The 91探花 is No. 8 on the 2025-26 U.S. News & World Report鈥檚 Best Global Universities rankings, 聽on Tuesday. The 91探花maintained its No. 2 ranking among U.S. public institutions.

The 91探花also placed in the top 10 in eight subject areas ranked by U.S. News.

Harvard University, Massachusetts Institute of Technology and Stanford University topped the list in that order. The University of Oxford is No. 4, followed by University of Cambridge, the University of California, Berkeley, University College London and the UW. Yale University and Columbia University rounded out the top 10.

鈥淯nquestionably, the 91探花is advancing discovery that saves and improves lives, promotes prosperity, makes our nation stronger and expands human knowledge for the good of all,鈥� said 91探花President Ana Mari Cauce. 鈥淚鈥檓 very proud to see this extraordinary impact recognized through this latest ranking.鈥�

The U.S. News ranking聽聽鈥斅燽ased on data and metrics provided by Clarivate 鈥� weighs factors that measure a university鈥檚 global and regional research reputation and academic research performance. For the overall rankings, this includes bibliometric indicators such as the number of publications, citations and international collaboration.

The overall Best Global Universities ranking encompasses 2,250 institutions spread across 105 countries, according to U.S. News.

Here are the 91探花fields of study that are in the top 10 in U.S. News鈥� subject rankings:

Molecular biology and genetics 鈥� No. 6

Clinical medicine 鈥� No. 6

Public, environmental and occupational health 鈥� No. 6

Microbiology 鈥� No. 7

Biology and biochemistry 鈥� No. 8 (up from 9)

Infectious diseases 鈥� No. 9

Marine and freshwater biology 鈥� No. 9

Social sciences and public health 鈥� No. 9

The 91探花 rose from No. 7 to No. 6 on the聽, released on Tuesday. The 91探花maintained its No. 2 ranking among U.S. public institutions.

U.S. News also ranked several subjects, and the 91探花placed in the top 10 in 10 subject areas, including immunology (No. 4), molecular biology and genetics (No. 5) and clinical medicine (No. 6).

In another ranking out this week, Times Higher Education World University Rankings 2023 by Subject, six subject areas at the 91探花placed in the top 25.

鈥淎s a global public research university, the UW鈥檚 mission is to create and accelerate change for the public good,鈥� 91探花President Ana Mari Cauce said. 鈥淚鈥檓 proud that these rankings reflect the outstanding and wide-ranging work of our faculty, staff and students to expand knowledge and discovery that is changing people鈥檚 lives for the better, particularly in the health sciences.鈥�

The U.S. News ranking 鈥斅� based on Web of Science data and metrics provided by Clarivate Analytics InCites 鈥� weighs factors that measure a university鈥檚 global and regional research reputation and academic research performance. For the overall rankings, this includes bibliometric indicators such as publications, citations and international collaboration.

The overall Best Global Universities ranking, now in its ninth year, encompasses the top 2,000 institutions spread across 90 countries, according to U.S. News.聽American universities make up eight of the top 10 spots.

Here are all the top 10 91探花rankings in U.S. News鈥� subject rankings:

• Immunology 鈥� No. 4
• Molecular biology and genetics 鈥� No. 5
• Clinical medicine 鈥� No. 6
• Geosciences 鈥� No. 7
• Infectious diseases 鈥� No. 7
• Public, environmental and occupational health 鈥� No. 7
• Social sciences and public health 鈥� No. 7
• Biology and biochemistry 鈥� No. 8
• Microbiology 鈥� No. 10

In the rankings, UW鈥檚 programs in these areas placed in the top 25:

• : No. 15
• (includes agriculture and forestry, biological sciences, veterinary science and sport science): No. 16
• (includes medicine, dentistry and other health subjects): No. 17
• (includes communication and media studies, politics and international studies 鈥� including development studies, sociology and geography): No. 18
• (includes mathematics and statistics, physics and astronomy, chemistry, geology, environmental sciences, and Earth and marine sciences): No. 19
• (includes education, teacher training, and academic studies in education): No. 23

The subject tables employ the same used in the overall聽; however, the methodology is recalibrated for each subject, with the weightings changed to suit the individual fields.

The most common organism in the oceans, and possibly on the entire planet, is a family of single-celled marine bacteria called SAR11. These drifting organisms look like tiny jelly beans and have evolved to outcompete other bacteria for scarce resources in the oceans.

We now know that this group of organisms thrives despite 鈥� or perhaps because of 鈥� the ability to host viruses in their DNA. A published in May in Nature Microbiology could lead to new understanding of viral survival strategies.

91探花 oceanographers discovered that the bacteria that dominate seawater, known as Pelagibacter or SAR11, hosts a unique virus. The virus is of a type that spends most of its time dormant in the host鈥檚 DNA but occasionally erupts to infect other cells, potentially carrying some of its host鈥檚 genetic material along with it.

鈥淢any bacteria have viruses that exist in their genomes. But people had not found them in the ocean’s most abundant organisms,鈥� said co-lead author , a 91探花associate professor of oceanography. 鈥淲e suspect it’s probably common, or more common than we thought 鈥� we just had never seen it.鈥�

This virus鈥� two-pronged survival strategy differs from similar ones found in other organisms. The virus lurks in the host鈥檚 DNA and gets copied as cells divide, but for reasons still poorly understood, it also replicates and is released from other cells.

