Tufts University will continue to teach local students about the possibilities of genetics work thanks to a $100,000 grant from Cummings Foundation.

Tufts University's popular Bioinformatics Inquiry through Sequencing (BioSeq) program will continue to teach local students about the possibilities of genetics work thanks to a $100,000 grant from Cummings Foundation.

BioSeq uses an interactive curriculum that emphasizes the value of genetics in personally relevant contexts, preparing students for research careers and enhancing understanding of how genetics work can shape and save lives.

The BioSeq program is part of Tufts and Cummings Foundation's legacy of support for science, technology, engineering and mathematics (STEM) education opportunities for students in greater Boston.

Started with funding from the National Institutes of Health Science Education Partnership Award and now in its fifth year, BioSeq has reached over 1,000 students in Medford, Somerville and Malden schools.

Until recently, genetic sequencing was labor-intensive, slow and expensive. Thanks to next-generation sequencing, however, scientists are employing new tools to gather genetic data and to draw meaningful conclusions on how the data can push the boundaries of medical knowledge and bring the promise of personalized medicine closer to reality. Despite these tremendous advances, this technology is largely out of the reach of the high school audience.

Due to cost and curriculum restraints, students in low-income and diverse urban communities often have limited opportunities to interact with genetics science, though within their lifetimes, current high school students will have to understand how their genetics may influence the treatments they receive and the drugs they are prescribed. The BioSeq program works to expose students to the possibilities of genetic sequencing so they will be more comfortable and better informed as genomics plays an increasingly influential role in health and medicine.

BioSeq engages and challenges students in their high school classrooms by focusing on inquiry-based experiments that relate to them directly. This grant will enable the program to continue to support classroom experiments such as "The Microbiome Portrait Experiment" in which students analyze their own DNA as well as local students and classes with their genomic science fair projects and will provide scholarships for the BioSeq summer program, run by Tufts Summer Studies.

"We're very grateful for Cumming Foundation's generosity and its continued commitment to both Tufts University and the goal of enhancing STEM education for young students from our local communities. Because of Cummings Foundation's support, students will have opportunities to learn by asking and answering their own questions about genetics," said Matthew Fierman, Ph.D., BioSeq's program administrator.

Cummings Foundation, Inc., founded by Tufts alumnus and trustee emeritus Bill Cummings and his wife, Joyce Cummings, has awarded more than $170 million in grants to non-profit organizations serving a broad range of causes in greater Boston and around the world, including human services, education, health care, and social justice. Cummings Foundation is active internationally through aid to the post-genocide rebuilding of Rwanda and support of education to help prevent future genocides and other intercultural violence and injustice. The Cummings' philanthropy has had a significant impact on the Tufts community in particular, including a naming gift in support of Cummings School of Veterinary Medicine at Tufts University.

For more information about the BioSeq program, including sample classroom activities, please visit: http://ase.tufts.edu/chemistry/walt/sepa/index.html

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Cummings grants Tufts $100K to bolster genetics program - Wicked Local Medford

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Wisconsin State Farmer 4:57 p.m. CT June 13, 2017

Select Sires Inc., and Accelerated Genetics will join forces this summer.(Photo: Select Sires Inc.)

BARABOO, WI - Two well known A.I. organizations will join forces this summer.

The board of directors for Select Sires Inc., and Accelerated Genetics reached a unanimous decision to unify the two cooperatives. Under the planned agreement, Select Sires will acquire the assets of Accelerated Genetics, joining together employees and independent sales representatives in each of their geographical member organizations.

This decision coincides with an already collaborative business relationship that began in 2001, where each shares ownership of World Wide Sires, Ltd. World Wide Sires serves as the international marketing arm for both companies in Europe, Africa, Asia, the Middle East and Oceania.

On June 22, 2017, Accelerated Genetics delegates will come together to cast the final vote on the direction of the cooperative. The goal is to create a unified cooperative that is second-to-none in the market place dedicated to the producer, according to company officials.

This impending endeavor is expected to create a well-rounded genetics program and solution-based animal health care product line that will fit the needs of dairy and beef producers worldwide. Producers can expect to continue working with highly qualified, passionate individuals, who know and understand the cattle breeding industry.

Based in Plain City, OH, Select Sires Inc. is North Americas largest A.I. organization and is comprised of nine farmer-owned and -controlled cooperatives

Read or Share this story: http://www.wisfarmer.com/story/news/state/2017/06/13/select-sires-inc-and-accelerated-genetics-join-forces/394333001/

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Select Sires Inc., and Accelerated Genetics to join forces - Wisconsin State Farmer

Cystic fibrosis is a common genetic disease, relatively speaking. About one in 25 to 30 Caucasians are carriers of a cystic fibrosis mutation. But there are more than 1,700 mutations of the cystic fibrosis gene that can result in different disease symptoms.

Researchers and companies working on cystic fibrosis treatments are increasingly paying attention to which mutations a patient carries, and tailoring drugs to certain mutations.

Just recently, the FDA expanded its approval for one cystic fibrosis drug called Kalydeco. It had been approved for use in the case of ten of the mutations. Now its approved for 33.

They did it without a full clinical trial. The reason: each mutation is so rare, there just arent the hundreds of people a lab needs to do a clinical drug trial.

You just cant do it, said Art Caplan, Professor of Bioethics at New York University's Langone Medical Center.

Some of the things we usually see, like a randomized trial with hundreds or thousands of subjects, are not going to work because of the ability to pick out genetic differences among subjects, making it harder to do the big studies, he said.

Another fundamental shift in this area of medicine has to do with how drugs are used. Labs are now investigating how a the same drug might treat a wide range of maladies.

Some diseases that we dont even think of as related -- lets say, ALS, muscular dystrophy, and severe depression they may turn out to have the same chemical pathway that you can block with a drug, Caplan said.

It is huge and it is the future.

