<img loading="lazy" decoding="async" class="alignright size-full wp-image-3516" title="istock_000000440662xsmall" src="https://blog-api.23andme.com/wp-content/uploads/2009/05/istock_000000440662xsmall.jpg" alt="" width="366" height="274" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/05/istock_000000440662xsmall.jpg 400w, https://blogcms.23andme.com/wp-content/uploads/2009/05/istock_000000440662xsmall-300x225.jpg 300w" sizes="auto, (max-width: 366px) 100vw, 366px" />
Even the safest drugs can be dangerous for some people.
Acetaminophen (Tylenol ®), for example, is responsible for more than a third of the approximately 2000 cases of <a href="http://emedicine.medscape.com/article/177354-overview" target="_blank" rel="noopener">acute liver failure</a> that occur each year in the United States.   An estimated 10% of the patients experiencing liver failure due to acetaminophen were taking the recommended dose.   Even among people who do not have liver failure in response to acetaminophen, about a third show temporarily increased liver enzyme levels, a sign of toxicity.
A team of researchers led by David Threadgill at North Carolina State University has used a two-stage approach, which starts in mice and then moves to humans, to investigate whether genetics play a part in determining who will suffer from acetaminophen liver toxicity.   Their results, published online this week in the journal <a href="https://dx.doi.org/10.1101/gr.090241.108 " target="_blank" rel="noopener">Genome Research</a>, suggest that variations in the immune system may be important.
The researchers fed acetaminophen to several genetically distinct strains of mice and found that some had elevated levels of a liver enzyme called ALT, while others were unaffected.   Genetic mapping in these mice revealed several variations that could be responsible for these differences.
The researchers then looked at equivalent variations in human volunteers taking acetaminophen for seven days.   They found an association between a SNP in the CD44 gene and ALT levels: having one copy of a T and one copy of a C at this SNP led to higher ALT levels than having two Cs.
“One of the fascinating things that came out of this study was that the genetic variation in acetaminophen toxicity is not what all the toxicologists would have predicted in the first place.   CD44 doesn’t have anything to do with the rate of metabolism of the drug, but it does have something to do with the immune system,” said Ken Paigen, an executive research fellow at the Jackson Laboratory and a study co-author, in a statement.
There are limits on the interpretation of this study, however. The one person out of the 121 studied who had two Ts at actually had lower ALT levels after taking acetaminophen than people with either CT or CC at this SNP.   This person could be just an anomaly, but more research on this rare genotype will be needed.   Also, the researchers measured only modest elevations in ALT levels in response to normal doses of acetaminophen. Additional studies will be needed to understand if genetic predisposition to these small increases can predict which individuals are more susceptible to the more severe toxicity seen in overdose situations.
According to Threadgill, the success of his two-stage approach has broad implications for drug testing in general.   Genetic variations in humans have not traditionally been taken into account during pre-clinical drug testing in animals.
“If genetic differences are included in early safety testing, more accurate predictions of clinical response will be obtained.   The end result will be safer drugs,” Threadgill said in a statement.

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Genetic Variation In Immune System Protein May Mediate Adverse Reactions To Acetaminophen

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3492" title="mri" src="https://blog-api.23andme.com/wp-content/uploads/2009/05/mri.jpg" alt="" width="346" height="229" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/05/mri.jpg 426w, https://blogcms.23andme.com/wp-content/uploads/2009/05/mri-300x199.jpg 300w" sizes="auto, (max-width: 346px) 100vw, 346px" />
The benign and malignant forms of neuroblastoma may have different genetic underpinnings, a new study published online this week in <a href="https://dx.doi.org/10.1038/ng.374" target="_blank" rel="noopener noreferrer">Nature Genetics</a> suggests.
Neuroblastomas develop from primitive nerve cells in an embryo or fetus and are one of the most common solid tumors in childhood.   They generally occur in infants and very young children and are rarely found in children over the age of 10.   In many cases the tumor is easily treated or disappears on its own.   But about 50% of the time the cancer spreads throughout the body.   Unfortunately, only about 35% of children with this aggressive form of the disease survive, despite intense treatment.
Recent work showed that DNA variations on chromosome 6 are associated with neuroblastoma, and, more specifically, with the aggressive form of the disease.   In this latest study, the same research team that found the chromosome 6 SNPs further investigated the possibility that different forms of neuroblastoma have different causes.
The scientists compared DNA from about 760 people with high-risk, aggressive neuroblastoma to more than 4,100 disease-free controls and identified several SNPs within the BARD1 gene on chromosome 2 that are associated with the most serious form of disease.   Additional analysis showed that one SNP alone could account for the effects they saw.   Each copy of a C at this SNP increased the odds of aggressive neuroblastoma by 1.68 times.
When the researchers went back and analyzed DNA from a collection of low- and intermediate-risk neuroblastoma cases, they found that there was no association with .
“Our data suggest that genetic initiating events may predispose not only to cancer, but to a particular subphenotype of the disease, and thus to disease outcome.   This may have implications for both screening and identifying critical pathways for targeted therapeutics,” the authors write.
The protein encoded by the BARD1 gene binds to the BRCA1 protein and is considered to be essential for the latter’s ability to keep cells cancer free.   But although mutations in the BRCA1 gene are a known risk factor for breast cancer, BARD1 mutations have not been implicated in that disease.   The association of variations in the BARD1 gene with neuroblastoma reported in this study is the first evidence that this gene is involved in cancer susceptibility.   The authors say that ongoing studies are now focusing on how the SNPs they identified affect the BARD1 gene and ultimately cancer development.

