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Andrea Ghez wins 2020 Nobel Prize in physics

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Photo of Andrea Ghez

Andrea Ghez, UCLA’s Lauren B. Leichtman and Arthur E. Levine Professor of Astrophysics, has been awarded the 2020 Nobel Prize in physics. Photo Credit: Elena Zhukova

Andrea Ghez, UCLA’s Lauren B. Leichtman and Arthur E. Levine Professor of Astrophysics, today was awarded the 2020 Nobel Prize in physics.

Ghez shares half of the prize with Reinhard Genzel of UC Berkeley and the Max Planck Institute for Extraterrestrial Physics. The Nobel committee praised them for “the discovery of a supermassive compact object at the centre of our galaxy.” The other half of the prize was awarded to Roger Penrose of the University of Oxford “for the discovery that black hole formation is a robust prediction of the general theory of relativity.”

In July 2019, the journal Science published a study by Ghez and her research group that is the most comprehensive test of Albert Einstein’s iconic general theory of relativity near the monstrous black hole at the center of our galaxy. Although she concluded that “Einstein’s right, at least for now,” the research group is continuing to test Einstein’s theory, which she says cannot fully explain gravity inside a black hole.

Ghez studies more than 3,000 stars that orbit the supermassive black hole. Black holes have such high density that nothing can escape their gravitational pull, not even light. The center of the vast majority of galaxies appears to have a supermassive black hole, she said.

“I’m thrilled and incredibly honored to receive a Nobel Prize in physics,” said Ghez, who is director of the UCLA Galactic Center Group. “The research the Nobel committee is honoring today is the product of a wonderful collaboration among the scientists in the UCLA Galactic Center Orbits Initiative and the University of California’s wise investment in the W.M. Keck Observatory.

“We have cutting-edge tools and a world-class research team, and that combination makes discovery tremendous fun. Our understanding of how the universe works is still so incomplete. The Nobel Prize is fabulous, but we still have a lot to learn.”

UCLA Chancellor Gene Block lauded Ghez for her accomplishments.

“The UCLA community is exceedingly proud of Professor Ghez’s achievements, including this extraordinary honor,” Block said. “We are inspired by her research uncovering the secrets of our universe and its potential to help us better understand the cosmos.”

David Haviland, chair of the Nobel Committee for Physics, said: “The discoveries of this year’s Laureates have broken new ground in the study of compact and supermassive objects. But these exotic objects still pose many questions that beg for answers and motivate future research. Not only questions about their inner structure, but also questions about how to test our theory of gravity under the extreme conditions in the immediate vicinity of a black hole.”

Ghez and her team have made direct measurements of how gravity works near a supermassive black hole — research she describes as “extreme astrophysics.”

Einstein’s general theory of relativity is the best description of how gravity works. “However, his theory is definitely showing vulnerability,” Ghez said in 2019. “[A]t some point we will need to move beyond Einstein’s theory to a more comprehensive theory of gravity that explains what a black hole is.”

Less than two months after her publication in Science, she and her research group reported in Astrophysical Journal Letters the surprising finding that the supermassive black hole is having an unusually large meal of interstellar gas and dust — and they do not yet understand why.

“We have never seen anything like this in the 24 years we have studied the supermassive black hole,” she said at the time. “It’s usually a pretty quiet, wimpy black hole on a diet. We don’t know what is driving this big feast.”

In January 2020, her team reported the discovery of a new class of bizarre objects — objects that look like gas and behave like stars — at the center of our galaxy, not far from the supermassive black hole.

Ghez and her team conducted their research at the W.M. Keck Observatory in Hawaii. They are able to see the impact of how space and time get comingled near the supermassive black hole, which is some 26,000 light-years away.

“Making a measurement of such fundamental importance has required years of patient observing, enabled by state-of-the-art technology,” Richard Green, director of the National Science Foundation’s division of astronomical sciences, said in 2019.

“Andrea is one of our most passionate and tenacious Keck users,” Keck Observatory director Hilton Lewis said, also in 2019. “Her latest groundbreaking research is the culmination of unwavering commitment over the past two decades to unlock the mysteries of the supermassive black hole at the center of our Milky Way Galaxy.”

The National Science Foundation funded Ghez’s research for the past 25 years. More recently, her research has also been funded by the W.M. Keck Foundation, the Gordon and Betty Moore Foundation and the Heising-Simons Foundation, Lauren Leichtman and Arthur Levine, and Howard and Astrid Preston.