Originally posted here:
Discoveries in Genetics Are Changing the Way Drugs Are Tested - WCAI

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Genetics: Recipe for intelligence - Nature.com

Sessions/Tracks

ConferenceSeries LLC provides the perfect platform for global networking and we are truly delighted to invite you to attend our 9thInternational Conference on Genomics & Pharmacogenomics, during June 15-16, 2017London, UK. Genomics-2017 is a global platform to discuss and learn about Genomics & Pharmacogenomics and its allied areas Bioinformatics, Transcriptomics, Biotechnology, Molecular Biology, Molecular Genetics and Genetic Engineering.

Track 1:Cancer Genomics

TumorGenomicsis the investigation ofhereditarytransformationsin charge of malignancy, utilizinggenomesequencingandbioinformatics. Diseasegenomicsis to enhance growth treatment and results lies in figuring out which sets of qualities and quality associations influence diverse subsets of tumors. UniversalCancer GenomeConsortium (ICGC) is a deliberate experimental association that gives a discussion to joint effort among the world's driving growth andgenomic analysts.

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Track 2:Functional Genomics

UtilitarianGenomicsuse incomprehensible abundance of information created bygenomic transcriptomictasks to portray quality capacities and cooperations. Patterns inFunctional Genomicsare Affymetrix developed as an early trend-setter around there by imagining a commonsense approach to examine quality capacity as a framework.

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Track 3:Next Generation Sequencing

Cutting edge sequencing(NGS) is regularly alluded to as greatly parallel sequencing, which implies that a large number of little parts ofDNAcan be sequenced in the meantime, making a gigantic pool of information. Cutting edge sequencing (NGS), hugely parallel or profound sequencing is connected terms that portray aDNA sequencinginnovation which has upsetgenomic research.

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Track 4:Biomarkers & Molecular Markers

Biomarkerscan be trademark organic properties or particles that can be distinguished and measured in parts of the body such as the blood or tissue.Biomarkerscan be particular cells, atoms, or qualities, quality items, chemicals, orhormones.Atomicmarkeris a section of DNA that is connected with a specific area inside of thegenome. Atomic markers are utilized as a part of sub-atomic science andbiotechnologyto distinguish a specific grouping of DNA in a pool of obscure DNA.

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Track: 5Pharmacogenomics & Personalized Medicine

Pharmacogenomicsis a piece of a field called customized solution that means to tweak human services, with choices and medications custom-made to every individual patient inside and out conceivable.Pharmacogenomicsandpharmacogenomicsmanages new developments in the field of customized meds and advancements in modified medication revelation utilizingproteomeinnovation.

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Track 6:Clinical Genomics

Clinical Genomicsis the utilization of genome sequencing to educate understanding analysis and care.Genome sequencingis relied upon to have the most effect in: portraying and diagnosinghereditary infection; stratifying patients for fittingmalignancytreatment; and giving data around an individual'simaginable reactionto treatment to lessen antagonistic medication responses.

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Track 7:Micro RNA

MicroRNAscomprise a novel class of small, non-coding endogenous RNAs that regulategene expressionby directing their targetmRNAsfor degradation or translational repression. miRNAs represent smallRNA moleculesencoded in thegenomesofplantsand animals. These highly conserved 22 nucleotides longRNA sequencesregulate the expression of genes by binding to the 3'-untranslated regions (3'-UTR) of specific mRNAs. A growing body of evidence shows that mRNAs are one of the key players in cell differentiation and growth, mobility andapoptosis.

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Track 8:mRNA Analysis

mRNAis a subtype of RNA. AmRNAatom conveys a segment of the DNA code to different parts of the cell for preparing.mRNAis made amid interpretation. Amid the translation handle, a solitary strand ofDNAis decoded by RNA polymerase, and mRNA is incorporated. Physically, mRNA is a strand of nucleotides known asribonucleiccorrosive, and is single-stranded.

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Track9:BioinformaticsinGenomics

Bioinformaticsis the exploration of gathering and breaking down complex organic information, for example,hereditary codes. Sub-atomic solution requires the joining and examination of genomic, sub-atomic, cell, and additionallyclinical informationand it in this way offers a momentous arrangement of difficulties to bioinformatics.

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Track 10:Comparative Genomics

SimilarGenomicsandgenomicmedicinenewfieldofnaturalexaminationinwhichthegenomegroupins of variousspecies- human, mouse and a wide assortment of different life forms from yeast to chimpanzees-are looked at. The assessment of likenesses and contrasts betweengenomesof various life forms; can uncover contrasts in the middle of people and species and also transformative connections.

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Track 11:Plant Genomics

Late mechanical headways have generously extended our capacity to dissect and comprehendplantgenomesand to diminish the crevice existing in the middle of genotype and phenotype. The quick advancing field of genomics permits researchers to dissect a huge number of qualities in parallel, to comprehend the hereditary building design ofplant genomesfurthermore to separate the qualities in charge oftransformations.

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Track 12:Personal Genomics

Individualgenomicsis the branch of genomics worried with thesequencingand examination of the genome of a person. Thegenotypingstage utilizes diverse strategies, includingsingle-nucleotide polymorphism(SNP) examination chips or incomplete or fullgenome sequencing.

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Track 13:Microbial Genomics

MicrobialGenomicsappliesrecombinantDNA,DNAsequencingroutines,andbioinformaticsto succession, gather, and dissect the capacity and structure of genomes in organisms. Amid the previous 10 years, genomics-based methodologies have profoundly affected the field ofmicrobiologyand our comprehension of microbial species. In view of their bigger genome sizes,genome sequencingendeavors on growths and unicellular eukaryotes were slower to begin than ventures concentrated on prokaryotes.