Researchers Identify Genetic Variations Associated With Aggressive Neuroblastoma

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3504" title="puppy Weimaraner" src="https://blog-api.23andme.com/wp-content/uploads/2009/05/istock_000003691151xsmall.jpg" alt="" width="309" height="308" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/05/istock_000003691151xsmall.jpg 347w, https://blogcms.23andme.com/wp-content/uploads/2009/05/istock_000003691151xsmall-150x150.jpg 150w, https://blogcms.23andme.com/wp-content/uploads/2009/05/istock_000003691151xsmall-300x300.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/05/istock_000003691151xsmall-271x271.jpg 271w" sizes="auto, (max-width: 309px) 100vw, 309px" />Stanford researchers are also studying narcoleptic dogs.
Ten years ago, the daytime drowsiness, irregular nighttime sleep and sudden loss of muscle tone and strength associated with narcolepsy were traced to the lack of a protein called hypocretin.   Further research showed that narcoleptics’ brains are missing the cells that produce this important wakefulness-promoting hormone.
Scientists didn’t know exactly why the hypocretin-secreting cells were missing in the brains of narcoleptics, but they did have a hunch.   More than 90% of people with narcolepsy carry a particular variation in an immune molecule that helps the body distinguish itself from foreign invaders like bacteria and viruses.   This led some researchers to suggest that narcolepsy is an autoimmune disease.
But 20% of people without narcolepsy also carry the immune molecule variation, indicating that there must be other genetic and/or environmental factors at work.  Now a new report, published online yesterday in the journal <a href="https://dx.doi.org/10.1038/ng.372" target="_blank" rel="noopener noreferrer">Nature Genetics</a>, adds more evidence to the autoimmune theory of narcolepsy by showing that variations in another immune-related gene are also associated with this condition that affects about one out of every 2,000 people.
In a sample of approximately 1,800 people (about 800 with narcolepsy and 1,000 without), all with European ancestry and all carrying the immune molecule variation found in most narcoleptics, researchers led by Stanford’s Emmanuel Mignot found that variations in the TRA@ gene, which encodes a receptor found on specialized immune cells called T cells, are associated with narcolepsy.
The scientists confirmed their findings in a second group of Caucasians, as well as in Asian (Japanese and Korean) and African American samples, although the size of the African American sample was too small for statistically significant data to be gathered. In a statement, Mignot said that he thinks it is likely that the T cell receptor variations identified in this study and the immune molecule variation previously found in narcoleptics interact to kill hypocretin-secreting cells, but that more research will be needed to understand exactly how this happens.   He went on to say that once these interactions are understood, scientists might be able to identify people at risk for narcolepsy and perhaps stop development of the disease.
In addition to shedding light on the biology of narcolepsy, the authors of the study think their findings will help researchers studying other autoimmune diseases such as multiple sclerosis and type 1 diabetes.
“I’m sure immunologists are going to be very excited.   If we can work out what happens specifically in patients with narcolepsy, we’ll be able to better understand the role of T cells in other autoimmune diseases that are more complicated and difficult to detect,” Mignot said in a statement.

