p.m. ET.

Posted-In: Earnings News Eurozone Commodities Offerings Global Intraday Update Markets

2017 Benzinga.com. Benzinga does not provide investment advice. All rights reserved.

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Mid-Afternoon Market Update: Cancer Genetics Gains After Q4 Results; Heat Biologics Shares Slide - Benzinga

MOVES-Deutsche Bank head of restructuring finance joins RBC -sources

March 23 Mark Cohen, the head of restructuring finance at Deutsche Bank AG, will join Royal Bank of Canada as head of its U.S. capital solutions group in New York in June, people familiar with the matter said on Thursday.

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BRIEF-Atossa Genetics files for public offering of up to 4 mln units - Reuters

Listen to the conversation on KCUR's Central Standard.

Geneticist Scott Hawley has a way with words especially when it comes to explaining science to non-scientists.

For example, he remembers the connections he made the first time he saw "Star Wars"when he was in graduate school.

Heres this Imperial Death Star that can stay in space forever, and heres Luke Skywalker in this little X-wing fighter, he told host Gina Kaufmann on KCURs Central Standard.

Luke comes down on the surface of the Death Star, he recalled, and goes in a little canal and loops around. Then, he fires a photon torpedo, which goes into the Death Star and theres a huge explosion of energy.

And I turn to the girl I was with and I go, thats fertilization!

And shed never go out with me again, he added. Which is why you dont date science nerds.

Hawley runs a lab at the Stowers Institute, where hes also the Dean of the Graduate School. He studies the process of meiosis in fruit flies. Meiosis is how the body manages, every time it makes a sperm or an egg, to get the right number of chromosomes into that egg.

He describes chromosomes as gigantic moving vans that carry your genes and enables cells to move genes around in a convenient fashion.

Each of us has 46 chromosomes, he said. But when we build a sperm or egg, we have to get 23 of those 46 those chromosomes in there. Not only do we have to get 23; it has to be the right 23.

As for how two chromosomes pairs, thats part of the mystery.

I mean, I have to tell you, at the moment, pretty much the best mechanism we have for how pairing works is: and then a miracle happens.

What drives his research is how this affects people.

One night, about 20 years ago, a chromosome segregation had gone wrong in a normal fruit fly. Hawley couldnt find a reason for it, he said, and that really bugged him.

One of his post-doctorate fellows said, You really do think meiosis is perfect, dont you? Cant you just let it make a mistake every now and then?

Well, it does makes mistakes every now and then, Hawley said. And the problem is, in human beings, when mistakes are made the consequences are either a zygote that cant flourish in other words, a zygote thats not going to be able to make it to term or, in certain cases, individuals who are going to have to cope with a complex set of effects resulting from having the wrong number of chromosomes.

And these are people and theyre trying to deal with very difficult disorders. And these are people, many of whom I know and I hear their stories, and its something that really matters to me. I want to understand how this process works.

Hawleys interest and drive started in a high school P.E. class.

When he was about 12 or 13, he had a series of three epileptic seizures. That bothered the state of California, where he lived at the time, so he couldnt be in a regular P.E. class; he was placed in a modified" P.E. class.

For the next four years, for an hour a day, five days a week, he was in a class with kids who had severe disabilities mostly disabilities they had been born with, he said.

And I saw how the world treated them, Hawley recalled.

One day after class, he was walking down the hall with a kid from this P.E. class when one of the high school superstars deliberately tripped him.

He fell forward and his face hit the floor. According to Hawley, there was blood, the boy was crying and everyone was laughing.

When he got up, it just didnt bother him that hed fallen. It didnt bother him that he was bleeding, Hawley said. He couldnt understand why people were laughing at him. He couldnt figure out why this was funny. And I couldnt explain it.

It just kept making me angrier and angrier.

This was the late 1960s, when Hawley said advocacy was booming. He decided to become a lawyer to do something for these kids.

But when he got to college, he was randomly assigned an advisor: CrellinPauling, a geneticist and the son of Linus Pauling (who won the Nobel Prize for his research of the chemical bond).

After listening to Hawley rant, Pauling said, I dont know if youre nave or just stupid."

Look at what people will discriminate against minor things. You think youre going to get them to not discriminate against serious developmental defects? You want to do something to help these kids? Why dont you try and fix it or prevent it?

Hawley had never taken a genetics class. Pauling let Hawley into his class, where Hawley said he did badly. But he realized that maybe someday, they could do something about these issues. And, on a selfish level, he said, he fell in love with the intellectual beauty of genetics as a science.