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Track 14:Future trends in Genomics

Genomics researchholds the way to meeting a considerable lot of the difficulties of the coming years. Right now, the greatest test is in information investigation. We can produce a lot of information modestly, yet that overpowers our ability to comprehend it. The significant test of theGenomeResearch is we have to imbuegenomic datainto restorative practice, which is truly hard.

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Originally posted here:
Worlds Leading Genomics Conference | Global Meetings ...

Researchers from Vrije Universiteit Amsterdam and elsewhere have identified seven risk genes for insomnia.

Insomnia is one of the most common health problems. Image credit: Dan Fa.

Insomnia is among the most frequent complaints in general practice. Even after treatment, poor sleep remains a persistent vulnerability for many people.

A research team led by Vrije Universiteit Professor Danielle Posthuma has come closer to unraveling the biological mechanisms that cause the predisposition for insomnia.

Our findings are the start of a path towards an understanding of insomnia at the level of communication within and between neurons, and thus towards finding new ways of treatment, Vrije Universiteit Professor Van Someren, co-author of the study.

As compared to the severity, prevalence and risks of insomnia, only few studies targeted its causes. Insomnia is all too often dismissed as being all in your head. Our research brings a new perspective. Insomnia is also in the genes.

To identify genetic factors for insomnia complaints, Prof. Posthuma, Prof. Someren and their colleagues performed a genome-wide association study and a genome-wide gene-based association study in 113,006 individuals.

As a result, the researchers identified seven genes associated with insomnia.

These genes play a role in the regulation of transcription, the process where DNA is read in order to make an RNA copy of it, and exocytosis, the release of molecules by cells in order to communicate with their environment, the authors said.

One of the identified genes, MEIS1, has previously been related to two other sleep disorders: periodic limb movements of sleep (PLMS) and restless legs syndrome (RLS).

Variants in the MEIS1 gene seem to contribute to all three disorders, they added.

Strikingly, PLMS and RLS are characterized by restless movement and sensation, respectively, whereas insomnia is characterized mainly by a restless stream of consciousness.

The team also found a strong genetic overlap with other traits, such as anxiety disorders, depression and neuroticism, and low subjective wellbeing.

This is an interesting finding, because these characteristics tend to go hand in hand with insomnia, said study first author Anke Hammerschlag, a PhD student at Vrije Universiteit.

We now know that this is partly due to the shared genetic basis.

The researchers also studied whether the same genetic variants were important for men and women.

Part of the genetic variants turned out to be different. This suggests that, for some part, different biological mechanisms may lead to insomnia in men and women, Prof. Posthuma said.

We also found a difference between men and women in terms of prevalence: in the sample we studied, including mainly people older than fifty years, 33% of the women reported to suffer from insomnia. For men this was 24%.

The teams findings were published today in the journal Nature Genetics.

_____

Anke R. Hammerschlag et al. Genome-wide association analysis of insomnia complaints identifies risk genes and genetic overlap with psychiatric and metabolic traits. Nature Genetics, published online June 12, 2017; doi: 10.1038/ng.3888

Read more:
Scientists Discover First Genes for Insomnia - Sci-News.com

LOS ANGELES, June 12, 2017 /PRNewswire/ --B-Real, DNA Genetics and PRHBTD Media,have joined forces to produce a new digital first reality series titled, "Pimp My Grow," aimed at cannabis enthusiasts.

DNA Genetics, one of the oldest and most respected genetics and grow experts in the Cannabis industry will visit Cannabis growers around the country and "Pimp Their Grows."Some growers may be new to the industry, looking to set-up their first personal grow for medical reasons, while others are building out industrial-sized indoor operations. All of them have one thing in common; they are looking to harness DNA's best-in-class expertise.

"We're psyched to meet with amateurs as well as experienced growers to help them grow the biggest, healthiest and most special plants!And we're going to bring along a few of our friends to help out," said DNA's Don/Aaron.

B-Real added, "I've seen a ton of good and bad growers and grows in this space. Nothing compares to the work that the DNA guys do.They will literally pimp out some grows.This is going to be unreal and unprecedented."

See more at http://www.prohbtd.com/pimpmygrow.

Drake Sutton-Shearer and Josh Otten from PRHBTD Media added, "Viewers will experience the thrill of growing with some of the best technology available. DNA and B-Real are experts in what they do, so it's a pleasure for us to help them show the world just what it takes to pimp out a grow."

The completed video series will result in seven episodes that showcase each grow operationand the hosts' expertise in helping each grower with their set-up.The series will initially be distributed across the PRHBTD MEDIA network to millions of viewers and then licensed for global content distribution.

B-Real and DNA Genetics will be working with some of their friends to provide product and service support when optimizing each grow. From lighting and nutrients to harvesting and storage, these world-class companies offer some of the best products and services on the market to ensure the highest quality plants and yield.

Added Greg Muller, CEO of leading LED lighting company Spectrum King: "We're excited to be a part of this series and work with these cannabis industry leaders to help show audiences how our technology can help increase potency yield and significant cost savings for growers."

Learn more atwww.prohbtd.com/pimpmygrow

About B-REAL

With his work in the pioneering hip-hop group Cypress Hill, rapper B-Real became something of a hip-hop legend for several reasons. Most immediately, his trademark rhyming style, featuring an exaggeratedly nasal whine and a jazz singer's skill at staying just behind DJ Muggs' already sluggish beats, was one of the most instantly recognizable flows of the 1990s. Furthermore, B-Real and his partners Sen Dog and DJ Muggs were the first Latino hip-hop stars, ushering in a richly varied sub-genre of hip-hop that thrives to this day. Finally, Cypress Hill's fervent proselytizing on the subject of marijuana legalization both brought the subject to its highest public awareness since the days of Cheech & Chong and paved the way for a generation of weed-happy middle-class high-school kids to discover and identify with hip-hop to an even greater degree than before.