In 1998, Ghez answered one of astronomy’s most important questions, helping to show that a supermassive black hole resides at the center of the Milky Way galaxy. The question had been a subject of much debate among astronomers for more than a quarter of a century.

Ghez helped pioneer a powerful technology called adaptive optics, which corrects the distorting effects of the Earth’s atmosphere in real time and opened the center of our galaxy as a laboratory for exploring black holes and their fundamental role in the evolution of the universe. With adaptive optics at the Keck Observatory, she and her colleagues have revealed many surprises about the environments surrounding supermassive black holes, discovering, for example, young stars where none were expected and a lack of old stars where many were anticipated.

In 2000, Ghez and her research team reported that for the first time, astronomers had seen stars accelerate around the supermassive black hole. In 2003, she and her team reported that the case for the Milky Way’s black hole had been strengthened substantially and that all of the proposed alternatives could be excluded.

In 2005, Ghez and her colleagues took the first clear picture of the center of the Milky Way, including the area surrounding the black hole, at the Keck Observatory.

Ghez has earned numerous honors for her research, including election to the National Academy of Sciences and the American Academy of Arts and Sciences; she was the first woman to receive the Royal Swedish Academy of Sciences’ Crafoord Prize, and she was named a MacArthur Fellow in 2008. In 2019, she was awarded an honorary degree by Oxford University.

She earned a bachelor’s degree in physics from MIT in 1987 and a doctorate from Caltech in 1992, and she has been a member of the UCLA faculty since 1994. When she was young, she wanted to be the first woman to walk on the moon.

Ghez is the eighth UCLA faculty member to be named a Nobel laureate, joining Willard Libby (chemistry, 1960), Julian Schwinger (physics, 1965), Donald Cram (chemistry, 1987), Paul Boyer (chemistry, 1997), Louis Ignarro (physiology or medicine, 1998), Lloyd Shapley (economics, 2012) and J. Fraser Stoddart (2016). Stoddart was a Northwestern University faculty member when he received the honor, but much of the work for which he was recognized was conducted at UCLA from 1997 to 2008.

In addition, seven UCLA alumni have been awarded the Nobel Prize.

Ghez is also the fourth woman to receive the physics prize, following Marie Curie in 1903, Maria Goeppert Mayer in 1963 and Donna Strickland in 2018.

This article, written by Stuart Wolpert, originally appeared in the UCLA Newsroom.

A photo of a sleeping baby.

UCLA-led team of scientists discovers why we need sleep

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A photo of a sleeping baby.

A UCLA-led team of scientists explains why sleep is so vital to our health and shows for the first time that a dramatic change in the purpose of sleep occurs at the age of about 2-and-a-half. (Photo Credit: Shutterstock.com)

Prolonged sleep deprivation can lead to severe health problems in humans and other animals. But why is sleep so vital to our health? A UCLA-led team of scientists has made a major advance in answering this question and has shown for the first time that a dramatic change in the purpose of sleep occurs at the age of about 2-and-a-half.

Before that age, the brain grows very rapidly. During REM sleep, when vivid dreams occur, the young brain is busy building and strengthening synapses — the structures that connect neurons to one another and allow them to communicate.

“Don’t wake babies up during REM sleep — important work is being done in their brains as they sleep,” said senior study author Gina Poe, a UCLA professor of integrative biology and physiology who has conducted sleep research for more than 30 years.

After 2-and-a-half years, however, sleep’s primary purpose switches from brain building to brain maintenance and repair, a role it maintains for the rest of our lives, the scientists report Sept. 18 in the journal Science Advances. This transition, the researchers say, corresponds to changes in brain development.

All animals naturally experience a certain amount of neurological damage during waking hours, and the resulting debris, including damaged genes and proteins within neurons, can build up and cause brain disease. Sleep helps repair this damage and clear the debris — essentially decluttering the brain and taking out the trash that can lead to serious illness.

Nearly all of this brain repair occurs during sleep, according to senior author Van Savage, a UCLA professor of ecology and evolutionary biology and of computational medicine, and his colleagues.

“I was shocked how huge a change this is over a short period of time, and that this switch occurs when we’re so young,” Savage said. “It’s a transition that is analogous to when water freezes to ice.”

The research team, which included scientists with expertise in neuroscience, biology, statistics and physics, conducted the most comprehensive statistical analysis of sleep to date, using data from more than 60 sleep studies involving humans and other mammals. They examined data on sleep throughout development — including total sleep time, REM sleep time, brain size and body size — and built and tested a mathematical model to explain how sleep changes with brain and body size.