The new study shows that as many as 3% of the SAR11 cells can have the virus multiply and split, or lyse, the cell 鈥� a much higher percentage than for most viruses that inhabit a host鈥檚 genome. This produces a large number of free viruses and could be key to its survival.

鈥淭here are 10 times more viruses in the ocean than there are bacteria,鈥� Morris said. 鈥淯nderstanding how those large numbers are maintained is important. How does a virus survive? If you kill your host, how do you find another host before you degrade?鈥�

The study could prompt basic research that could help clarify host鈥搗irus interactions in other settings.

鈥淚f you study a system in bacteria, that is easier to manipulate, then you can sort out the basic mechanisms,鈥� Morris said. 鈥淚t鈥檚 not too much of a stretch to say it could eventually help in biomedical applications.鈥�

The 91探花oceanography group had published a previous paper in 2019 looking at how marine phytoplankton, including SAR11, use sulfur. That allowed the researchers to cultivate two new strains of the ocean-dwelling organism and analyze one strain, NP1, with the latest genetic techniques.

Co-lead author collected samples off the coast of Oregon during a research cruise. She diluted the seawater several times and then used a sulfur-containing substance to grow the samples in the lab 鈥� a difficult process, for organisms that prefer to exist in seawater.

The team then sequenced this strain鈥檚 DNA at the in Seattle.

鈥淚n the past we got a full genome, first try,鈥� Morris said. 鈥淭his one didn’t do that, and it was confusing because it’s a very small genome.鈥�

The researchers found that a virus was complicating the task of sequencing the genome. Then they discovered a virus wasn鈥檛 just in that single strain.

鈥淲hen we went to grow the NP2 control culture, lo and behold, there was another virus. It was surprising how you couldn鈥檛 get away from a virus,鈥� said Cain, who graduated in 2019 with a 91探花bachelor鈥檚 in oceanography and now works in a 91探花research lab.

Cain鈥檚 experiments showed that the virus鈥� switch to replicating and bursting cells is more active when the cells are deprived of nutrients, lysing up to 30% of the host cells. The authors believe that bacterial genes that hitch a ride with the viruses could help other SAR11 maintain their competitive advantage in nutrient-poor conditions.

鈥淲e want to understand how that has contributed to the evolution and ecology of life in the oceans,鈥� Morris said.

Co-authors are postdoctoral researcher and associate professor in the 91探花Department of Biochemistry. The study was funded by the National Science Foundation and the National Institutes of Health鈥檚 National Institute of Allergy and Infectious Disease.

For more information, contact Morris at morrisrm@uw.edu or 206-221-7228 and Cain at kcain97@uw.edu.

DNA testing services like 23andMe, Ancestry.com and MyHeritage are making it easier for people to learn about their ethnic heritage and genetic makeup. People can also use genetic testing results to connect to potential relatives by using third-party sites, like, where they can compare their DNA sequences to others in the database who have uploaded test results.

But a less happy ending is also possible. Researchers at the 91探花 have found that GEDmatch is vulnerable to multiple kinds of security risks. An adversary can use only a small number of comparisons to extract someone’s sensitive genetic markers. A malicious user could also construct a fake genetic profile to impersonate someone’s relative.

The team Oct. 29. The researchers have also had this research accepted at the and will present these results in February in San Diego.

“People think of genetic data as being personal 鈥� and it is. It’s literally part of their physical identity,” said lead author, a postdoctoral researcher in the 91探花Paul G. Allen School of Computer Science & Engineering. “This makes the privacy of genetic data particularly important. You can change your credit card number but you can’t change your DNA.”

The mainstream use of genetic testing results for genealogy is a relatively recent phenomenon. The initial benefits may have obscured some underlying risks, the researchers say.

“When we have a new technology, whether it is smart automobiles or medical devices, we as a society start with ‘What can this do for us?’ Then we start looking at it from an adversarial perspective,” said co-author, a professor in the Allen School. “Here we’re looking at this system and asking: ‘What are the privacy issues associated with sharing genetic data online?'”

To look for security issues, the team created a research account on GEDmatch. The researchers uploaded experimental genetic profiles that they created by mixing and matching genetic data from multiple databases of anonymous profiles. GEDmatch assigned these profiles an ID that people can use to do one-to-one comparisons with their own profiles.

For the one-to-one comparisons, GEDmatch produces graphics with information about how much of the two profiles match. One graphic is a bar for each of the 22 non-sex chromosomes. Each bar changes length depending on how similar the two profiles are for that chromosome. A longer bar shows that there are more matching regions, while a series of shorter bars means that there are short regions of similarity interspersed with areas that are different.

The team wanted to know if an adversary could use that bar to find out a specific DNA sequence within one region of a target’s profile, such as whether or not the target has a mutation that makes them susceptible to a disease. For this search, the team designed four “extraction profiles” that they could use for one-to-one comparisons with a target profile they created. Based on whether the bar stayed in one piece 鈥� indicating that the extraction profile and the target matched 鈥� or split into two bars 鈥� indicating no match 鈥� the team was able to deduce the target’s specific sequence for that region.