Genetics is kind of the algebra of biology. Its a way of thinking, he said. Its the ability to go into a genome that has 26,000 genes, or 14,000 like fruit flies, and be able to identify the small number of genes that specifically control the process youre interested in, understand what those genes do, how they function, and then begin to understand what happens when they dont do their job when theyre not right.

Genetics is about cherishing the exceptions, he said.

Hawley also writes poetry. He paraphrases a quote: How am I supposed to know what I feel until I know what Ive written?

Words mean a lot to me, he said. Poetry is a powerful way for him to communicate with people who matter in his life, especially when words fail him.

And poetry allows him to fail, he said. He usually writes and re-writes a poem multiple times. In that process, he learns what does and doesnt work.

He writes about anything, he said, including science. The beauty of an image inspires him. He has a framed picture on his desk of when his lab first visualized this structure inside the meiotic cell.

When he first saw it, he said, it took him a minute or two to step back and say, OK, what are we actually looking at? What does this tell us? What questions does this answer and what questions do we need to ask? How do we make sure this is the right thing?

The usual sort of self-questioning things that are science, he said. But for the first minute or two, I was just struck by this image is so beautiful.

Jen Chen is associate producer forKCUR'sCentral Standard. Reach out to her atjen@kcur.org.

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'Cherishing The Exceptions': KC Scientist Scott Hawley On The Beauty Of Genetics - KCUR

This article is a non-technical introduction to the subject. For the main encyclopedia article, see Genetics.

A long molecule that looks like a twisted ladder. It is made of four types of simple units and the sequence of these units carries information, just as the sequence of letters carries information on a page.

They form the rungs of the DNA ladder and are the repeating units in DNA. There are four types of nucleotides (A, T, G and C) and it is the sequence of these nucleotides that carries information.

A package for carrying DNA in the cells. They contain a single long piece of DNA that is wound up and bunched together into a compact structure. Different species of plants and animals have different numbers and sizes of chromosomes.

A segment of DNA. Genes are like sentences made of the "letters" of the nucleotide alphabet, between them genes direct the physical development and behavior of an organism. Genes are like a recipe or instruction book, providing information that an organism needs so it can build or do something - like making an eye or a leg, or repairing a wound.

The different forms of a given gene that an organism may possess. For example, in humans, one allele of the eye-color gene produces green eyes and another allele of the eye-color gene produces brown eyes.

The complete set of genes in a particular organism.

When people change an organism by adding new genes, or deleting genes from its genome.

An event that changes the sequence of the DNA in a gene.

Genetics is the study of geneswhat they are, what they do, and how they work. Genes inside the nucleus of a cell are strung together in such a way that the sequence carries information: that information determines how living organisms inherit various features (phenotypic traits). For example, offspring produced by sexual reproduction usually look similar to each of their parents because they have inherited some of each of their parents' genes. Genetics identifies which features are inherited, and explains how these features pass from generation to generation. In addition to inheritance, genetics studies how genes are turned on and off to control what substances are made in a cellgene expression; and how a cell dividesmitosis or meiosis.

Some phenotypic traits can be seen, such as eye color while others can only be detected, such as blood type or intelligence. Traits determined by genes can be modified by the animal's surroundings (environment): for example, the general design of a tiger's stripes is inherited, but the specific stripe pattern is determined by the tiger's surroundings. Another example is a person's height: it is determined by both genetics and nutrition.

Chromosomes are tiny packages which contain one DNA molecule and its associated proteins. Humans have 46 chromosomes (23 pairs). This number varies between speciesfor example, many primates have 24 pairs. Meiosis creates special cells, sperm in males and eggs in females, which only have 23 chromosomes. These two cells merge into one during the fertilization stage of sexual reproduction, creating a zygote. In a zygote, a nucleic acid double helix divides, with each single helix occupying one of the daughter cells, resulting in half the normal number of genes. By the time the zygote divides again, genetic recombination has created a new embryo with 23 pairs of chromosomes, half from each parent. Mating and resultant mate choice result in sexual selection. In normal cell division (mitosis) is possible when the double helix separates, and a complement of each separated half is made, resulting in two identical double helices in one cell, with each occupying one of the two new daughter cells created when the cell divides.