Genetic Study Strengthens Case For Autoimmune Cause of Narcolepsy

<img loading="lazy" decoding="async" class="alignright size-full wp-image-2759" title="heartman" src="https://blog-api.23andme.com/wp-content/uploads/2009/02/heartman.jpg" alt="" width="350" height="260" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/02/heartman.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/02/heartman-300x223.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
A common genetic variation may influence how well a person recovers from heart surgery, a study published online yesterday in the <a href="https://dx.doi.org/10.1681/ASN.2008080915" target="_blank" rel="noopener noreferrer">Journal of the American Society of Nephrology</a> suggests.
Coronary artery bypass surgery, which involves using blood vessels from elsewhere in the body to reroute blood around clogged arteries feeding the heart, increases the risk of low blood pressure and shock.   Norepinephrine can be used to bring blood pressure back up to acceptable levels, but a variation in the gene for an enzyme critical to the metabolism of this drug, COMT, may make some people less responsive.
Researchers studied 260 people who had had bypass surgery and found that those who carried an A at both copies of went into shock more often compared to those with other genotypes (69% vs. 57% in AG people and 46.6% in GG people). The A version of produces a less efficient version of the COMT enzyme.
Prolonged shock, lasting more than 48 hours, was also more frequent in people with two As (25% vs. 13% for AG and 6.8% for GG). Because the body responds to shock by restricting blood flow to the kidneys, people with two As at also had greater frequency of acute kidney injury.
The median hospital stay after bypass surgery was longer for people with two As at : nine days vs. eight days for AG and seven days for GG.
More research on the effects of the COMT variation investigated in this study and variations in other genes that could also affect recovery after bypass surgery will be needed.   But if confirmed, the researchers suggest that their findings could help tailor drug regimens and lead to better outcomes.
“If confirmed in larger trials, preoperative COMT genotyping together with known clinical risk factors could aid in preoperative risk stratification to anticipate occurrence of circulatory and renal dysfunction, and prolonged recovery.   Patients thus identified may benefit from an individualized treatment…” the authors conclude.

Genetic Variation May Influence Heart Surgery Recovery

When scientific research is published, the authors often confess that they wish they&#8217;d collected more data. Critical reviews of research studies often say the same thing. Indeed, if there&#8217;s anything scientists love, it&#8217;s more data.<img loading="lazy" decoding="async" src="https://blog-api.23andme.com/wp-content/uploads/2016/08/Africa_icon-300x244.jpg" alt="" class="alignright size-medium wp-image-24241" width="300" height="244" srcset="https://blogcms.23andme.com/wp-content/uploads/2016/08/Africa_icon-300x244.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2016/08/Africa_icon-768x625.jpg 768w, https://blogcms.23andme.com/wp-content/uploads/2016/08/Africa_icon-1024x834.jpg 1024w, https://blogcms.23andme.com/wp-content/uploads/2016/08/Africa_icon-880x717.jpg 880w, https://blogcms.23andme.com/wp-content/uploads/2016/08/Africa_icon-1180x961.jpg 1180w, https://blogcms.23andme.com/wp-content/uploads/2016/08/Africa_icon.jpg 2014w" sizes="auto, (max-width: 300px) 100vw, 300px" />
Which is why the members of an international team of genetic anthropologists led by Sarah Tishkoff of the University of Pennsylvania are probably quite pleased with themselves. In a new study published this week in <a href="http://www.sciencemag.org/cgi/content/abstract/1172257" target="_blank" rel="noopener noreferrer">Science</a>, the team took the concept of &#8220;more is more&#8221; to heart by collecting and analyzing the DNA of thousands of people, mostly from Africa, so that they might uncover more clues to not only the genetic make-up of modern Africans, but also the genetic history of Africans and non-Africans alike.