The data were remarkably consistent: All species experienced a dramatic decline in REM sleep when they reached the human developmental equivalent of about 2-and-half years of age. The fraction of time spent in REM sleep before and after that point was roughly the same, whether the researchers studied rabbits, rats, pigs or humans.

REM sleep decreases with the growth in brain size throughout development, the scientists found. While newborns spend about 50% of their sleep time in REM sleep, that falls to about 25% by the age of 10 and continues to decrease with age. Adults older than 50 spend approximately 15% of their time asleep in REM. The significant dropoff in REM sleep at about 2-and-a-half happens just as the major change in the function of sleep occurs, Poe said.

“Sleep is as important as food,” Poe said. “And it’s miraculous how well sleep matches the needs of our nervous system. From jellyfish to birds to whales, everyone sleeps. While we sleep, our brains are not resting.”

A chronic lack of sleep likely contributes to long-term health problems such as dementia and other cognitive disorders, diabetes, and obesity, to name a few, Poe said. When you start to feel tired, she said, don’t fight it — go to bed.

“I fought sleep and pulled all-nighters when I was in college, and now think that was a mistake,” Savage said. “I would have been better off with a good night’s sleep. Now when I feel tired, I don’t have any guilt about sleeping.”

For most adults, a regular seven-and-a-half hours of sleep a night is normal — and time lying awake doesn’t count, Poe says. While children need more sleep, babies need much more, roughly twice as much as adults. The large percentage of REM sleep in babies is in stark contrast to the amount of REM sleep observed in adult mammals across an enormous range of brain sizes and body sizes. Adult humans have five REM cycles during a full night of sleep and can have a few dreams in each cycle.

A good night’s sleep is excellent medicine, Poe says. And it’s free.

Co-authors of the study are Junyu Cao, who conducted research in Savage’s laboratory and is now an assistant professor at the University of Texas at Austin; Alexander Herman, an assistant professor of psychiatry at the University of Minnesota, Twin Cities; and Geoffrey West, a physicist who is the Shannan Distinguished Professor at the Santa Fe Institute.

Funding sources included the National Science Foundation and the Eugene and Clare Thaw Charitable Trust.

This article originally appeared in the UCLA Newsroom.

A photo of two N95 respirators.

Single-use N95 respirators can be decontaminated and used again, study finds

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A photo of two N95 respirators.

N95 respirators reduce exposure to airborne infectious agents, including SARS-CoV-2, the virus that causes COVID-19. (Photo Credit: CDC/Debora Cartagena)

N95 respirators, which are widely worn by health care workers treating patients with COVID-19 and are designed to be used only once, can be decontaminated effectively and used up to three times, according to research by UCLA scientists and colleagues.

An early-release version of their study has been published online, with the full study to appear in September in the journal Emerging Infectious Diseases.

N95 respirators reduce exposure to airborne infectious agents, including SARS-CoV-2, the virus that causes COVID-19, and are one of the key pieces of personal protective equipment used by clinical workers in preventing the spread of the virus. Critical shortages of these masks have driven efforts to find new decontamination methods that can extend their use.

“Although N95 respirators are designed for just one use before disposal, in times of shortage, N95 respirators can be decontaminated and reused up to three times,” said James Lloyd-Smith, a co-author of the study and a UCLA professor of ecology and evolutionary biology. “But the integrity of the respirator’s fit and seal must be maintained.”

In a controlled laboratory setting, the researchers tested several decontamination methods on small sections of N95 filter fabric that had been exposed to SARS-CoV-2. The methods included vaporized hydrogen peroxide, dry heat at 70 degrees Celsius (158 degrees Fahrenheit), ultraviolet light and a 70% ethanol spray. All four methods eliminated detectable viable virus traces from the N95 fabric test samples.

The investigators then treated fully intact, clean respirators with the same decontamination methods to test their reuse durability. Employees with the National Institutes of Health’s Rocky Mountain Laboratories in Montana volunteered to wear the masks for two hours to determine if they maintained a proper fit and seal over the face. The scientists decontaminated each mask three times, using the same procedure with each.

The masks treated with vaporized hydrogen peroxide experienced no failures, suggesting they potentially could be reused three times, Lloyd-Smith said. Those treated with ultraviolet light and dry heat began showing fit and seal problems after three decontaminations, suggesting these respirators potentially could be reused twice.

The study authors concluded that vaporized hydrogen peroxide was the most effective method because no traces of the virus could be detected after only a 10-minute treatment. They found that ultraviolet light and dry heat are also acceptable decontamination procedures, as long as the methods are applied for at least 60 minutes.