Chromosomes all contain DNA made up of four nucleotides, abbreviated C (cytosine), G (guanine), A (adenine), or T (thymine), which line up in a particular sequence and make a long string. There are two strings of nucleotides coiled around one another in each chromosome: a double helix. C on one string is always opposite from G on the other string; A is always opposite T. There are about 3.2 billion nucleotide pairs on all the human chromosomes: this is the human genome. The order of the nucleotides carries genetic information, whose rules are defined by the genetic code, similar to how the order of letters on a page of text carries information. Three nucleotides in a rowa tripletcarry one unit of information: a codon.

The genetic code not only controls inheritance: it also controls gene expression, which occurs when a portion of the double helix is uncoiled, exposing a series of the nucleotides, which are within the interior of the DNA. This series of exposed triplets (codons) carries the information to allow machinery in the cell to "read" the codons on the exposed DNA, which results in the making of RNA molecules. RNA in turn makes either amino acids or microRNA, which are responsible for all of the structure and function of a living organism; i.e. they determine all the features of the cell and thus the entire individual. Closing the uncoiled segment turns off the gene.

Heritability means the information in a given gene is not always exactly the same in every individual in that species, so the same gene in different individuals does not give exactly the same instructions. Each unique form of a single gene is called an allele; different forms are collectively called polymorphisms. As an example, one allele for the gene for hair color and skin cell pigmentation could instruct the body to produce black pigment, producing black hair and pigmented skin; while a different allele of the same gene in a different individual could give garbled instructions that would result in a failure to produce any pigment, giving white hair and no pigmented skin: albinism. Mutations are random changes in genes creating new alleles, which in turn produce new traits, which could help, harm, or have no new effect on the individual's likelihood of survival; thus, mutations are the basis for evolution.

Genes are pieces of DNA that contain information for synthesis of ribonucleic acids (RNAs) or polypeptides. Genes are inherited as units, with two parents dividing out copies of their genes to their offspring. This process can be compared with mixing two hands of cards, shuffling them, and then dealing them out again. Humans have two copies of each of their genes, and make copies that are found in eggs or spermbut they only include one copy of each type of gene. An egg and sperm join to form a complete set of genes. The eventually resulting offspring has the same number of genes as their parents, but for any gene one of their two copies comes from their father, and one from their mother.[1]

The effects of this mixing depend on the types (the alleles) of the gene. If the father has two copies of an allele for red hair, and the mother has two copies for brown hair, all their children get the two alleles that give different instructions, one for red hair and one for brown. The hair color of these children depends on how these alleles work together. If one allele dominates the instructions from another, it is called the dominant allele, and the allele that is overridden is called the recessive allele. In the case of a daughter with alleles for both red and brown hair, brown is dominant and she ends up with brown hair.[2]

Although the red color allele is still there in this brown-haired girl, it doesn't show. This is a difference between what you see on the surface (the traits of an organism, called its phenotype) and the genes within the organism (its genotype). In this example you can call the allele for brown "B" and the allele for red "b". (It is normal to write dominant alleles with capital letters and recessive ones with lower-case letters.) The brown hair daughter has the "brown hair phenotype" but her genotype is Bb, with one copy of the B allele, and one of the b allele.

Now imagine that this woman grows up and has children with a brown-haired man who also has a Bb genotype. Her eggs will be a mixture of two types, one sort containing the B allele, and one sort the b allele. Similarly, her partner will produce a mix of two types of sperm containing one or the other of these two alleles. When the transmitted genes are joined up in their offspring, these children have a chance of getting either brown or red hair, since they could get a genotype of BB = brown hair, Bb = brown hair or bb = red hair. In this generation, there is therefore a chance of the recessive allele showing itself in the phenotype of the childrensome of them may have red hair like their grandfather.[2]

Many traits are inherited in a more complicated way than the example above. This can happen when there are several genes involved, each contributing a small part to the end result. Tall people tend to have tall children because their children get a package of many alleles that each contribute a bit to how much they grow. However, there are not clear groups of "short people" and "tall people", like there are groups of people with brown or red hair. This is because of the large number of genes involved; this makes the trait very variable and people are of many different heights.[3] Despite a common misconception, the green/blue eye traits are also inherited in this complex inheritance model.[4] Inheritance can also be complicated when the trait depends on interaction between genetics and environment. For example, malnutrition does not change traits like eye color, but can stunt growth.[5]

Some diseases are hereditary and run in families; others, such as infectious diseases, are caused by the environment. Other diseases come from a combination of genes and the environment.[6]Genetic disorders are diseases that are caused by a single allele of a gene and are inherited in families. These include Huntington's disease, Cystic fibrosis or Duchenne muscular dystrophy. Cystic fibrosis, for example, is caused by mutations in a single gene called CFTR and is inherited as a recessive trait.[7]