<h6>Genetic Diversity</h6>
The scientists&#8217; first step was to collect DNA from a diverse set of Africans. Africa is the most culturally and linguistically diverse place on Earth, so it was important to take a wide sample of individuals from all corners of the continent. In total, they collected 2,432 DNA samples from 113 diverse and distinct groups of people from across the African continent as well as 60 non-African groups. They sampled everyone from the Mozabite Berbers of Morocco to the hunter-gatherer San of the Kalahari Desert, and many in between.
But the hard work didn&#8217;t stop there. The scientists then examined 1,327 genetic markers across the human genome for each individual studied. While many studies focus on a particular part of the genome such the mitochondrial DNA or the Y chromosome, this study took a comprehensive approach. Finally, the researchers used sophisticated statistical techniques, piecing together how these populations from Africa and around the world were the same, and how they were different.
The results confirmed that Africa has the highest genetic diversity of any continent, as many scientists have proposed. In fact, the authors found genetic diversity to decrease the further one traveled away from Africa. Genetic diversity is often used as a measure of how long ago humans inhabited a region – conventional wisdom places the earliest humans in East Africa, which had exceptionally high genetic diversity according to this study, though an analysis by the researchers put the origin of the human expansion farther south near the border of Namibia and Angola.
The study also shed light on the incredible genetic diversity among African populations, said Roy King, a professor of psychiatry and anthropological geneticist from Stanford University:
<blockquote>
Not only did farming and pastoral communities differ from hunter-gatherers, but within the broad range of agricultural populations of West and West-Central Africa – from which many African Americans derive their ancestry – the authors also found some genetic diversity. For example, the Dogon of Mali, although geographically near the Mandinka of Senegal, cluster with North African Berber populations. Thus, this study supports the notion that not only is Africa varied in culture – art, music, religion and language – but also harbors a rich genetic diversity across its multitude of ethnic groups.
</blockquote>
<h6>Languages</h6>
The authors also found a loose connection between the genetics of a population and its language. However, there were a few exceptions, most often the result of a population adopting a new language within the last few thousand years.
The sheer size and diversity of the DNA samples collected allowed the researchers to construct a human family tree based on their analyses. Not unexpectedly, the tree they constructed fits well with current theories on the genetic relationship between Africans and non-Africans; namely that all non-Africans are descended from a particular group or groups of people who were the first humans to migrate out of Africa tens of thousands of years ago.
This study is important for a multitude of reasons. It has been able to confirm theories from the archaeological, cultural, and linguistic records on the origins and movements of Africans and non-Africans.
&#8220;It fits nicely with earlier genetic studies, while subverting the early 20th century colonialist idea of sub-Saharan Africa as constituting a homogeneous genetic an cultural unit,&#8221; King said.
It also creates a new resource that historians, linguists, archaeologists and scientists from a range of other disciplines can use in their own work. If we are lucky, this study will bring forth a flurry of activity surrounding the origins and history of the African continent, and the people who live there.
Credit: istockphoto/Erie

Scientists Publish Largest-Ever Study on the Genetics of Modern Africans

I spent the better part of my undergraduate career lugging around massive biology textbooks.  
General biology, genetics, embryology: It didn&#8217;t matter, they all weighed a ton. I pored over endless chapters of text, highlighting the important sentences, always wishing for more photos, more diagrams, more graphs. A single well-made diagram or image was easier to understand than the preceding 10 paragraphs about the same topic.   I always wished that my textbooks were a little more visual and a little less wordy.   An added benefit, I thought, would be that I could shave a few pounds from my backpack.
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My college days are long over. But my wish may have finally come true, in the form of a new graphic guide to genetics entitled The Stuff of Life: A Graphic Guide to Genetics and DNA, by Mark Schultz.   Published in December, it takes a more visual approach to presenting the most current knowledge on a particular branch of the biological sciences close to my heart: genetics.

The Stuff of Life is centered around a group of aliens who are trying to understand the genetics of all life on earth.  These aliens are both rather ugly (the illustrator has drawn them to resemble sea cucumbers) and rather arrogant.  They can&#8217;t seem to understand why a lowly, hairy primate has come to dominate the planet and make such amazing advances in science and technology. In the style of a comic book, with various windows and balloons leading us from the origins of the earth 4.6 billion years ago to modern day applications of genetics and DNA, it falls flat in oddly juxtaposing complex information and somewhat juvenile humor.
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For anyone who hasn&#8217;t taken a college (or advanced high school level) biology class, the information presented will seem overwhelming at best, and confusing at worst.  For those who are well versed in the biological sciences, the information may be understandable but the humor will seem trite and silly.   After the first few chapters of the cucumberesque aliens repeatedly exclaiming that they can&#8217;t believe humans have managed to understand how genes are passed down from parents to children, that they can&#8217;t believe humans have been able to sequence DNA, understand the genetics of cancer, and create genetically modified organisms, I began to dread their appearances. I stopped reading the sections focused on them, instead skipping to the parts that contained actual information. Once I did I began to enjoy the book much more.
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The organization of the book is similar to a standard introductory genetics textbook.   It begins with a description of the structure of the cell, DNA, and how the genes housed within our DNA can determine thousands of physical traits.   Schultz then moves quickly forward, presenting important genetics concepts such as inheritance, dominant vs. recessive alleles, and why my cat has two different colors of fur.   Finally, he spends the last one-third of the book examining modern-day applications to the study of genetics.
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The strategy works well by allowing the reader to understand the practical value of understanding the basic genetics concepts that were brought up in earlier chapters.   Indeed, having more applications-centric lectures during college might have silenced the students who never understood why this field is so important.   Undoubtedly, this section was written with the more general reader in mind.   It is easily the best section of the entire book.
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Though the constant banter from the sea cucumber-like aliens should not interest anyone over the age of 10, this book would be of use to those currently taking an introductory course in biology, as it might help solidify more difficult concepts that might prove difficult to students.   For educators, this book could prove useful in providing fresh ideas on how to present some of the most important genetics concepts.
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The uneven feeling I got from reading The Stuff of Life is something that must constantly be a fear for anyone who is trying to make science fun and accessible to the general populace.   Presenting such important topics as genetics and DNA that are easy for anyone to understand, scientifically accurate, AND enjoyable, is no easy feat.   And, while The Stuff of Life may have stumbled in some aspects, it is most certainly a noble effort, and may lighten the load in biology majors&#8217; backpacks in the coming months.   I sincerely hope that Schultz continues with more volumes, though I could do without those sea cucumbers next time.