About DNA Genetics

DNA Genetics, one of the most important seed companies in the world, has been at the forefront of the cannabis industry and culture for over a decade.DNA has won more than 150 awards worldwide at the most prestigious events and trade shows for their contributions to the cannabis industry, making it the most-awarded company in the world. DNA has won the illustrious High Times 'Top 10 Strain of the Year' award more than five times, is the only seed company to have received every award presented at the High Times Cannabis Cup events and was inducted into the High Times Seedbank Hall of Fame in 2009. Working with the medical and scientific community has been a priority, helping to provide alternative solutions to the current pharmaceutical approach. Collaborations with the Unconventional Foundation for Autism and Israeli Research are some of the examples. DNA Genetics is also very proud of their new partnership with Canadian Licensed Medical Producers, Tweed in Ontario, Canada. When working within the medical community, DNA Genetics is committed not only to effective medicine, but also to combining all beneficial parts of the plant for a better experience and more effective results for the patients.

About PRHBTD MEDIA

PRHBTD MEDIA provides world-class video production, digital marketing and branding solutions for more than 50 brand partners in the cannabis industry. As the leading content studio, PRHBTD also produces original video and editorial with multi-platform distribution across the PRHBTD Media Network, which includes prohbtd.com, AppleTV, Amazon Prime, Roku, Metacafe, Dailymotion and more, reaching 100+ million monthly consumers and business owners.

To learn more, contact whatsgood@prohbtd.com

Media Contact: handsonpr@aol.com

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To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/b-real-dna-genetics-and-prohbtd-media-announce-digital-first-reality-series-pimp-my-grow-300472088.html

SOURCE PROHBTD

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Western Australia's chief scientist Peter Klinken said he was "gobsmacked" when he found he had been made a Companion of the Order of Australia.

Professor Klinken has been recognised for service to medical research and biochemistry through his contributions to understanding the genetics of diseases.

He had also been recognised for promoting science and innovation in WA.

Professor Klinken said the Queen's Birthday honour was unexpected.

"Gobsmacked to be honest, it was just mind-blowing when I got the information. I had to read the letter several times to actually get it to sink in. It is such an honour," he said.

"I didn't go into what I'm doing now with the expectation of receiving accolades, but hopefully what I've done has contributed to the good of our society and I'm just blown away by this honour."

Professor Klinken was born in Singapore, and educated in Perth, where he did a PhD.

He said it was when he went to the United States in the 1980s to do some studies at the National Cancer Institute that he became interested in cancer genetics.

"I spent the vast majority of my scientific career trying to identify these genes that go wrong," he said.

"Working out why they go wrong and how you can try and fix them up in leukaemias and certain cancers."

Professor Klinken said this area of research marked out the achievements he was most proud of.

"Actually identifying that cells, which were apparently committed to one particular function or one job, could actually change their functions change their job description, so to speak," he said.

"At that stage, that was unheard of.

"I was able to introduce a couple of genes into these cells and turn them from what were essentially antibody producing cells into macrophages, which are scavenger cells, and that just broke all the dogma at the time.

"I'm particularly proud of the genes that we've discovered that can go wrong in cases of leukaemias and slowly trying to work out, well, how do they go wrong? What are the steps we can take to try and prevent them from causing cancers and leukaemias?"

After he returned to Perth, Professor Klinken took up a position at RPH, and in 1998 became the director of the WA Institute of Medical Research [later the Harry Perkins Institute of Medical Research].

In 2014, he was asked to be Western Australia's chief scientist.

"It has been a remarkable opportunity, a rare privilege ... to see the breadth and depth and quality of science in Western Australia and play a small role in trying to shape it and explain it to policymakers ... to get them to value science and innovation and how important it is to the state," he said.

"And also to spread the word within the community about how science is such an integral part of our life that we sometimes take it for granted."

Topics: awards-and-prizes, science-awards, perth-6000

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Chief scientist Peter Klinken recognised for work in disease genetics - ABC Online

The study of the genetics and archaeogenetics of the ethnic groups of South Asia aims at uncovering these groups' genetic history. The geographic position of the Indian subcontinent makes its biodiversity important for the study of the early dispersal of anatomically modern humans across Asia.

Studies based on mtDNA variation have reported genetic unity across various Indian subpopulations.[1][2][3][4] Conclusions of studies based on Y Chromosome variation and Autosomal DNA variation have been varied, although many researchers argue that most of the ancestral nodes of the phylogenetic tree of all the mtDNA types originated in the subcontinent. Recent genome studies appear to show that most South Asians are descendants of two major ancestral components, one restricted to South Asia (Ancestral South Indian) and the other component (Ancestral North Indian) more closely related to those in Central Asia, West Asia and Europe.[5][6]

It has been found that the ancestral node of the phylogenetic tree of all the mtDNA types typically found in Central Asia, the West Asia and Europe are also to be found in South Asia at relatively high frequencies. The inferred divergence of this common ancestral node is estimated to have occurred slightly less than 50,000 years ago.[7] In India the major maternal lineages, or mitochondrial DNA haplogroups are M, R and U, whose coalescence times have been approximated to 50,000 BP.[7]

The major paternal lineages represented by Y chromosomes are haplogroups R1a1, R2, H, L and J2.[8] Many Indian researchers have argued that Y-DNA Haplogroup R1a1 (M17) is of autochthonous Indian origin.[9][10] However, proposals for a Central Asian origin for R1a1 are also quite common as it is additionally supported by linguistics and archeology.[11][12]

All the mtDNA and Y-chromosome lineages outside Africa descend from three founder lineages:

All these six founder haplogroups can be found in the present day populations of South Asia. Moreover, the mtDNA haplogroup M and the Y-chromosome haplogroups C and D are restricted to the area east of South Asia. All the West Eurasian populations derive from the N and R haplogroups of mtDNA and the F haplogroup of the Y-chromosome.