Other diseases are influenced by genetics, but the genes a person gets from their parents only change their risk of getting a disease. Most of these diseases are inherited in a complex way, with either multiple genes involved, or coming from both genes and the environment. As an example, the risk of breast cancer is 50 times higher in the families most at risk, compared to the families least at risk. This variation is probably due to a large number of alleles, each changing the risk a little bit.[8] Several of the genes have been identified, such as BRCA1 and BRCA2, but not all of them. However, although some of the risk is genetic, the risk of this cancer is also increased by being overweight, drinking a lot of alcohol and not exercising.[9] A woman's risk of breast cancer therefore comes from a large number of alleles interacting with her environment, so it is very hard to predict.

The function of genes is to provide the information needed to make molecules called proteins in cells.[1] Cells are the smallest independent parts of organisms: the human body contains about 100 trillion cells, while very small organisms like bacteria are just one single cell. A cell is like a miniature and very complex factory that can make all the parts needed to produce a copy of itself, which happens when cells divide. There is a simple division of labor in cellsgenes give instructions and proteins carry out these instructions, tasks like building a new copy of a cell, or repairing damage.[10] Each type of protein is a specialist that only does one job, so if a cell needs to do something new, it must make a new protein to do this job. Similarly, if a cell needs to do something faster or slower than before, it makes more or less of the protein responsible. Genes tell cells what to do by telling them which proteins to make and in what amounts.

Proteins are made of a chain of 20 different types of amino acid molecules. This chain folds up into a compact shape, rather like an untidy ball of string. The shape of the protein is determined by the sequence of amino acids along its chain and it is this shape that, in turn, determines what the protein does.[10] For example, some proteins have parts of their surface that perfectly match the shape of another molecule, allowing the protein to bind to this molecule very tightly. Other proteins are enzymes, which are like tiny machines that alter other molecules.[11]

The information in DNA is held in the sequence of the repeating units along the DNA chain.[12] These units are four types of nucleotides (A,T,G and C) and the sequence of nucleotides stores information in an alphabet called the genetic code. When a gene is read by a cell the DNA sequence is copied into a very similar molecule called RNA (this process is called transcription). Transcription is controlled by other DNA sequences (such as promoters), which show a cell where genes are, and control how often they are copied. The RNA copy made from a gene is then fed through a structure called a ribosome, which translates the sequence of nucleotides in the RNA into the correct sequence of amino acids and joins these amino acids together to make a complete protein chain. The new protein then folds up into its active form. The process of moving information from the language of RNA into the language of amino acids is called translation.[13]

If the sequence of the nucleotides in a gene changes, the sequence of the amino acids in the protein it produces may also changeif part of a gene is deleted, the protein produced is shorter and may not work any more.[10] This is the reason why different alleles of a gene can have different effects in an organism. As an example, hair color depends on how much of a dark substance called melanin is put into the hair as it grows. If a person has a normal set of the genes involved in making melanin, they make all the proteins needed and they grow dark hair. However, if the alleles for a particular protein have different sequences and produce proteins that can't do their jobs, no melanin is produced and the person has white skin and hair (albinism).[14]

Genes are copied each time a cell divides into two new cells. The process that copies DNA is called DNA replication.[12] It is through a similar process that a child inherits genes from its parents, when a copy from the mother is mixed with a copy from the father.

DNA can be copied very easily and accurately because each piece of DNA can direct the creation of a new copy of its information. This is because DNA is made of two strands that pair together like the two sides of a zipper. The nucleotides are in the center, like the teeth in the zipper, and pair up to hold the two strands together. Importantly, the four different sorts of nucleotides are different shapes, so for the strands to close up properly, an A nucleotide must go opposite a T nucleotide, and a G opposite a C. This exact pairing is called base pairing.[12]

When DNA is copied, the two strands of the old DNA are pulled apart by enzymes; then they pair up with new nucleotides and then close. This produces two new pieces of DNA, each containing one strand from the old DNA and one newly made strand. This process is not predictably perfect as proteins attach to a nucleotide while they are building and cause a change in the sequence of that gene. These changes in DNA sequence are called mutations.[15] Mutations produce new alleles of genes. Sometimes these changes stop the functioning of that gene or make it serve another advantageous function, such as the melanin genes discussed above. These mutations and their effects on the traits of organisms are one of the causes of evolution.[16]

A population of organisms evolves when an inherited trait becomes more common or less common over time.[16] For instance, all the mice living on an island would be a single population of mice: some with white fur, some gray. If over generations, white mice became more frequent and gray mice less frequent, then the color of the fur in this population of mice would be evolving. In terms of genetics, this is called an increase in allele frequency.