Connections Between Brain Cells May Be Key To Autism Puzzle

Editor&#8217;s note: Some of the tools described in this post no longer reflect the current 23andMe product offerings.
Every family has its legends.
Maybe it&#8217;s a story about how they&#8217;re descended from a passenger on the Mayflower, a Confederate soldier or <a href="http://www.theatlantic.com/doc/200205/olson" target="_blank" rel="noopener noreferrer">Charlemagne</a>.
<div id="attachment_3400" style="width: 279px" class="wp-caption alignright"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-3400" class="wp-image-3400 size-full" src="http://35.88.189.111/wp-content/uploads/2009/04/pocahontas.jpg" alt="" width="269" height="350" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/04/pocahontas.jpg 269w, https://blogcms.23andme.com/wp-content/uploads/2009/04/pocahontas-231x300.jpg 231w" sizes="auto, (max-width: 269px) 100vw, 269px" />Pocahontas.</div>
Of all the classic American family legends, stories of a Native American ancestor are among of the most common. Many times there&#8217;s a well-documented link to a Native forbear: Two First Ladies (Edith Wilson and Nancy Reagan) and one Duchess of Windsor (Wallis Simpson) are proven descendants of Pocahontas.
Other times, the evidence amounts to little more than vague tales about a rugged pioneer and a Cherokee princess. (Learn what&#8217;s wrong with that scenario <a href="http://www.native-languages.org/princess.htm" target="_blank" rel="noopener noreferrer">here.</a>)
Now 23andMe customers who are curious about whether they may have Native American ancestors can look for evidence of it in their genes.
The Native American Ancestry Finder uses some existing 23andMe features – Ancestry Painting, <a href="https://www.23andme.com/you/haplogroup/maternal/" target="_self" rel="noopener noreferrer">Maternal Line</a> and <a href="https://www.23andme.com/you/haplogroup/paternal/" target="_self" rel="noopener noreferrer">Paternal Line</a> – to look for genetic signatures that are likely to have come from a Native American ancestor.