Endicott et al. state that these facts are consistent with the hypothesis of a single exodus from East Africa 65,000 years ago via a southern coastal route, with the West Eurasian lineages separating from the South Asian lineages somewhere between East/Northeast Africa and South Asia.

The most frequent mtDNA haplogroups in the Indian subcontinent are M, R and U (where U is a descendant of R).[8]

Arguing for the longer term "rival Y-Chromosome model",[9]Stephen Oppenheimer believes that it is highly suggestive that India is the origin of the Eurasian mtDNA haplogroups which he calls the "Eurasian Eves". According to Oppenheimer it is highly probable that nearly all human maternal lineages in Central Asia, the Middle East and Europe descended from only four mtDNA lines that originated in South Asia 50,000-100,000 years ago.[15]

The macrohaplogroup M which is considered as a cluster of the proto-Asian maternal lineages,[7] represents more than 60% of Indian MtDNA.[16]

The M macrohaplotype in India includes many subgroups that differ profoundly from other sublineages in East Asia especially Mongoloid populations.[7] The deep roots of M phylogeny clearly ascertain the relic of Indian lineages as compared to other M sub lineages (in East Asia and elsewhere) suggesting 'in-situ' origin of these sub-haplogroups in South Asia, most likely in India. These deep rooting lineages are not language specific and spread over all the language groups in India.[16]

Virtually all modern Central Asian MtDNA M lineages seem to belong to the Eastern Eurasian (Mongolian) rather than the Indian subtypes of haplogroup M, which indicates that no large-scale migration from the present Turkic-speaking populations of Central Asia occurred to India. The absence of haplogroup M in Europeans, compared to its equally high frequency among Indians, eastern Asians and in some Central Asian populations contrasts with the Western Eurasian leanings of South Asian paternal lineages.[7]

Most of the extant mtDNA boundaries in South and Southwest Asia were likely shaped during the initial settlement of Eurasia by anatomically modern humans.[17]

The macrohaplogroup R (a very large and old subdivision of macrohaplogroup N) is also widely represented and accounts for the other 40% of Indian MtDNA. A very old and most important subdivision of it is haplogroup U that, while also present in West Eurasia, has several subclades specific to South Asia.

Most important South Asian haplogroups within R:[17]

Haplogroup U is a sub-haplogroup of macrohaplogroup R.[17] The distribution of haplogroup U is a mirror image of that for haplogroup M: the former has not been described so far among eastern Asians but is frequent in European populations as well as among Indians.[18] Indian U lineages differ substantially from those in Europe and their coalescence to a common ancestor also dates back to about 50,000 years.[1]

It is also found in SW Arabia.

It is also found in Oman.

The major Y chromosome DNA haplogroups in the subcontinent are Haplogroup F's descendant haplogroups R (mostly R1a1, R2 and R2a), L, H and J (mostly J2).[8]

The South Asian Y-chromosomal gene pool is characterized by five major lineages: R1a, R2, H, L and J2. Their geographical origins are listed as follows, according to the latest scholarship:

Haplogroup H (Y-DNA) is found at a high frequency in South Asia. H is rarely found outside of the South Asia but is common among the Romanis, particularly the H-M82 subgroup. Haplogroup H is frequently found among populations of India, Sri Lanka, Nepal, Pakistan and Maldives. All three branches of Haplogroup H (Y-DNA) are found in Indian-subcontinent.

It is a branch of Haplogroup F and descends from GHIJK family. Haplogroup H is believed to have arisen in South Asia between 30,000 and 40,000 years ago.[19] Its probable site of introduction is South Asia, since it is concentrated there. It seems to represent the main Y-Chromosome haplogroup of the paleolithic inhabitants of Indian-Subcontinent. Some individuals in South Asia have also been shown to belong to the much rarer subclade H3 (Z5857).[19] Haplogroup H is by no means restricted to specific populations. For example, H is possessed by about 28.8% of Indo-Aryan castes.[9][20] and in tribals about 25-35%.[11][20]

Haplogroup J2 reflects presence from neolithic period in the subcontinent.[21] The frequency of J2 is higher in South Indian castes (19%) than in North Indian castes (11%) or Pakistan (12%).[9]Haplogroup J2 frequency is higher among south Indian middle castes at 21%, followed by upper castes at 18.6%, and lower castes 14%.[9] J2 is present in tribals too and has a frequency of 11% in Austro-Asiatic tribals. Among the Austro-Asiatic tribals, the predominant J2 occurs in the Lodha(35%).[9] J2 is also present in the South Indian hill tribe Toda at a frequency of 38.46%[22] and in the Kol tribe of Uttar Pradesh at a frequency of 33.34%.[23] Haplogroup J-P209 was found to be more common in India's Shia Muslims, of which 28.7% belong to haplogroup J, with 13.7% in J-M410, 10.6% in J-M267 and 4.4% in J2b (Eaaswarkhanth 2009).

In Pakistan, the highest frequencies of J2-M172 were observed among the Parsis at 38.89%, the Dravidian speaking Brahui's at 28.18% and the Makrani Balochs at 24%.[24] It also occurs at 18.18% in Makrani Siddis and at 3% in Karnataka Siddis.[24][25]

J2-M172 is found at an overall frequency of 16.1% in the people of Sri Lanka.[26] In Maldives, 22% of Maldivian population were found to be haplogroup J2 positive.[citation needed]

Haplogroup L shows time of neolithic expansion.[21] The clade is present in the Indian population at an overall frequency of ca.7-15%.[9][11][27][20] There are three subbranches of Haplogroup L and all three are found mostly in South Asia. Haplogroup L has higher frequency among south Indian castes (ca. 17-19%) and reaches up to 68% in some castes in Karnataka but is somewhat rarer in north Indian castes (ca. 5-6%).[9][28] They make a case for an indigenous origin of L-M76 in South Asia as the spatial distributions of both L-M76 HG frequency and associated microsatellite variance show a pattern of spread emanating from southern India.[9] The presence of haplogroup L is quite rare among tribal groups (ca. 5,6-7%)[9][11][20]

Haplogroup L3 (M357) is found frequently among Burusho (approx. 12%[29]) and Pashtuns (approx. 7%[29]), Its highest frequency can be found in south western Balochistan province along the Makran coast (28%) to Indus River delta. L3a (PK3) is found in approximately 23% of Nuristani in northwest Pakistan,[29]

The clade is present in moderate distribution among the general Pakistani population (approx. 11.6%[29]).