Alleles become more or less common either by chance in a process called genetic drift, or by natural selection.[17] In natural selection, if an allele makes it more likely for an organism to survive and reproduce, then over time this allele becomes more common. But if an allele is harmful, natural selection makes it less common. In the above example, if the island were getting colder each year and snow became present for much of the time, then the allele for white fur would favor survival, since predators would be less likely to see them against the snow, and more likely to see the gray mice. Over time white mice would become more and more frequent, while gray mice less and less.

Mutations create new alleles. These alleles have new DNA sequences and can produce proteins with new properties.[18] So if an island was populated entirely by black mice, mutations could happen creating alleles for white fur. The combination of mutations creating new alleles at random, and natural selection picking out those that are useful, causes adaptation. This is when organisms change in ways that help them to survive and reproduce. Many such changes, studied in evolutionary developmental biology, affect the way the embryo develops into an adult body.

Since traits come from the genes in a cell, putting a new piece of DNA into a cell can produce a new trait. This is how genetic engineering works. For example, rice can be given genes from a maize and a soil bacteria so the rice produces beta-carotene, which the body converts to Vitamin A.[19] This can help children suffering from Vitamin A deficiency. Another gene being put into some crops comes from the bacterium Bacillus thuringiensis; the gene makes a protein that is an insecticide. The insecticide kills insects that eat the plants, but is harmless to people.[20] In these plants, the new genes are put into the plant before it is grown, so the genes are in every part of the plant, including its seeds.[21] The plant's offspring inherit the new genes, which has led to concern about the spread of new traits into wild plants.[22]

The kind of technology used in genetic engineering is also being developed to treat people with genetic disorders in an experimental medical technique called gene therapy.[23] However, here the new gene is put in after the person has grown up and become ill, so any new gene is not inherited by their children. Gene therapy works by trying to replace the allele that causes the disease with an allele that works properly.

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Introduction to genetics - Wikipedia

The Jekyll Island Authority Historic Preservation and Conservation Committee is hoping to find out if the recently discovered bobcats living on Jekyll Island are from the same genealogy as the bobcats on Cumberland Island.

According to Ben Carswell, director of conservation for the authority, the first bobcat genetic samples have been sent off to Penn State University for analysis.

A recently confirmed sighting of the mate and two kittens of a bobcat known to live on the island was announced last month.

Motion-triggered cameras placed throughout the island captured pictures of the bobcat family.

Bobcat sightings have been reported throughout the years on Jekyll Island, however, Sept. 1, 2014, was the first documented sighting.

Its been suggested that the male, in his search to establish territory, may have wondered over to Jekyll Island from the mainland.

The DNA analysis from Penn State could provide some insight into the origins of these particular cats.

Bobcats have been sighted on the Downing Musgrove Causeway in the past. Reportedly, its possible for them to either cross the bridge or swim Jekyll Creek to get to the island.

In the late 1980s, bobcats were successfully reintroduced on neighboring Cumberland Island. As native predators to Coastal Georgia, they are part of the areas biological diversity.

With a yellowish, gray, or reddish-brown, leopard print coat and short, stubby tail, bobcats are about twice the size of an average house cat. Adult males weigh between 18 to 25 pounds and adult females weigh 15 to 20 pounds.

Though the bobcats are predators, Carswell said previously they pose no threat to humans, but cautioned residents to keep a close eye on their pets, something he said should be done anyway.

According to Carswell, the bobcats are feeding on deer on Jekyll Island, a natural and important occurrence for the ecosystems balance and health.

The authoritys conservation team continues to monitor the cats to track, analyze and understand the population.

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Penn State University to study Jekyll bobcats' genetics - The News (subscription)

How does one set of genes result in huge horns in males and none at all in females?

Picture a lion: The male has a luxuriant mane, the female doesnt. This is a classic example of what biologists call sexual dimorphism the two sexes of the same species exhibit differences in form or behavior. Male and female lions pretty much share the same genetic information, but look quite different.