The Maternal Line and Paternal Line elements of the Finder are pretty straightforward; certain mitochondrial DNA (maternal) and Y chromosome (paternal) haplogroups are often found among Native Americans.
These include mitochondrial haplogroups A2, B2, C1, D1 and X2a – which are found exclusively among Native Americans. People in some other branches of the A, B, C and D haplogroups may also have Native American ancestry, but their maternal lines could also trace to Asia. On the paternal side, only Q3 is exclusive to Native Americans, though anyone with a Y chromosome in the C, C3 or Q haplogroup could conceivably have Native American forbears.
<div id="attachment_3392" style="width: 251px" class="wp-caption alignleft"><img loading="lazy" decoding="async" aria-describedby="caption-attachment-3392" class="wp-image-3392 size-full" src="http://35.88.189.111/wp-content/uploads/2009/04/natamwoman.png" alt="" width="241" height="350" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/04/natamwoman.png 241w, https://blogcms.23andme.com/wp-content/uploads/2009/04/natamwoman-207x300.png 207w" sizes="auto, (max-width: 241px) 100vw, 241px" />An example of a Native American&#8217;s ancestry painting.</div>
The part of the Finder that uses Ancestry Painting to find evidence for Native American forbears is a little more complicated. It relies on the fact that people of full Native American descent have Ancestry Paintings that are consistently about 75% orange (Asian) and 25% blue (European).
This is due to the fact that Native Americans are ultimately descended from populations that lived in northern and central Asia about 15,000 to 20,000 years ago, and the fact that those regions are intermediate between the reference populations that Ancestry Painting classifies as fully Asian (Japanese and Chinese) and fully European (European-Americans living in Utah).
Then the Finder compares your Ancestry Painting proportions to a table that contains the results of an extensive series of simulations that we performed to determine what would happen to that three-to-one Asian/European proportion over the generations if a Native American and a partner of all-European descent had a child who then reproduced with another all-European partner, and so on. We did the same analysis for a Native American marrying into an all-Asian pedigree.
Unfortunately, partly due to inadequate sampling of Africa&#8217;s genetic diversity, this method cannot yet establish Native American ancestry for African Americans.
We found that it takes at least five generations after the appearance of a single Native American in an otherwise all- European pedigree for the percentage of Asian (orange) DNA to reach zero. In an otherwise all-Asian pedigree that process is much faster – in two generations, the grandchild of that single Native American can have no trace of European in his or her Ancestry Painting.
There are, of course, plenty of Eurasian populations that also have blue-and-orange Ancestry Paintings. So the Native American Ancestry Finder performs a second analysis that can distinguish people of South Asian, Central Asian, Middle Eastern and Ashkenazi descent from those with Native American ancestry.
Unfortunately, there is still some uncertainty when it comes to distinguishing people with Native American ancestry.
It&#8217;s still a work in progress – that&#8217;s what Labs are all about. But we hope customers will help us by trying out the Native American Ancestry Finder and letting us know if anything doesn&#8217;t mesh with what they know about their genealogy.
You can also contribute by taking the &#8220;<a href="https://www.23andme.com/you/23andwe/surveys/" target="_self" rel="noopener noreferrer">Where Are You From?</a>&#8221; survey in <a href="https://www.23andme.com/you/23andwe/surveys/" target="_self" rel="noopener noreferrer">23andWe</a>.

New 23andMe Lab Searches Genome for Native American Ancestry

<img loading="lazy" decoding="async" class="alignright size-full wp-image-3410" title="istock_000002436798xsmall" src="https://blog-api.23andme.com/wp-content/uploads/2009/04/istock_000002436798xsmall.jpg" alt="" width="374" height="248" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/04/istock_000002436798xsmall.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2009/04/istock_000002436798xsmall-300x199.jpg 300w" sizes="auto, (max-width: 374px) 100vw, 374px" />
DNA Day was created in 2003 by a congressional resolution to celebrate two important milestones in the study of genetics: the 50th anniversary of the description of the double-helix structure of DNA by James D. Watson and Francis H.C. Crick and the completion of the Human Genome Project. DNA Day is usually celebrated on April 25th, but to accommodate classroom schedules, many activities will be taking place a day early on Friday April 24th.
<ul>
<li>DNA Day Chatroom: The National Human Genome Research Institute (NHGRI) will be hosting its annual <a href="https://www.genome.gov/20519689" target="_blank" rel="noopener noreferrer">DNA Day chatroom</a> from 8 a.m. to 6 p.m., EDT on April 24th. Genomics and genetics experts will answer questions from students, teachers and the general public on topics ranging from basic genomic research to the genetic basis of disease to ethical questions about genetic privacy. Transcripts from past chatrooms can be found <a href="https://www.genome.gov/20519689" target="_blank" rel="noopener noreferrer">here</a>.</li>
<li>Teaching Tools for DNA Day: To plan your own DNA Day activities, check out the NHGRI’s collection of <a href="https://www.genome.gov/20519692" target="_blank" rel="noopener noreferrer">teaching tools</a> and webcasts. &nbsp; And don&#8217;t miss our collection of DNA-themed activities.</li>
<li>DNA Day Online: National DNA Day is on Facebook and Twitter. &nbsp; You can compete to win a NHGRI mug in their DNA model photo contest. &nbsp; Pictures can be uploaded through April 24th. &nbsp; You can also send a virtual gene via Facebook (thanks to <a href="https://blog.23andme.com/2008/05/02/giving-the-gift-of-a-virtual-gene/" target="_blank" rel="noopener noreferrer">Genome Alberta</a>) or send a DNA Day e-card.</li>
</ul>
What are you doing to celebrate? &nbsp; Leave us a comment — we’d love to know. &nbsp; And if you know of any cool DNA Day happenings, let us know about those too!

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