鈥淕enetic information correlates to medical conditions and potentially other deeply personal traits,” said co-author, a professor in the Allen School. “Even in the age of oversharing information, this is most likely the kind of information one doesn鈥檛 want to share for legal, medical and mental health reasons. But as more genetic information goes digital, the risks increase.”

Next the researchers wondered if an adversary could use a similar technique to acquire a target’s entire profile. The team focused on another GEDmatch graphic that describes how well the profiles match by showing a line of colored pixels that mark how well each DNA segment in the query matches the target: green for a complete match, yellow for a half match 鈥� when one strand of DNA matched but not the other 鈥� and red for no match.

Then the team played a game of 20 questions: They created 20 extraction profiles that they used for one-to-one comparisons on a target profile that they created. Based on how the pixel colors changed, they were able to pull out information about the target sequence. For five test profiles, the researchers extracted about 92% of a test’s unique sequences with about 98% accuracy.

“So basically, all the adversary needs to do is upload these 20 profiles and then make 20 one-to-one comparisons to the target,” Ney said. “They could write a program that automatically makes these comparisons, downloads the data and returns the result. That would take 10 seconds.”

Once someone’s profile is exposed, the adversary can use that information to create a profile for a false relative. The team tested this by creating a fake child for one of their experimental profiles. Because children receive half their DNA from each parent, the fake child’s profile had their DNA sequences half matching the parent profile. When the researchers did a one-to-one comparison of the two profiles, GEDmatch estimated a parent-child relationship.

An adversary could generate any false relationship they wanted by changing the fraction of shared DNA, the team said.

鈥淚f GEDmatch users have concerns about the privacy of their genetic data, they have the option to delete it from the site,” Ney said. “The choice to share data is a personal decision, and users should be aware that there may be some risk whenever they share data. Security is a difficult problem for internet companies in every industry.鈥�

Prior to publishing their results, the researchers shared their findings with GEDMatch, which has been working to resolve these issues, according to the GEDmatch team. The 91探花researchers are not affiliated with GEDmatch, however, and can’t comment on the details of any fixes.

“We’re only beginning to scratch the surface,” Kohno said. “These discoveries are so fundamental that people might already be doing this and we don’t know about it. The responsible thing for us is to disclose our findings so that we can engage a community of scientists and policymakers in a discussion about how to mitigate this issue.”

This research was funded in part by the 91探花, which receives support from: the William and Flora Hewlett Foundation, the John D. and Catherine T. MacArthur Foundation, Microsoft, and the Pierre and Pamela Omidyar Fund at the Silicon Valley Community Foundation. This research also was funded by a grant from the Defense Advanced Research Projects Agency Molecular Informatics Program.

For more information, contact the team at dnasec@cs.washington.edu.

In patients with chronic lymphocytic leukemia (CLL), the rate of disease growth varies widely. In a new study from the Dana-Farber Cancer Institute, the Broad Institute of MIT and Harvard, Massachusetts General Hospital and the 91探花, scientists report that CLL growth is apt to follow one of three trajectories: relentlessly upward, steadily level or something in between. The particular course the disease takes is tightly linked to the genetic makeup of the cancer cells, particularly the number of growth-spurring 鈥渄river鈥� mutations they contain.

The , published online May 29 in the journal , contains a further insight: Genetic changes that occur very early in CLL development exert a powerful influence on the growth pattern the CLL cells will ultimately take. This raises the possibility that physicians may one day be able to predict the course of the disease by its molecular features at the time of diagnosis.

鈥淥ur findings provide a framework not only for understanding the differing patterns of CLL growth in patients but also for exploring the basic biological mechanisms that underlie these differences,鈥� said Dr. of Dana-Farber, the Broad Institute and Brigham and Women鈥檚 Hospital, who is co-corresponding author with of the Broad Institute and Massachusetts General Hospital. 鈥淯ltimately, we鈥檇 like to be able to tie the genotype of the disease 鈥� the particular genetic abnormalities in a patient鈥檚 cancer cells 鈥� to its phenotype, or how the cancer actually behaves.鈥�

CLL is a useful model for studying the pace of cancer growth because it progresses at widely different rates from one patient to another, said Wu. In many patients, it persists at a low level for many years before advancing to the point where treatment is necessary. In others, it progresses so rapidly that treatment is required shortly after diagnosis.

To see if there were different patterns of CLL growth among patients, researchers drew on data from 107 patients diagnosed with the disease. Beginning at diagnosis, each patient underwent periodic blood tests to track disease progress over the succeeding months and years, and continued until the disease reached a stage where treatment would begin. Each test consisted of a white blood cell count, which served as a proxy measure of CLL: the greater the number of white cells within a blood sample, the greater the burden of the disease. The tests were conducted over a period ranging from two years in one patient to 19 years in another.

The serial testing allowed researchers to calculate growth rates over time for CLL in each patient. They used a statistical model to determine if the rates were consistent with various patterns of cancer growth.

鈥淲e found that some cases of CLL show exponential growth, in which it expands without any apparent limit, while other cases show 鈥榣ogistic鈥� growth, in which it plateaus at a fairly consistent level,鈥� said co-lead author , a 91探花assistant professor of applied mathematics.

Cases that didn鈥檛 fit either category were classified as indeterminate.