The ethanol spray, the scientists discovered, damaged the integrity of the respirator’s fit and seal after two sessions, and they do not recommend it for decontaminating N95 respirators.

The researchers stressed that anyone decontaminating an N95 respirator should closely check the fit and seal over the face before each reuse.

Co-authors of the study include Amandine Gamble, a UCLA postdoctoral researcher in Lloyd-Smith’s laboratory, as well as researchers with Rocky Mountain Laboratories, part of the NIH’s National Institute of Allergy and Infectious Diseases.

Funding sources included the National Institute of Allergy and Infectious Diseases, the Defense Advanced Research Projects Agency, and the National Science Foundation.

In a widely cited study, Lloyd-Smith and colleagues reported in March that the virus that causes COVID-19 remains for several hours to days on surfaces and in aerosols.

This article originally appeared in the UCLA Newsroom.

 

Picture of Tracy Johnson

Tracy Johnson named dean of the UCLA Division of Life Sciences

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Tracy Johnson, professor of molecular, cell, and developmental biology and holder of the Keith and Cecilia Terasaki Presidential Endowed Chair, has been named dean of the division of life sciences in the UCLA College, effective Sept. 1.

Picture of Tracy Johnson

Tracy Johnson. Photo Credit: Hadar Goren

An award-winning scientist whose research focuses on understanding the mechanisms of gene regulation, particularly RNA splicing, chromatin modification and the intersection between these reactions, Johnson has been a member of the faculty since 2013 and has served as associate dean for inclusive excellence in the division of life sciences since January 2015.

“I am deeply humbled to serve as UCLA’s next dean of the division of life sciences. Our life sciences researchers and educators are consistently at the leading edge of scientific and educational innovation, and our international reputation for excellence has allowed the division to attract truly exceptional students,” said Johnson, who is also a Howard Hughes Medical Institute professor.

“These extraordinary times provide an opportunity for UCLA Life Sciences to exercise leadership in new and previously unimaginable ways across the UCLA campus, the city of Los Angeles, the state of California, the nation and beyond,” Johnson said. “I am honored to be a steward of these incredible opportunities to build on a foundation of excellence as we move forward into an exciting future.”

Prior to her appointment at UCLA, Johnson was a member of the UC San Diego biological sciences faculty from 2003 to 2013, and a Jane Coffin Childs postdoctoral research fellow at the California Institute of Technology.

Recognized for her scientific leadership and contributions to educational innovation, and as a champion of diversity, equity and inclusion, Johnson serves as a member of the UCLA Human Pluripotent Stem Cell Research oversight committee; chair and director of the biomedical research minor; co-director and steering committee member for the Bruins in Genomics summer program; and co-director/co-principal investigator for the National Institutes of Health–funded UPLIFT/IRACDA program, which supports postdoctoral researchers preparing for academic careers.

Johnson also started the UCLA-HHMI Pathways to Success program, which is funded through the Howard Hughes Medical Institute to support the success of students from diverse backgrounds in STEM fields. She is also the principal investigator for a second HHMI grant aimed at promoting greater access and success for students studying life sciences who transfer from community colleges.

Additionally, Johnson has served on numerous campus committees, including the faculty advisory committees for the Ralph J. Bunche Center for African American Studies and the UCLA Center for the Study of Women, the Moreno Report Implementation Committee, Jonsson Comprehensive Cancer Center executive committee, and diversity in research committee.

“Chancellor Block and I are confident that the division of life sciences will continue to thrive under Tracy’s capable leadership. Please join me in congratulating her and welcoming her to this new role,” said Emily Carter, UCLA executive vice chancellor and provost, who also thanked Dean Victoria Sork for her leadership of the division of life sciences.

Beyond UCLA, Johnson has served as chair of an NIH Molecular Genetics Study Section, the National Cancer Institute Board of Scientific Counselors, the executive committee for the Annual Biomedical Research Conference for Minority Students, and the executive board of the Society of Howard Hughes Medical Institute Professors.

She is the recipient of numerous awards, including the National Science Foundation CAREER Award; the Presidential Early Career Award for Scientists and Engineers; the UCLA Academic Senate Award for Career Commitment to Diversity, Equity and Inclusion; and the UCLA Life Sciences Award for Inclusive Excellence through teaching, mentorship, service and research.

Johnson earned her bachelor’s degree in biochemistry and cell biology at UC San Diego and her doctorate in biochemistry and molecular biology at UC Berkeley.

This article originally appeared in the UCLA Newsroom.

Image of interstellar comet.

New NASA image provides more details about first observed interstellar comet

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Image of interstellar comet.