In South Asia R1a1 has been observed often with high frequency in a number of demographic groups,[10][30][31] as well as with highest STR diversity which lead some to see it as the locus of origin.[32][33][34]

While R1a originated ca. 22,000[33] to 25,000 years ago, its subclade M417 (R1a1a1) diversified ca. 5,800 years ago. The distribution of M417-subclades R1-Z282 (including R1-Z280) in Central- and Eastern Europe and R1-Z93 in Asia suggests that R1a1a diversified within the Eurasian Steppes or the Middle East and Caucasus region. The place of origin of these subclades plays a role in the debate about the origins of Indo-Europeans.

In India, high percentage of this haplogroup is observed in West Bengal Brahmins (72%) [30] to the east, Konkanastha Brahmins (48%) [30] to the west, Khatris (67%)[31] in north, Iyengar Brahmins (31%) in the south.[30] It has also been found in several South Indian Dravidian-speaking Tribals including the Chenchu (26%)[32] and Valmikis of Andhra Pradesh as well as the Yadav and Kallar of Tamil Nadu suggesting that M17 is widespread in these Southern Indians tribes.[32] Besides these, studies show high percentages in regionally diverse groups such as Manipuris (50%) [31] to the extreme North East and in among Punjabis (47%)[32] to the extreme North West.

In Pakistan it is found at 71% among the Mohanna of Sindh Province to the south and 46% among the Baltis of Gilgit-Baltistan to the north.[31]

23% of the Sinhalese people out of a sample of 87 subjects were found to be R1a1a (R-SRY1532) positive according to a 2003 research.[32]

In Maldives, 24% of the Maldivian people were found to be R1a1a (M17) positive.[citation needed]

People in Terai Region, Nepal show R1a1a at 69%.[37]

In South Asia, the frequency of R2 and R2a lineage is around 10-15% in India and Sri Lanka and 7-8% in Pakistan. At least 90% of R-M124 individuals are located in the Indian sub-continent.[38] It is also reported in Caucasus and Central Asia at lower frequency.

Among regional groups, it is found among West Bengalis (23%), New Delhi Hindus (20%), Punjabis (5%) and Gujaratis (3%).[32] Among tribal groups, Karmalis of West Bengal showed highest at 100%[10] followed by Lodhas (43%)[39] to the east, while Bhil of Gujarat in the west were at 18%,[33]Tharus of north showed it at 17%,[4]Chenchu and Pallan of south were at 20% and 14% respectively.[10][9] Among caste groups, high percentages are shown by Jaunpur Kshatriyas (87%), Kamma Chaudhary (73%), Bihar Yadav (50%), Khandayat (46%)and Kallar (44%).[10]

It is also significantly high in many Brahmin groups including Punjabi Brahmins (25%), Bengali Brahmins (22%), Konkanastha Brahmins (20%), Chaturvedis (32%), Bhargavas (32%), Kashmiri Pandits (14%) and Lingayat Brahmins (30%).[33][12][4][10]

North Indian Muslims have a frequency of 19% (Sunni) and 13% (Shia),[12] while Dawoodi Bohra Muslim in the western state of Gujarat have a frequency of 16% and Mappla Muslims of South India have a frequency of 5%.[40]

The R2 haplogroup is found in 14% of the Burusho people.[29] Among the Hunza it is found at 18% while the Parsis show it at 20%. It is also found in the northeastern part of Afghanistan.[citation needed]

39% of the Sinhalese of Sri Lanka were found to be R2 positive according to a 2003 research.[32]

13% of the Maldivian people of Maldives are found to have R2[citation needed]

In Nepal, R2 percentages range from 2% to 26% within different groups under various studies. Newars show a significantly high frequency of 26% while people of Kathmandu show it at 10%.

The Indian Genome Variation Consortium (2008), divides the population of the subcontinent into four linguistic groups Indo-European, Dravidian, Tibeto-Burman and Austro-Asiatic.[41][42][43][45] The molecular anthropology studies use three different type of markers: Mitochondrial DNA (mtDNA) variation which is maternally inherited and highly polymorphic, Y Chromosome variation which involves uniparental transmission along the male lines, and Autosomal DNA variation.[4]:04

Most of the studies based on mtDNA variation have reported genetic unity of Indian populations across language, caste and tribal groups.[1][2][3] It is likely that haplogroup M was brought to Asia from East Africa along the southern route by earliest migration wave 60,000 years ago.[1]

According to Kivisild et al. (1999), "Minor overlaps with lineages described in other Eurasian populations clearly demonstrate that recent immigrations have had very little impact on the innate structure of the maternal gene pool of Indians. Despite the variations found within India, these populations stem from a limited number of founder lineages. These lineages were most likely introduced to the Indian subcontinent during the Middle Palaeolithic, before the peopling of Europe and perhaps the Old World in general."[1] Basu et al. (2003) also emphasizes underlying unity of female lineages in India.[27]

Conclusions based on Y Chromosome variation have been more varied than those based on mtDNA variation. While Kivisild et al. (2003) proposes an ancient and shared genetic heritage of male lineages in India, Bamshad et al. (2001) suggests an affinity between Indian male lineages and west Eurasians proportionate to caste rank and places caste populations of southern Indian states closer to East Europeans.[46]