To explore whether genetic differences were at the root of these divergent growth patterns, the researchers performed whole-exome sequencing on several CLL samples collected from each patient prior to receiving therapy. Whole-exome sequencing provides a letter-by-letter readout of the regions of DNA that encode for cellular proteins.

They found that exponentially growing CLL typically carried a large number of driver mutations 鈥� those that confer a competitive advantage in growth 鈥� and quickly reached the stage where treatment was called for. In contrast, logistically growing CLL had fewer genetic alterations and fewer types of alterations and progressed relatively slowly toward the level that requires treatment. Seventy-five percent of patients with exponential growth eventually warranted treatment; by comparison, 21% of those with logistic growth and 67% of those with indeterminate growth eventually required treatment.

By analyzing patients鈥� serial blood samples collected over a period of time, researchers found that exponential CLL not only grows faster but also evolves faster, spinning off new subtypes of cancer cells, each with a particular set of genetic abnormalities. Whole-exome sequencing revealed that exponential CLL is marked by a great variety of tumor cell types and subtypes, while logistic CLL is marked by a relatively less diverse collection of tumor cells.

The information from whole-exome sequencing further enabled researchers to discover the growth rates of those subpopulations of cells within each patient鈥檚 leukemia that could be identified on the basis of a subset of mutations, some of them putative driver mutations. These measurements clearly revealed that many of the mutations, which were suspected to be centrally involved in CLL growth, did in fact provide subpopulations with preferential growth acceleration compared to populations lacking these putative drivers. Their results further indicate that the eventual course of CLL growth is inscribed in the genes of tumor cells early in the disease鈥檚 development.

鈥淚f the course of the disease isn鈥檛 altered by therapeutic treatment, the rate and pattern of CLL growth over time seems to 鈥榩lay out鈥� according to a predetermined set of genetic instructions,鈥� said Wu.

鈥淭he discovery that CLL growth accelerates in the presence of large numbers of driver mutations is compelling evidence that these mutations do, in fact, confer a growth advantage to cells 鈥� that they truly do 鈥榙rive鈥� the disease,鈥� said co-lead author Dr. of Dana-Farber, the Broad Institute and the Medical University of Vienna.

Bozic and co-lead authors and at the Broad Institute developed methods to jointly model possible phylogenetic relationships of cancer cell subpopulations 鈥� which are a description of each subpopulation鈥檚 history and relationships to each other during the evolution of the cancer 鈥� as well as integrate growth rates with subclone-specific genetic information.

鈥淐ombining clinical data with computational and mathematical modeling, we show that the growth of many CLLs seems to follow specific mathematical equations 鈥� exponential and logistic 鈥� each associated with distinct underlying genetics and clinical outcomes,鈥� said Bozic. 鈥淚ntegrating tumor burden and whole-exome sequencing data allowed us to quantify the growth rates of different tumor subpopulations in individual CLLs, methodology that could potentially inform personalized therapy in the future.鈥�

Co-authors of the study are: Kristen Stevenson, Oriol Olive, Reaha Goyetche, Stacey M. Fernandes, Jing Sun, Wandi Zhang and Donna Neuberg of Dana-Farber; Dr. Jennifer R. Brown of Dana-Farber and Brigham and Women鈥檚 Hospital; Laura Rassenti and Dr. Thomas J. Kipps of the Moores Cancer Center at the University of California, San Diego; Daniel Rosebrock, Amaro Taylor-Weiner, Chip Stewart, Alicia Wong and Carrie Cibulskis of the Broad Institute; Johannes G. Reiter, Jeffrey M. Gerold and Martin A. Nowak of Harvard University; Dr. John G. Gribben of the Barts Cancer Institute at the University of London; Dr. Kanti R. Rai of Hofstra North Shore-LIJ School of Medicine; and Michael J. Keating of the MD Anderson Cancer Center.

The study funded by the National Cancer Institute; the CLL Global Research Foundation; the National Heart, Lung, and Blood Institute; the European Union; and the Leukemia and Lymphoma Society.

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For more information, contact Bozic at ibozic@uw.edu.

Grant numbers: 5P01CA081534-14, 1R01CA155010-01A1, P01CA206978, U10CA180861, 1RO1HL103532-0, PIOF-2013-624924

Adapted from a by the Dana-Farber Cancer Institute.

People who have submitted photos to the have selected images of family members, favorite places and tasty food that will be preserved for years in the form of synthetic DNA. Now this collection 鈥� which currently contains more than 3,000 images and is still growing 鈥� will be headed to the final frontier: space.

The , which creates archives that can survive for a long time in space, that it will be partnering with researchers at the 91探花, Microsoft and Twist Bioscience to include media stored in DNA in its newest shipment, which is destined to go to the moon in less than two years.

Researchers at the at the 91探花 and Microsoft plan to provide both the #MemoriesInDNA project and a DNA archive of e-books for this mission. The Arch Mission Foundation’s will also include instructions for how to sequence DNA and how to access the contents of the archive.

To prepare the DNA for its life in space, the researchers have been developing new methods to package and protect the information it stores.

“Sending DNA into space is a great opportunity for us to make our storage system more robust,” said , a professor in the UW鈥檚 Paul G. Allen School of Computer Science & Engineering. “How can we protect the DNA so that it will still be readable thousands of years into the future?”