The interstellar comet Comet 2I/Borisov (blueish image at right) near a spiral galaxy (left), in an image taken Nov. 16. Photo credit: NASA, ESA and David Jewitt/UCLA

A new image from NASA’s Hubble Space Telescope provides important new details about the first interstellar comet astronomers have seen in our solar system.

The comet, called Comet 2I/Borisov (the “I” stands for interstellar), was spotted near a spiral galaxy known as 2MASX J10500165-0152029. It was approximately 203 million miles from Earth when the image was taken on Nov. 16.

“Data from the Hubble Space Telescope give us the best measure of the size of comet 2I/Borisov’s nucleus, which is the really important part of the comet,” said David Jewitt, a UCLA professor of planetary science and astronomy who analyzed and interpreted the data from the new image.

Jewitt collaborated on the new analysis with colleagues from the University of Hawaii, Germany’s Max Planck Institute for Solar System Research, the Space Telescope Science Institute in Baltimore and Johns Hopkins University’s Applied Physics Laboratory. The scientists were surprised to learn that the nucleus has a radius measuring only about half of a kilometer — or less than one-fifteenth the size that earlier investigations suggested it might be.

“That is important because knowing its size helps us to determine the total number, and mass, of other similar objects in the solar system and the Milky Way,” Jewitt said. “2I/Borisov is the first known interstellar comet, and we would like to learn how many others there are.”

The comet is traveling at a breathtaking speed of 110,000 miles per hour — one of the fastest comets ever seen, Jewitt said. More commonly, comets travel at about half that speed.

Crimean astronomer Gennady Borisov discovered the comet on Aug. 30, using a telescope he built. Based on precise measurements of its changing position, the International Astronomical Union’s Minor Planet Center calculated a likely orbit for the comet, which shows that it came from elsewhere in the galaxy. Jewitt said its precise point of origin is unknown.

A second Hubble Space Telescope image of the comet, taken on Dec. 9, shows the comet even closer to Earth, approximately 185 million miles from Earth, he said.

Comets are icy bodies thought to be fragments left behind when planets form in the outer parts of planetary systems.

Observations by numerous telescopes show that the comet’s chemical composition is similar to that of comets previously observed in our solar system, which provides evidence that comets also form around other stars, Jewitt said. By mid-2020, the comet will have zoomed past Jupiter on its way back into interstellar space, where it will drift for billions of years, Jewitt said.

This article originally appeared in the UCLA Newsroom.

Photo of student smiling.

Meet UCLA Student Researcher Julia Nakamura

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Photo of student smiling.

Fourth-year UCLA student researcher Julia Nakamura

Meet fourth-year UCLA student researcher Julia Nakamura!

Julia majors in Psychobiology with a minor in Gerontology and is in our Undergraduate Research Scholars Program. The title of her research project is “The Role of Social Support in the Association between Early Life Stress, Depression, and Inflammation in Older Adults.”

 

How did you first get interested in your research project?

UCLA’s Cluster course “Frontiers in Human Aging” initially sparked my interest in aging populations. Through a service learning project at ONEgeneration Adult Day Care Center, I directly witnessed the burden of chronic disease in later-life adults and realized the pressing need to understand the mechanisms underlying these adverse health outcomes. Through my coursework in psychology, I became interested in the psychological factors that influence biological mechanisms and have the potential to positively impact the trajectory of chronic disease outcomes.

I began research in psychology in Dr. Julienne Bower’s Mind-Body Lab under the direction of Dr. Kate Kuhlman. We study the effects of childhood adversity on biological and behavioral responses to psychological stress. My experiences in this lab led me to wonder what factors could mitigate adverse physical and mental health outcomes from stressful experiences, specifically in older adults. My honors research project examines if social support moderates the relationship between early-life stress, depressive symptoms, and inflammation in older adults using data from the Health and Retirement Study.

What has been the most exciting aspect of your research so far?

Getting to test my own research questions has been the best part of this project. Specifically, it has been really exciting for me to run my own data analyses for the first time with Dr. Kuhlman’s guidance. Experiencing the “behind-the-scenes” of research and systematically moving through the steps of conducting an independent project has been really informative. This project has helped me to feel that I am truly developing the skill set of an independent researcher, which is very exciting!

What has surprised you about your research or the research process?

The immensely collaborative nature of research in academia was quite surprising to me when I first started on this project. Through my research, I’ve had the privilege of working with several scientists and professors who are experts in their respective areas of study. They have all welcomed me and helped to make my project as scientifically sound and comprehensive as possible. Research really builds on itself. Learning from other people’s projects and ideas, even if they are outside of your immediate area of study, can result in high levels of collaboration and really interesting research!