Basu et al. (2003) concludes that AustroAsiatic tribal populations entered India first from the Northwest corridor and much later some of them through Northeastern corridor.[27] Whereas, Kumar et al. (2007) analyzed 25 Indian Austro-Asiatic tribes and found strong paternal genetic link among the sub-linguistic groups of the Indian Austro-Asiatic populations.[39] Mukherjee et al. (2001) places North Indians between west Asian and Central Asian populations,[47] whereas Cordaux et al. (2004) argues that the Indian caste populations are closer to Central Asian populations.[20] Sahoo et al. (2006) and Sengupata et al. (2006) suggest that Indian caste populations have not been subject to any recent admixtures.[9][10] Sanghamitra Sahoo concludes his study with:[10]

It is not necessary, based on the current evidence, to look beyond South Asia for the origins of the paternal heritage of the majority of Indians at the time of the onset of settled agriculture. The perennial concept of people, language, and agriculture arriving to India together through the northwest corridor does not hold up to close scrutiny. Recent claims for a linkage of haplogroups J2, L, R1a, and R2 with a contemporaneous origin for the majority of the Indian castes paternal lineages from outside the subcontinent are rejected, although our findings do support a local origin of haplogroups F* and H. Of the others, only J2 indicates an unambiguous recent external contribution, from West Asia rather than Central Asia. The current distributions of haplogroup frequencies are, with the exception of the lineages, predominantly driven by geographical, rather than cultural determinants. Ironically, it is in the northeast of India, among the TB groups that there is clear-cut evidence for large-scale demic diffusion traceable by genes, culture, and language, but apparently not by agriculture.

Results of studies based upon autosomal DNA variation have also been varied. In a major study (2009) using over 500,000 biallelic autosomal markers, Reich hypothesized that the modern Indian population was the result of admixture between two genetically divergent ancestral populations dating from the post-Holocene era. These two "reconstructed" ancient populations he termed "Ancestral South Indians" (ASI) and "Ancestral North Indians" (ANI). According to Reich: "ANI ancestry is significantly higher in Indo-European than Dravidian speakers, suggesting that the ancestral ASI may have spoken a Dravidian language before mixing with the ANI."[48]

Further building on Reich et al.'s characterization of the South Asian population as historically based on admixture of ANI (Ancestral North Indian) and ASI (Ancestral South Indian) populations, a 2013 paper by Moorjani et al. states that a major mixture between populations in India occurred 1,9004,200 years BP characterized by the deurbanization of the Indus civilization and population shift to the Gangetic system.[6]

Basu et al. (2003) suggests concludes that "Dravidian tribals were possibly widespread throughout India before the arrival of the Indo-European-speaking nomads" and that "formation of populations by fission that resulted in founder and drift effects have left their imprints on the genetic structures of contemporary populations".[27] The geneticist PP Majumder (2010) has recently argued that the findings of Reich et al. (2009) are in remarkable concordance with previous research using mtDNA and Y-DNA:[49]

Central Asian populations are supposed to have been major contributors to the Indian gene pool, particularly to the northern Indian gene pool, and the migrants had supposedly moved into India through what is now Afghanistan and Pakistan. Using mitochondrial DNA variation data collated from various studies, we have shown that populations of Central Asia and Pakistan show the lowest coefficient of genetic differentiation with the north Indian populations, a higher differentiation with the south Indian populations, and the highest with the northeast Indian populations. Northern Indian populations are genetically closer to Central Asians than populations of other geographical regions of India... . Consistent with the above findings, a recent study using over 500,000 biallelic autosomal markers has found a north to south gradient of genetic proximity of Indian populations to western Eurasians. This feature is likely related to the proportions of ancestry derived from the western Eurasian gene pool, which, as this study has shown, is greater in populations inhabiting northern India than those inhabiting southern India.

Studies by Watkins et al. (2005) and Kivisild et al. (2003) based on autosomal markers conclude that Indian caste and tribal populations have a common ancestry.[50][51] Reddy et al. (2005) found fairly uniform allele frequency distributions across caste groups of southern Andhra Pradesh, but significantly larger genetic distance between caste groups and tribes indicating genetic isolation of the tribes and castes.[52]

Viswanathan et al. (2004) in a study on genetic structure and affinities among tribal populations of southern India concludes, "Genetic differentiation was high and genetic distances were not significantly correlated with geographic distances. Genetic drift therefore probably played a significant role in shaping the patterns of genetic variation observed in southern Indian tribal populations. Otherwise, analyses of population relationships showed that all Indian and South Asian populations are still similar to one another, regardless of phenotypic characteristics, and do not show any particular affinities to Africans. We conclude that the phenotypic similarities of some Indian groups to Africans do not reflect a close relationship between these groups, but are better explained by convergence."[53]

A 2011 study published in the American Journal of Human Genetics[5] indicates that Indian ancestral components are the result of a more complex demographic history than was previously thought. According to the researchers, South Asia harbours two major ancestral components, one of which is spread at comparable frequency and genetic diversity in populations of Central Asia, West Asia and Europe; the other component is more restricted to South Asia. However, if one were to rule out the possibility of a large-scale Indo-Aryan migration, these findings suggest that the genetic affinities of both Indian ancestral components are the result of multiple gene flows over the course of thousands of years.[5]

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Created: 2017-05-31 Last Modified: 2017-06-09

the basic unit of genetic material - a defined portion of a chromosome that encodes for a particular trait or substance such as hair color, blood type, etc.

the different forms a particular gene can occur in (e.g. brown, blue, green eyes) - you have two copies of each gene (one from mom and one from dad) so there are two potential alleles for each

codominant/incomplete dominace

neither masks the other so both are expressed (AB blood type)

the makeup of the genes - which 2 alleles are present

what actually gets expressed - what you "see"

type A- antigen on red blood cell's surface; type B - B antigen on surface; type AB - both A and B antigens on surface; type O - neither A or B antigen on surface