Storing electronic data in DNA molecules saves a lot of storage space. Data centers require acres of land and account for in the United States, but DNA molecules can store information millions of times more compactly using less energy.

“DNA is so dense that we can store a lot of information in a single gram,” said Ceze. “This is huge because room is so limited in space missions.”

The basic process converts digital data’s strings of ones and zeroes into the four basic building blocks of DNA sequences: adenine, guanine, cytosine and thymine. The team is working with to create synthetic DNA molecules in a lab. This DNA doesn’t come from living organisms. Instead, it is synthesized from scratch base by base (letter by letter).

In space, stray cosmic rays could break DNA strands, making them unreadable. So Ceze and his team have been working on methods to ensure that they can still decode all the information, even if some of the DNA degrades.

The first method, called physical redundancy, involves adding multiple copies of each strand of DNA to the archive. So if one copy is destroyed, there are still many other copies with the same information. The team is considering adding billions of copies of each strand to account for degradation over time, Ceze said.

The second method, called , attaches information about the data within the DNA itself, like adding information about how two puzzle pieces go together. That way if all copies of a DNA strand go missing, the researchers can piece together what was lost and still get all of the data.

For example, to store two numbers 鈥� two and three 鈥� researchers would also store the information that two plus three equals five. So if something happened to the number two, the numbers five and three would still exist. That logic could be reversed to conclude that the missing information is five minus three 鈥� or two.

Now that the team is working with the Arch Mission Foundation, it has a strict deadline to finalize all packaging and storage plans: The Lunar Library is expected to be .

“We鈥檙e proud that this partnership with Arch continues to push the boundaries of what鈥檚 possible in increasingly exciting ways and remarkable directions,鈥� said collaborator , a senior researcher at Microsoft and a 91探花affiliate associate professor of computer science and engineering. “This is an incredibly exciting project and we have a great multidisciplinary team working on it: coding theorists, computer architects, engineers and molecular biologists, all coming together to make this new technology a reality.”

For more details about how to include your own images in the #MemoriesInDNA project, visit the or email lunarlibrary@memoriesindna.com. Note: To be included in the DNA image collection, photographs cannot be copyrighted by any other party and must be free of violent or inappropriate content. The image dataset will be preserved in DNA indefinitely and shared with researchers worldwide.

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For more information, contact misl-info@cs.washington.edu or visit the #MemoriesInDNA Project website: .

Through photosynthesis, they use sunlight and carbon dioxide to make food, belching out the oxygen that we breathe as a byproduct. This evolutionary innovation is so central to plant identity that nearly all land plants use the same pores 鈥� called stomata 鈥� to take in carbon dioxide and release oxygen.

Stomata are tiny, microscopic and critical for photosynthesis. Thousands of them dot on the surface of the plants. Understanding how stomata form is critical basic information toward understanding how plants grow and produce the biomass upon which we thrive.

In published May 7 in the journal , a 91探花-led team describes the delicate cellular symphony that produces tiny, functional stomata. The scientists discovered that a gene in plants known as MUTE orchestrates stomatal development. MUTE directs the activity of other genes that tell cells when to divide and not to divide 鈥� much like how a conductor tells musicians when to play and when to stay silent.

鈥淭he MUTE gene acts as a master regulator of stomatal development,鈥� said senior author , a 91探花professor of biology and investigator at the . 鈥淢UTE exerts precision control over the proper formation of stomata by initiating a single round of cell division 鈥� just one 鈥� in the precursor cell that stomata develop from.鈥�

Stomata resemble doughnuts 鈥� a circular pore with a hole in the middle for gas to enter or leave the plant. The pore consists of two cells 鈥� each known as a guard cell. They can swell or shrink to open or close the pore, which is critical for regulating gas exchange for photosynthesis, as well as moisture levels in tissues.

鈥淚f plants cannot make stomata, they are not viable 鈥� they cannot 鈥榖reathe,鈥欌�� said Torii, who also is a professor at Nagoya University in Japan.

Torii and her team investigated which genes governed stomata formation in Arabidopsis thaliana, a small weed that is one of the most widely studied plants on the planet. Past research by Torii鈥檚 team and other researchers had indicated that, in Arabidopsis, MUTE plays a central role in the formation of stomata. The MUTE gene encodes instructions for a cellular protein that can control the 鈥渙n鈥� or 鈥渙ff鈥� state of other plant genes.

The researchers created a strain of Arabidopsis that can artificially produce a lot of the MUTE protein, so they could easily identify which genes the MUTE protein turned on or off. They discovered that many of the activated genes control cell division 鈥� a process that is critical for stomatal development.

In Arabidopsis, as in nearly all plants, stomata form from precursor cells known as guard mother cells, or GMCs. To form a working stoma 鈥� singular for stomata 鈥� a GMC divides once to yield to paired guard cells. Since their data showed that MUTE proteins switched on genes that regulated cell division, Torii and her team wondered if MUTE is the gene that activates this single round of cell division. If so, it would have to be a tightly regulated process. The genetic program would have to switch on cell division in the GMC, and then quickly switch it right back off to ensure that only a single round of division occurs.

Torii鈥檚 team showed that one of the genes activated by the MUTE protein to its DNA is CYCD5;1, a gene that causes the GMC to divide. The researchers also found that MUTE proteins turn on two genes called FAMA and FOUR LIPS. This was an important discovery because, while CYCD5;1 turns on cell division of the GMC, FAMA and FOUR LIPS turn off 鈥� or repress 鈥� the cell division program.