Were used to thinking of genes as responsible for the traits an organism develops. But different forms of a trait mane or no mane can arise from practically identical genetic information. Further, traits are not all equally sexually dimorphic. While the tails of peacocks and peahens are extremely different, their feet, for example, are pretty much the same.

Understanding how this variation of form what geneticists call phenotypic variation arises is crucial to answering several scientific questions, including how novel traits appear during evolution and how complex diseases emerge during a lifetime.

So researchers have taken a closer look at the genome, looking for the genes responsible for differences between sexes and between traits within one sex. The key to these sexually dimorphic traits appears to be a kind of protein called a transcription factor, whose job it is to turn genes on and off.

In our own work with dung beetles, my colleagues and I are untangling how these transcription factors actually lead to the different traits we see in males and females. A lot of it has to do with something called alternative gene splicing a phenomenon that allows a single gene to encode for different proteins, depending on how the building blocks are joined together.

Over the years, different groups of scientists independently worked with various animals to identify genes that shape sexual identity; they realized that many of these genes share a specific region. This gene region was found in both the worm gene mab-3 and the insect gene doublesex, so they named similar genes containing this region DMRT genes, for doublesex mab-related transcription factors.

These genes code for DMRT proteins that turn on or off the reading, or expression, of other genes. To do this, they seek out genes in DNA, bind to those genes, and make it either easier or harder to access the genetic information. By controlling what parts of the genome are expressed, DMRT proteins lead to products characteristic of maleness or femaleness. They match the expression of genes to the right sex and trait.

DMRTs almost always confer maleness. For instance, without DMRT, testicular tissue in male mice deteriorates. When DMRT is experimentally produced in female mice, they develop testicular tissue. This job of promoting testis development is common to most animals, from fish and birds to worms and clams.

DMRTs even confer maleness in animals where individuals develop both testes and ovaries. In fish that exhibit sequential hermaphroditism where gonads change from female to male, or vice versa, within the same individual the waxing and waning of DMRT expression results in the appearance and regression of testicular tissue, respectively. Likewise, in turtles that become male or female based on temperatures experienced in the egg, DMRT is produced in the genital tissue of embryos exposed to male-promoting temperatures.

The situation is a little different in insects. First, the role of DMRT (doublesex) in generating sexual dimorphism has extended beyond gonads to other parts of the body, including mouthparts, wingspots and mating bristles aptly named sex combs.

Secondly, male and female insects generate their own versions of the doublesex protein through whats called alternative gene splicing. This is a way for a single gene to code for multiple proteins. Before genes are turned into proteins, they must be turned on; that is, transcribed into instructions for how to build the protein.

But the instructions contain both useful and extraneous regions of information, so the useful parts must be stitched together to create the final protein instructions. By combining the useful regions in different ways, a single gene can produce multiple proteins. In male and female insects, its this alternative gene splicing that results in the doublesex proteins behaving differently in each sex.

So in a female, instructions from the doublesex gene might include sections 1, 2 and 3, while in a male the same instruction might include only 2 and 3. The different resulting proteins would each have their own effect on what parts of the genetic code are turned on or off leading to a male with huge mouthparts and a female without, for instance.

How do male and female forms of doublesex regulate genes to produce male and female traits? Our research group answered this question using dung beetles, which are exceptionally numerous in species (over 2,000), widespread (inhabiting every continent except Antarctica), versatile (consuming about every type of dung) and show amazing diversity in a sexually dimorphic trait: horns.

We focused on the bull-headed dung beetle Onthophagus taurus, a species in which males produce large, bull-like head horns but females remain hornless. We found that doublesex proteins can regulate genes in two ways.

In most traits, it regulates different genes in each sex. Here, doublesex is not acting as a switch between two possible sexual outcomes, but instead bestowing maleness and femaleness to each sex independently. Put another way, these traits dont face a binary decision between becoming male or female, they are simply asexual and poised for further instruction.

The story is different for the dung beetles head horns. In this case, doublesex acts more like a switch, regulating the same genes in both sexes but in opposite directions. The female protein suppressed genes in females that would otherwise be promoted by the male protein in males. Why would there be an evolutionary incentive to do this?

Our data hinted that the female doublesex protein does this to avoid what is known as sexual antagonism. In nature, fitness is sculpted by both natural and sexual selection. Natural selection favors traits increasing survival, whereas sexual selection favors traits increasing access to mates.