O is recessive - to have type O blood, an individual must be homozygous (OO); A is dominant- to have type A blood, an individual can be either (AA or AO); type B is also dominant - to have type B you can be either (BB or BO); AB blood has an AB genotype, because the genes are codominant.

in blood donations/transfusions, what will happen

you will react (produce antibodies) against the type(s) you don't have even without prior exposure

can receive from A or O, can donate to A or AB

can receive from B or O, can donate to B or AB

can receive from A, B, AB, or Ol can donate to AB

can receive from O; can donate to A, B, AB, or O

transfusion reactions with the Rh blood system

you will once again react (produce antibodies) against the type(s) / antigen(s) you don't have - in this case, Rh- individuals react against Rh+ cells but only after prior exposure

when an Rh- mother is carrying a Rh+ child. after she is exposed to Rh+ RBC's during the first pregnancy, she may produce IgG antibodies which will cross the placenta and attack deal RBC's in later pregnancies. this is known as hemolytic disease of the newborn or Rh disease

the most common x-inked disorder - a defect in clotting proteins (a recessive trait, designated by a small h)

when can males and females be considered hemopheliac

males - XhY; females XhXh. for females to have it, they have to have both X chromosomes with the h

most common form of color blindness

defect in the production of melanin

a change of a single nucleotide of the hemoglobin b gene (molecule that carries oxygen) - RBC's have typical sickle shape

phenylketonuria - a defect in the enzyme that normally converts Phe to Tyr leads to buildup of phenylalanine in the bloodstream and neurological problems

CF. enzyme defect causes the production of abnormal mucus which causes problems in both the respiratory and gastrointestinal tracts

what does the term autosomal recessive disorder refer to

you must have 2 copies of the bad gene in order for it to be expressed because the trait is on chromosomes other than the sex chromosomes. it must be recessive (cc). if its (Cc) you are a carrier of the gene but do not have the disorder

autosomal dominant disorders

because the gene is dominant, you only need one copy to have the disorder - therefore just one paren needs to have the gene/allele, not both - there are no "carriers"

an invariably fatal neurological disorder which does not show up until 30 or 40 years of age - after the person has had children and possibly passed the gene on

chromosomal and structural disorders general concepts

these involve physical or structural defects in the chromosomes rather than in the genes - they often result fro nondisjunction, where one or more chromosome pairs do not separate during mitosis or meiosis - this leads to cells having too many or too few chromosomes due to unequal distribution during cell division

refers to more than the usual amount of a particular chromosome

also known as trisomy 21 due to the fact that there are 3 copies of that chromosome rather than 2 - associated with structural defects of the face and neurological problems. other examples are XXY (Klinefelter syndrome) or XYY

only one copy of the chromosomes - an example is women with only one X chromosome (turners syndrome)

Dan is a nucleic acid - composed of 4 bases or nucleotides - A, G, C, and T. the three main components of a nucleotide are a 5-carbon sugar, a nitrogenous base (purine or pyrimidine) and a phosphate group

the two strands of DNA are connected by hydrogen bonding between bases in the two strands. known as base pairing. A only pairs with T and G only pairs with C.

the two strands of DNA form a ...

a DNA sequence that triggers gene expression/ transcription

what is the difference in base pairing with RNA vs. DNA

in RNA there is U (uracil) instead of T, so the pairing is A-U and G-C

the initial step is the splitting of the two strand to form a replication fork - it involves helices enzymes - each single stranded DNA will then serve as the template for the synthesis of a complementary (not identical) new strand (e.g. where there is a G in the old strand there will be a C in the new strand). The enzyme primarily responsible for this process is DNA polymerase - gaps in the lagging DNA strand are joined by DNA ligase. DNA polymerase (along with a target specific primer and heat) is a key part of a testing procedure known as the Polymerase Chain reaction (PCR) which can amplify small amount of DNA or RNA being looked for

one strand of the DNA molecule is read to produce RNA - transcription. the mRNA attaches to ribosomes to trigger the production of protein (translation) - the condons in the mRNA are "read" by transfer RNA (tRNA) to place the appropriate amino acids in their place

a DNA sequence that triggers gene expression/transcription

are a cluster of genes controlled by a single promoter (the lac operon is often used as an example of this)

refers to a permanent change in the structure of the DNA which is passed on to the offspring of the effected cell - it may or n=may not have a xnoticebaleeffect and the effect may be either helpful or harmful

a single base is changed - this leads to a change in the codon ( e.g. UGC --> UGG) which in turn leads to the production of a different amino acid. the "sense" or meaning of the codon has been changed. a change in the first two of the three letters in a codon will have the greatest impact

a single base is changed. this leads to a change in the codon (e.g. UAG, UAC) so that it becomes a stop codon which terminates the synthesis of the protein at that point in the mRNA instead of at the real end of the protein - how near this is to the start or end of the message determines its impact

the way the codons in the mRNA are read is messed up by adding or removing bases (the location of this change determines its impact - the closer it is to the start of the message, the more harmful it will be )

an extra base is inserted into the DNA molecule - this throws off the codon it ends up in and also all those "downstream" from that point (a major change)

in this case a base is deleted from the DNA molecule - this again throws off the codon it ends up in and also all those "downstream" from that point (a major change)

refers to the transfer of genetic information from one organism (the donor) to another (the recipient)

bacteria take up DNA from their surroundings through the cell wall of the recipient bacteria and integrated into its own DNA - this can also be done in the laboratory

involves transfer of a small piece of DNA (a plasmid) or possibly chromosomal DNA from one bacteria to another that is connected by a sex pilus - the donor bacteria are designated F+ of Hfr and the recipient bacteria F - ; antibiotic resistance and other genes can be transferred this way

a virus (bacteriophage) carries genetic information from one bacteria to another

transposable genetic elements - aka "jumping genes" - genetic elements that move from one place to another within a chromosome

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