What is one piece of advice you have for other UCLA students thinking about doing research?

I would advise students interested in research to actively pursue research opportunities. There are plenty of amazing opportunities to be involved in research at UCLA, but you have to seek them out. It can be intimidating to take the initial steps to reach out to professors and discuss their research interests, but it is so worthwhile to find a lab and professor that are a good fit! I would recommend that students find an area of study that they are really passionate about. I think that your passion for your area of study and your continued curiosity will drive your research questions and help you get the most out of each research experience.

What effect do you hope your research has in your field, at UCLA, in your community, or in the world?

I hope to spend my life contributing to our understanding of the biobehavioral processes that promote mental and physical health across the lifespan. As the number of older adults (a majority of whom have at least one chronic disease) increase in our society, it is now more important than ever to identify potential intervention targets that can improve the trajectory of chronic disease outcomes.

This article originally appeared on the Undergraduate Research Center website.

Picture of a valley oak tree.

One of California’s iconic tree species offers lessons for conservation

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Picture of a valley oak tree.

The valley oak, the largest oak in California, grows to over 100 feet tall and provides habitat and food for a variety of animals. Photo credit: Victoria Sork/UCLA

 

With increasing regularity, Californians are witnessing firsthand the destructive power of wildfires. But not everyone sees what happens after the flames die down, when debris is cleared, homes and lives rebuilt — and trees replanted to help nature recover.

New research led by UCLA evolutionary biologist Victoria Sork examines whether the trees being replanted in the wake of California’s fires will be able to survive a climate that is continuing to warm.

The study, which is published in the Proceedings of the Natural Academy of Sciences, focuses on California’s iconic valley oak. The research is among the first to demonstrate the potential of using genomics to inform conservation strategies — essentially giving species an evolutionary boost. The study showed that planting trees that are genetically better suited to higher temperatures makes them more likely to survive and grow to maturity.

“When we think about managing ecosystems under rapidly changing climates, we have to realize trees need to be able to survive past 50 years,” Sork said.

The paper also discovered something surprising: The valley oak, an essential component of many ecosystems in California, is already poorly adapted to its environment — even considering climate conditions in 2019.

“They actually seem to grow better in cooler climates than they’re in right now,” said Luke Browne, a postdoctoral scholar at the UCLA La Kretz Center for California Conservation Science and the study’s lead author. “They might grow better if climates were more like they were 21,000 years ago, during the last ice age.”

During the peak of the last ice age, summer temperatures were about 4 to 5 degrees Celsius colder, and ice covered most of Canada and mountainous areas of the U.S.

In the fields of conservation and land management, it is a common assumption that plants and animals are adapted to their environments — that’s how evolution and natural selection are supposed to work. The new research casts doubt on that assumption.

The study is part of an ongoing project initiated by Sork and Jessica Wright, an expert in conservation genetics at the USDA Forest Service, more than 10 years ago.

Researchers gathered 11,000 seeds from 94 locations throughout the trees’ range, which stretches from the Santa Monica Mountains to the Cascade foothills in the northern part of the state. They grew them to saplings in a greenhouse and planted them in two large experimental gardens, in Chico and Placerville, California. They tracked how well trees from different locations grew, and sequenced the genomes of their mother trees to link genetic information and growth rates.

The researchers then identified which genetic variants would be more likely to thrive as climate change continues to warm California. They predicted that, under predicted future warmer temperatures, trees containing beneficial genetic variations would have 11% higher growth rates than the average for all of the trees in the experiment, and 25% higher growth rates than the trees without the beneficial variations.

Information like that could help the U.S. Forest Service, for example, in its efforts to restore forests with species that have the best chance for long-term survival.

“Studies like this one provide valuable insights that help land managers make informed decisions on reforestation projects,” Wright said. “When planting trees in a particular location, managers have to decide where to collect the acorns.”

By 2070, average temperatures in the state are projected to be up to 4.8 degrees warmer than they were during the mid- to late 20th century.

“That’s going to have consequences for how fast these trees grow,” Browne said. “We’re at a challenging time to figure out the best way to do conservation science. This paper shows one approach we could use that takes advantage of modern genomics.”

The study did not determine why valley oaks are not well adapted to their environment. It might be because the climate has already warmed up so much, the trees’ long lifespans — up to 500 years — or some other, unknown factor.