鈥淥ur experiments showed that MUTE was turning on both activators of cell division and repressors of cell division, which seemed counterintuitive 鈥� why would it do both?鈥� said Torii. 鈥淭hat made us very interested in understanding the temporal regulation of these genes in the GMC and the stomata.鈥�

Through precise experiments, they gathered data on the timing MUTE activation of these cell division activators and repressors. They incorporated this information into a mathematical model, which simulated how MUTE acts to both activate and repress cell division in the GMC. First, MUTE turns on the activator CYCD5;1 鈥� which triggers one round of cell division. Then, FAMA and FOUR LIPS act to prevent further cell division, yielding one functional stomata consisting of two guard cells.

鈥淟ike a conductor at the podium, MUTE appears to signal its target genes 鈥� each of which has specific, and even opposite, parts to play in the ensuing piece,鈥� said Torii. 鈥淭he result is a tightly coupled sequence of activation and repression that gives rise to one of the most ancient structures on land plants.鈥�

Co-lead authors on the paper are Soon-Ki Han, a former 91探花postdoctoral researcher now at Nagoya University, and 91探花postdoctoral researcher Xingyun Qi. Additional co-authors are Jonathan Dang, Kristen Miller and Eun Deok Kim at the UW; Kei Sugihara and Takashi Miura at Kyushu University; and Takaho Endo at the RIKEN Center for Integrative Medical Sciences. The research was funded by the National Science Foundation, the Gordon and Betty Moore Foundation and the HHMI.

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For more information, contact Torii at 206-221-5701 or ktorii@uw.edu.

Grant numbers: MCB-0855659, GBMF-3035.

For biologists, a single cell is a world of its own: It can form a harmonious part of a tissue, or go rogue and take on a diseased state, like cancer. But biologists have long struggled to identify and track the many different types of cells hiding within tissues.

Researchers at the 91探花 and the have developed a new method to classify and track the multitude of cells in a tissue sample. In a published March 15 in the journal , the team reports that this new approach 鈥� known as SPLiT-seq 鈥� reliably tracks gene activity in a tissue down to the level of single cells.

鈥淐ells differ from each other based on the activity of their genes 鈥� which genes are switched off or switched on,鈥� said senior author , a 91探花associate professor in both the Department of Electrical Engineering and the Paul G. Allen School of Computer Science & Engineering. 鈥淯sing SPLiT-seq, it becomes possible to measure gene activity in individual cells, even if there are hundreds of thousands of different cells in a tissue sample.鈥�

SPLiT-seq 鈥� which stands for Split Pool Ligation-based Transcriptome sequencing 鈥� combines a traditional approach to measuring gene expression with a new twist. For more than a decade, scientists have measured gene expression in tissues by sequencing the genetic 鈥渓etters鈥� of RNA, the DNA-like molecule that is the first step in gene expression. This standard approach 鈥� known as RNA-sequencing 鈥� profiles RNA across the whole tissue. But this approach does not tell researchers how cells within the tissue differ from one another. Single-cell RNA-sequencing addresses this by sequencing RNA from isolated cells, but existing methods are costly and do not scale well.

SPLiT-seq makes it possible to perform single-cell RNA-sequencing without ever isolating individual cells. The researchers put the cells through four rounds of 鈥渟huffling鈥� 鈥� splitting them into separate pools and mixing them back together. At each shuffling step, they labeled the RNA in each pool with its own unique DNA 鈥渂arcode.鈥� At the end of four rounds of shuffling and labeling, RNA from each cell essentially contained its own unique combination of barcodes 鈥� and that barcode combination is included in the bulk sequencing of all the RNA in the tissue.

鈥淲ith these 鈥榮plit-pool barcoding steps,鈥� we solve a big problem in measuring gene expression: reliably identifying which RNA molecules came from which cell in the original tissue sample,鈥� said , who is also a researcher in the 91探花Molecular Engineering & Sciences Institute.

鈥淲ith that problem addressed, we can begin to ask biological questions about the different types of cells we define in the tissue,鈥� said co-author , Associate Director of Molecular Genetics at the Allen Institute for Brain Science.

The team performed SPLiT-seq on brain and spinal cord tissue samples from laboratory mice. Using SPLiT-seq, they could measure the gene activity of over 156,000 cells. Based on patterns of gene activity, they estimated that more than 100 different types of cells were present in those tissue samples 鈥� including neurons and glial cells at various stages of development and differentiation.

SPLiT-seq can deliver this rich array of biological data at a cost of 鈥渏ust a penny per cell,鈥� said Seelig in a 聽by the Allen Institute for Brain Science. This is a significantly lower cost than other single-cell RNA sequencing approaches, according to the researchers.

The researchers say that SPLiT-seq could answer important questions about how tissues develop, and identify minute changes in gene expression that precede the onset of complex diseases like Parkinson鈥檚 disease or cancer.