Sometimes these forces are in agreement, but not always. The large head horns of male O. taurus increase their access to mates, but the same horns would be a hassle for females who have to tunnel underground to raise their offspring. This creates a tension between the sexes, or sexual antagonism, that limits the overall fitness of the species. However, if the female doublesex protein turns off genes that in males are responsible for horn growth, the whole species does better.

Our ongoing research is addressing how doublesex has evolved to generate the vast diversity in sexual dimorphism in dung beetles. Across species, horns are found in different body regions, grow differently in response to different quality diets, and can even occur in females rather than males.

In Onthophagus sagittarius, for instance, its the female that grows substantial horns while males remain hornless. This species is only five million years diverged from O. taurus, a mere drop of time in the evolutionary bucket for insects. For perspective, beetles diverged from flies about 225 million years ago. This suggests that doublesex can evolve quickly to acquire, switch, or modify the regulation of genes underlying horn development.

How will understanding the role of doublesex in sexually dimorphic insect traits help us understand phenotypic variation in other animals, even humans?

Despite the fact that DMRTs are spliced as only one form in mammals and act primarily in males, the majority of other human genes are alternatively spliced; just like insects doublesex gene, most human genes have various regions that can be spliced together in different orders with varying results. Alternatively spliced genes can have distinct or opposing effects based on which sex or trait theyre expressed in. Understanding how proteins that are produced by alternatively spliced genes behave in different tissues, sexes and environments will reveal how one genome can produce a multitude of forms depending on context.

In the end, the humble dung beetles horns can give us a peek into the mechanisms underlying the vast complexity of animal forms, humans included.

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What dung beetles are teaching us about the genetics of sex differences - The Conversation US

How Cannabis Strain Genetics Influence the THC:CBD Ratio

Whydo strains like Blue Dream and Harlequin have such different effects? In large part, its because they have very different THC-to-CBD ratios.

THC and CBD are the two most abundant cannabinoids in most strains. THC is well known as the major psychoactive compound. CBD is best known for having a wide range of medical uses. While CBD lacks the psychoactive properties of THC, it does influence the effects of THC in the brain. This is why the THC:CBD ratio strongly influences a strains effects, and why that ratio is important when deciding which strain is right for you.

Heres the cool part: The THC:CBD ratio is largely determined by strain genetics. Each plants genetic code determines the way the plant produces the two compounds. Its a fascinating process that many consumers arent aware of.

THC and CBD are both made from another cannabinoid called cannabigerol (CBG). Within Cannabis plants, each of these compounds is actually present in a slightly different, acidic form. The plants are really making either THCA or CBDA out of CBGA (Figure 1). Its only after THCA and CBDA are decarboxylatedby heat that we get significant levels of THC and CBD. The heat energy from your vaporizer, lighter, or oven causes a chemical reaction that turns THCA and CBDA into THC and CBD, respectively.

THCA and CBDA dont have the same effects as their activated (decarboxylated) counterparts. Remember that scene in Super Trooperswhere the guy eats a bag of cannabis flower and goes out of his mind? That wouldnt really work, because flower contains mostly THCA, which isnt psychoactive. You would have to heat the flower at the right temperature first, turning the THCA into THC, before eating it would get you high.

A single CBGA molecule can turn into a single THCA or CBDA molecule, but not both. How does the plant decide which to make? That depends on the presence of an enzyme that comes in two flavors. Lets call them Enzyme 1 (E1) and Enzyme 2 (E2).

E1 takes CBGA and converts it into CBDA, while E2 converts CBGA into THCA (Figure 1). Some strains only have E1, some only have E2, and some have both.

Like most plants and animals, Cannabis plants inherit two copies of their genes (although there are rare exceptions to this). As it turns out, the E1 and E2 enzymes that turn CBGA into either CBDA or THCA are encoded by two different versions of the same gene. Because each plant gets two copies of that gene, there are only three possibilities: A plant can have two copies of the gene that encodes the E1 enzyme, it can have one copy each of the genes that encode E1 and E2, or it can have two copies of the gene that encodes E2 (Figure 2).

Importantly, these three possibilities are based solely on the THC:CBD ratio, and dont take into account other compounds that a particular strain might produce. The three broad THC:CBD ratio strain categories are:

Cannabis genetics limit THC and CBD production so that only these three broad categories of flower are possible. Hemp strains do not produce significant levels of THC, while most commercial strains fall into the high-THC categorythey have THC but negligible levels of CBD. Mixed strains produce both THC and CBD, but generally not as much THC as high-THC strains or as much CBD as the more potent hemp strains.