The valley oak is the largest oak in California; it grows to over 100 feet tall, and has dark green leaves and a deeply grooved trunk. It is considered a foundational species because it provides habitat and food for a variety of animals, including squirrels, birds, deer and insects. In parts of the state, it is one of the only species of tree that exists. Valley oaks provide benefits to humans, too: filtering water and providing shady places to escape the heat.

Although it focuses on the oak, the paper has broader implications for conservation science in a changing climate — especially for species that evolve and adapt slowly. That’s what Sork and Wright were thinking when they initiated the project.

At the time, they hoped to find conservation strategies that could eventually be implemented using genetic information alone — without extensive field experiments.

“Not everyone in the world is going to be able to collect 11,000 seeds and plant them in a common garden,” Sork said.

This article originally appeared in the UCLA Newsroom.

Study shows how serotonin and a popular anti-depressant affect the gut’s microbiota

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Senior author Elaine Hsiao says researchers hope to build on their current study to learn whether microbial interactions with antidepressants have consequences for health and disease. Photo: Reed Hutchinson/UCLA

A new study in mice led by UCLA biologists strongly suggests that serotonin and drugs that target serotonin, such as anti-depressants, can have a major effect on the gut’s microbiota — the 100 trillion or so bacteria and other microbes that live in the human body’s intestines.

Serotonin — a neurotransmitter, or chemical messenger that sends messages among cells — serves many functions in the human body, including playing a role in emotions and happiness. An estimated 90% of the body’s serotonin is produced in the gut, where it influences gut immunity.

The team — led by senior author Elaine Hsiao and lead author Thomas Fung, a postdoctoral fellow — identified a specific gut bacterium that can detect and transport serotonin into bacterial cells. When mice were given the antidepressant fluoxetine, or Prozac, the biologists found this reduced the transport of serotonin into their cells. This bacterium, about which little is known, is called Turicibacter sanguinis. The study is published this week in the journal Nature Microbiology.

“Our previous work showed that particular gut bacteria help the gut produce serotonin. In this study, we were interested in finding out why they might do so,” said Hsiao, UCLA assistant professor of integrative biology and physiology, and of microbiology, immunology and molecular genetics in the UCLA College; and of digestive diseases in the David Geffen School of Medicine at UCLA.

Hsiao and her research group reported in the journal Cell in 2015 that in mice, a specific mixture of bacteria, consisting mainly of Turicibacter sanguinis and Clostridia, produces molecules that signal to gut cells to increase production of serotonin. When Hsiao’s team raised mice without the bacteria, more than 50% of their gut serotonin was missing. The researchers then added the bacteria mixture of mainly Turicibacter and Clostridia, and their serotonin increased to a normal level.

That study got the team wondering why bacteria signal to our gut cells to make serotonin. Do microbes use serotonin, and if so, for what?

In this new study, the researchers added serotonin to the drinking water of some mice and raised others with a mutation (created by altering a specific serotonin transporter gene) that increased the levels of serotonin in their guts. After studying the microbiota of the mice, the researchers discovered that the bacteria Turicibacter and Clostridia increased significantly when there was more serotonin in the gut.

If these bacteria increase in the presence of serotonin, perhaps they have some cellular machinery to detect serotonin, the researchers speculated. Together with study co-author Lucy Forrest and her team at the National Institutes of Health’s National Institute of Neurological Disorders and Stroke, the researchers found a protein in multiple species of Turicibacter that has some structural similarity to a protein that transports serotonin in mammals. When they grew Turicibacter sanguinis in the lab, they found that the bacterium imports serotonin into the cell.

In another experiment, the researchers added the antidepressant fluoxetine, which normally blocks the mammalian serotonin transporter, to a tube containing Turicibacter sanguinis. They found the bacterium transported significantly less serotonin.

The team found that exposing Turicibacter sanguinis to serotonin or fluoxetine influenced how well the bacterium could thrive in the gastrointestinal tract. In the presence of serotonin, the bacterium grew to high levels in mice, but when exposed to fluoxetine, the bacterium grew to only low levels in mice.

“Previous studies from our lab and others showed that specific bacteria promote serotonin levels in the gut,” Fung said. “Our new study tells us that certain gut bacteria can respond to serotonin and drugs that influence serotonin, like anti-depressants. This is a unique form of communication between bacteria and our own cells through molecules traditionally recognized as neurotransmitters.”

The team’s research on Turicibacter aligns with a growing number of studies reporting that anti-depressants can alter the gut microbiota. “For the future,” Hsiao said, “we want to learn whether microbial interactions with antidepressants have consequences for health and disease.” Hsiao wrote a blog post for the journal about the new research.