Co-lead authors on the paper are 91探花electrical engineering postdoctoral researcher and , a 91探花doctoral student in the Department of Bioengineering. Additional 91探花co-authors are Richard Muscat, Anna Kuchina, Paul Sample and Sumit Mukherjee in the Department of Electrical Engineering; David Peeler in the Department of Bioengineering; Wei Chen in the Molecular Engineering & Sciences Institute; , a professor of bioengineering; and Drew Sellers, a research assistant professor of bioengineering and scientist with the 91探花Institute for Stem Cell and Regenerative Medicine. Additional co-authors from Allen Institute for Brain Science are Zizhen Yao and Lucas Gray. The research was funded by the National Institutes of Health, the National Science Foundation and the Allen Institute for Brain Science.

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For more information, contact Rosenberg at alex.b.rosenberg@gmail.com or 773-294-4109 and Seelig at gseelig@uw.edu or 206-294-8180.

If you could pick an image to be preserved for thousands of years, what would it be? A picture of your family, an endangered landscape, a page of poetry, or a snapshot that sends a message to the future?

Researchers from the at the 91探花 and Microsoft are looking to collect 10,000 original images from around the world to preserve them indefinitely in synthetic DNA manufactured by . DNA holds promise as a revolutionary storage medium that lasts much longer and is many orders of magnitude denser than current technologies.

The team has already encoded important compositions in DNA molecules, including The Universal Declaration of Human Rights, the top 100 books of Project Gutenberg, songs from the and an .

The invites the public to submit original photographs that they鈥檇 like to see preserved in DNA for millennia. The images 鈥� which can be uploaded at the 鈥� will be encoded in synthetic DNA and made available to researchers worldwide. The researchers also are encouraging people to share their images on social media with the hashtag #MemoriesInDNA and include a story about why the photograph or video is important to them.

鈥淚t鈥檚 your turn to show us what should be preserved in DNA forever,鈥� said , professor in the UW鈥檚 Paul G. Allen School of Computer Science & Engineering. 鈥淲e want people to go out and take a picture of something that they want the world to remember 鈥� it鈥檚 a fun opportunity to send a message to future generations and help our research in the process.鈥�

DNA data storage has emerged as a potential solution to bridge the growing gap between the amount of digital data generated today 鈥� by everything from commercial video to space imagery to medical records 鈥� and our ability to affordably and efficiently store that data.

Unlike data centers, which require acres of land and account for in the United States, DNA molecules can store information millions of times more compactly. The basic process converts the strings of ones and zeroes in digital data into the four basic building blocks of DNA sequences 鈥� adenine, guanine, cytosine and thymine. It employs synthetic DNA molecules created in a lab, not living DNA.

The team of 91探花computer scientists and electrical engineers, in collaboration with Microsoft researchers and working with Twist Bioscience, holds the for the amount of data stored in DNA.聽 So far they have been able to encode photographic images and video in DNA and retrieve and convert those individual molecular 鈥渇iles鈥� back into digital data.

Their next challenge involves exploring how to perform meaningful data processing directly in DNA 鈥� without having to convert the images back into their electronic form.

鈥淟et鈥檚 suppose you have a trillion images encoded in DNA and want to find all the photographs that have a red car in them, or to find out whether a person鈥檚 face exists in those images,鈥� said Ceze. 鈥淲e want to be able to do that information processing in DNA directly 鈥� to search in a smart way and make the molecules themselves carry out that computer vision work.鈥�

The team will encode approximately 10,000 of the crowdsourced images in manufactured snippets of DNA. The researchers鈥� approach to searching images directly in DNA relies on the fact that certain nucleotides stick to others 鈥� A binds to T and C binds to G.

They can introduce strips of DNA into the solution that contains a coded 鈥渜uery鈥� 鈥� essentially, a string of complementary DNA that causes all photographs with a red car or certain facial features or whatever meets the criteria of the query to bind to it. By attaching magnetic nanoparticles to the query DNA, they can use a magnet to pull out all the similar images that have stuck to it.

鈥淚t is thrilling to bring computer science and molecular biology together in this project,鈥� said Microsoft senior researcher and collaborator Karin Strauss. 鈥淭here has been amazing progress recently in both areas and, when combined, they can be very powerful in tackling problems created by the massive amounts of data we鈥檝e been generating.鈥�

鈥淗aving a set of diverse images from around the world will help us invent new ways to make molecules work with each other to carry out these computations directly,鈥� said Microsoft partner architect and collaborator .

The team will employ machine learning to devise methods to map and encode all the visual features contained in a photograph 鈥� such as colors, curves, lines and objects 鈥� in DNA. The main challenge is doing that in a way that allows scientists to extract similar things and perform meaningful data processing.

鈥淲e will use neural networks to explore ways to classify visual patterns in the images and video that we encode in DNA,鈥� said , 91探花associate professor of electrical engineering and in the Allen School. 鈥淔or example, are there more red cars than blue cars in a photograph? Or are there people riding bicycles?鈥�

鈥淲ith proof-of-concept achieved for DNA as a digital data storage media, we are working to drive down the cost of synthesizing DNA to enable its potential as a widely-available commercial solution for the growing body of precious data in digital format, such as archival data, financial and health record backups, and all long-term data retention where current media is not practical,鈥� said Emily M. Leproust, CEO of Twist Bioscience. 鈥淢emoriesInDNA is a fabulous project to showcase the technological, scientific and cultural importance of DNA worldwide and we look forward to our role in this historic event.鈥�

#MemoriesInDNA will provide an important library of images to be encoded in a separately funded project supported by the Defense Advanced Research Projects Agency (DARPA) . 91探花was recently awarded $6.3M to accelerate the pace at which data can be encoded in DNA, and to develop new capabilities to process this data through image search and classification. The work will build the foundation on which 91探花can advance its next-generation work in molecular information processing.