In the next article of this series, we will explore more precisely what the limits on THC and CBD levels are for each of these categories. Later on, well consider some of the effects you may experience when consuming strains with different THC:CBD ratios.

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How Strain Genetics Influence THC:CBD Ratios | Leafly - Leafly

Its often said that humans are 99.9% identical. and what makes us unique is a measly 0.1% of our genome. This may seem insignificant. But what these declarations fail to point out is that the human genome is made up of three billion base pairswhich means 0.1% is still equal to three million base pairs.

In those three million differences lie the changes that give you red hair instead of blonde, or green eyes instead of blue. You can find changes that increase your risk of obesity, or others that decrease your risk of heart disease; differences that make you taller or lactose intolerant, or allow you to run faster.

When I first started learning about genetic variation, I assumed these changesthe 0.1% that make us uniqueonly appeared in certain places, such as genes for height or inherited diseases like diabetes. I thought the rest of the genomethe other 99.9%was fixed; that the 0.1% that was different in me was more or less the same 0.1% that was different in you. But, as it turns out, the 0.1% of DNA that is different between people is not always the same 0.1%: Variation can happen anywhere in our genomes.

In fact, one group of scientists looking at 10,000 people found variants at 146 million unique positions, or about 4.8% of the genome. Another group collected the DNA from 15,000 people and found 254 million variants, roughly 8% of the genome. And as we continue to sequence 100,000, 100 million, or all seven billion people on the planet, we will find a lot more variation. This means that humans have many more differences than we first thought.

Imagine that your DNA is a car. There are certain obvious variants you can have: blue or white, two-door or four-door, convertible or sedan. These changes represent the 0.1%. Because the other 99.9%the engine, the seats, the steering wheel, the tireshas to be there for the car to work, we assume they are fixed.

But electric cars have shown us that we dont need the gas cap, the gas tank, or even a gas engine any more; we can replace those things with a variant like batteries and charging ports. And maybe one day well develop cars that have boosters instead of tires so we can hover over the ground.

In other words, what we believe is static may actually be variable. More than 0.1% of the car can change and it still be a car, just like the human genome.

With the rise of services that offer to sequence your DNA, more and more people are talking about the value of personal genomics and what you might uncover about yourself. These kinds of mail-in tests are an easy way to point to something tangiblelike your blue eyes or the waddle you and your grandmother shareand say It runs in the family. You might even say, Theres a gene for that!

But those examples of straight-forward, visible evidence are just starting points in the immense and only partially explored field of personal genomics. There are also many variations of our genomes that are invisible to the naked eye, like the way we metabolize caffeine, have a distaste for cilantro, or the more serious examples of predispositions toward certain types of cancers and diseases like Alzheimers and Parkinsons.

There are also all sorts of other gene variants we havent discovered yet. Because our data is limited by the amount of sequenced DNA available for study, scientists like myself have only explored a small portion of the genetic variation that exists in the world.

As access to personal genomics becomes a more practical option and more people opt in to research, this data pool grows every day. This means our theories will become much less theoretical in the months and years to come, and it soon wont be surprising to discover theres a gene for almost every trait.

So what does all this variation actually mean? What do we learn by cataloging all this information?

The consequences of sequencing millions of peoples DNA and identifying new genetic variants are both simultaneously predictable and unknown. On the predictable side, we are going to learn a lot more about human health and disease: Individual genetic variants and groups of genetic variants will be found to play a role in obesity, heart disease, and cancer, among other factors. We are going to find genetic variants responsible for rare diseases that have gone undiagnosed.

But its the unknown findings that get me excited. We dont know how many unique variants we will find. And while our current understanding of biology suggests some positions in DNA are not variable (because any change in these genes disrupts the basic function of being human), we may discover that these positions actually are variable and can change. Were also getting to a point where we will be able to better study the role of environmentwhat you are exposed to, the things you choose to eat, the activities you decided to engage inand how it interacts with your DNA. With this information, we will be able to better make predictions about you as an individual.

There is still so much for us to discover about human genetic variation. A variant that increases risk for a disease today might turn out to be protective for another disease tomorrow. The more people who get their DNA sequencedwhether for personal or research purposesthe more we will discover.

We each carry three billion base pairs of information inside us with the potential to unravel a piece of the mystery that makes us all so fundamentally human. At the end of the day, we are all still more similar than we are differentbut we are just beginning to understand how important our differences are.

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Genetics has proven that you're uniquejust like everyone else - Quartz