Note: To be included in the DNA image collection, photographs cannot be copyrighted by any other party and must be free of violent or inappropriate content. The image dataset will be preserved in DNA indefinitely and shared with researchers worldwide. For more details about how to upload and share images, visit the .

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For more information, contact misl-info@cs.washington.edu or visit the #MemoriesInDNA Project website: .

The findings, in the , shed new light on how the intricate interplay between genetics and environment impacts human health.

“These are important and surprising findings because 鈥� generally speaking 鈥� shorter chromosome ‘caps’ are associated with a higher burden of disease later in life,” said lead author , an assistant professor of anthropology at the 91探花.

The ‘caps’ Eisenberg and his co-authors measured are called telomeres. These are long stretches of DNA at the ends of our chromosomes, which protect our genes from damage or improper regulation. who studies telomeres has compared them to 鈥� the plastic or metal sheath covering ends of shoelaces. When aglets wear down, the shoelace is exposed to fraying and degradation from environmental forces.

Like aglets, telomeres don’t last forever. In most of our cells, telomeres get shorter each time that cell divides. And when they get too short, the cell either quits dividing or dies.

That makes telomere length particularly important for the cells of our immune system, especially the white blood cells circulating in our bloodstream. When activated against a pathogen, white blood cells undergo rapid rounds of cell division to raise a defensive force against the infectious invader. But if telomeres in white blood cells are already too short, the body may struggle to mount an effective immune response.

“Many studies 鈥� in laboratory animals and humans 鈥� have associated shorter telomeres with poor health outcomes, especially in adults,” said Eisenberg.

But few studies have addressed whether or not events early in a person’s life might affect telomere length.

To get at this question, Eisenberg turned to the , which has tracked the health of over 3,000 infants born in 1983-1984 in Cebu City in the Philippines. Researchers collected detailed data every two months from mothers on the health and feeding habits of their babies up through age two. Mothers reported how often their babies had diarrhea 鈥� a sign of infection 鈥� as well as how often they breastfed their babies.

As these babies grew up, scientists collected additional health data during follow-up surveys over the next 20 years. In 2005, 1,776 of these offspring donated a blood sample. By then, they were 21- or 22-year-old young adults.

Eisenberg measured telomere length in cells from those blood samples. He then combined the data on adult telomere length with information about their health and feeding habits as babies.

He found that babies with higher reported cases of diarrhea at 6 to 12 months also had the shortest telomeres as adults. This six-month period is the typical age for weaning infants, as well as a time of increasing mobility and exploration. It is also a time when infectious diseases in infants reach their peak. Based on the environment and public health situation in Cebu City at the time, these cases of diarrhea were most likely brought about by infection, Eisenberg said.

Diarrheal infection is a very serious global health concern as it is the second leading cause of death in children under age five. The association Eisenberg found between this infection and telomeres is large enough that it might influence aging in important ways. For example, those with an average level of diarrheal infection as babies, compared to those who with no reported infections, showed the equivalent of three additional years of telomere “aging” 鈥� based on the rate of telomere shortening among middle-aged adults.

One explanation is that the adults have shorter telomeres because they had more infections as infants. Infections spur increased cell replications and inflammation, both of which can shorten telomeres. But, Eisenberg said, another explanation is also possible.

“It could also be that they had shorter telomeres at birth,” said Eisenberg. “And perhaps as a result, they were more susceptible to infections at 6 to 12 months and maintained these short telomeres into adulthood.” If this were the case, then telomeres may be an important determinant of whether or not children around the world succumb to diarrheal infections.

Surprisingly, he found no association between breastfeeding by mothers and telomere length in their offspring as adults.

“We were expecting to see a relationship between breastfeeding and telomere length because babies receive maternally-produced antibodies through breastmilk, which can help them fight off pathogens while their own immune systems are developing,” said Eisenberg. “In addition, breastfed babies are less likely to be exposed to infectious agents through contaminated food and water.”

In addition, from 2016 reported that, among 121 Latino children in California, exclusive breastfeeding in the first six weeks after birth was associated with longer telomeres at age 4 or 5. But there are many reasons that could explain the difference between the 2016 study in California and this new study from the Philippines, Eisenberg said.

“If breastfeeding does effect telomere length, it could be that the effect goes away by age 21,” said Eisenberg. “Also, infants in these studies were from vastly different parts of the world 鈥� which likely affects the pathogens they were exposed to and the other typical parenting habits of women who breastfeed.”

Only more data on health, telomere length and environment can resolve the debate, Eisenberg concluded.

Co-authors on the study include and at Northwestern University and with the in the Philippines. The research was funded by the National Science Foundation, the Wenner-Gren Foundation, the National Institutes of Health and Northwestern University.

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For more information, contact Eisenberg at 206-221-9056 or dtae@uw.edu.

Grant numbers: BCS-0962282, 8111, TW05596, DK078150, RR20649, ES10126 and DK056350.