Other study co-authors are Helen Vuong, Geoffrey Pronovost, Cristopher Luna, Anastasia Vavilina, Julianne McGinn and Tomiko Rendon, all of UCLA; and Antoniya Aleksandrova and Noah Riley, members of Forrest’s team.

The research was supported by funding from the National Institutes of Health’s Director’s Early Independence Award, Klingenstein-Simons Fellowship Award, and David & Lucile Packard Foundation’s Packard Fellowship for Science and Engineering.

This article originally appeared in the UCLA Newsroom.

Biochemists discover new insights into what may go awry in brains of people with Alzheimer’s

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Photo of two researchers in lab.

Research by UCLA professor Steven Clarke and former graduate student Rebeccah Warmack, as well as UCLA colleagues, reveals new information about the brain’s biochemistry.

More than three decades of research on Alzheimer’s disease have not produced any major treatment advances for those with the disorder, according to a UCLA expert who has studied the biochemistry of the brain and Alzheimer’s for nearly 30 years. “Nothing has worked,” said Steven Clarke, a distinguished professor of chemistry and biochemistry. “We’re ready for new ideas.” Now, Clarke and UCLA colleagues have reported new insights that may lead to progress in fighting the devastating disease.

Scientists have known for years that amyloid fibrils — harmful, elongated, water-tight rope-like structures — form in the brains of people with Alzheimer’s, and likely hold important clues to the disease. UCLA Professor David Eisenberg and an international team of chemists and molecular biologists reported in the journal Nature in 2005 that amyloid fibrils contain proteins that interlock like the teeth of a zipper. The researchers also reported their hypothesis that this dry molecular zipper is in the fibrils that form in Alzheimer’s disease, as well as in Parkinson’s disease and two dozen other degenerative diseases. Their hypothesis has been supported by recent studies.

Alzheimer’s disease, the most common cause of dementia among older adults, is an irreversible, progressive brain disorder that kills brain cells, gradually destroys memory and eventually affects thinking, behavior and the ability to carry out the daily tasks of life. More than 5.5 million Americans, most of whom are over 65, are thought to have dementia caused by Alzheimer’s.

The UCLA team reports in the journal Nature Communications that the small protein beta amyloid, also known as a peptide, that plays an important role in Alzheimer’s has a normal version that may be less harmful than previously thought and an age-damaged version that is more harmful.

Rebeccah Warmack, who was a UCLA graduate student at the time of the study and is its lead author, discovered that a specific version of age-modified beta amyloid contains a second molecular zipper not previously known to exist. Proteins live in water, but all the water gets pushed out as the fibril is sealed and zipped up. Warmack worked closely with UCLA graduate students David Boyer, Chih-Te Zee and Logan Richards; as well as senior research scientists Michael Sawaya and Duilio Cascio.

What goes wrong with beta amyloid, whose most common forms have 40 or 42 amino acids that are connected like a string of beads on a necklace?

The researchers report that with age, the 23rd amino acid can spontaneously form a kink, similar to one in a garden hose. This kinked form is known as isoAsp23. The normal version does not create the stronger second molecular zipper, but the kinked form does.

“Now we know a second water-free zipper can form, and is extremely difficult to pry apart,” Warmack said. “We don’t know how to break the zipper.”

The normal form of beta amyloid has six water molecules that prevent the formation of a tight zipper, but the kink ejects these water molecules, allowing the zipper to form.

When one of its amino acids forms a kink, beta amyloid creates a harmful molecular zipper, shown here in green. Photo credit: Rebeccah Warmack/UCLA

When one of its amino acids forms a kink, beta amyloid creates a harmful molecular zipper, shown here in green.
“Rebeccah has shown this kink leads to faster growth of the fibrils that have been linked to Alzheimer’s disease,” said Clarke, who has conducted research on biochemistry of the brain and Alzheimer’s disease since 1990. “This second molecular zipper is double trouble. Once it’s zipped, it’s zipped, and once the formation of fibrils starts, it looks like you can’t stop it. The kinked form initiates a dangerous cascade of events that we believe can result in Alzheimer’s disease.”

Why does beta amyloid’s 23rd amino acid sometimes form this dangerous kink?

Clarke thinks the kinks in this amino acid form throughout our lives, but we have a protein repair enzyme that fixes them.

“As we get older, maybe the repair enzyme misses the repair once or twice,” he said. “The repair enzyme might be 99.9% effective, but over 60 years or more, the kinks eventually build up. If not repaired or if degraded in time, the kink can spread to virtually every neuron and can do tremendous damage.”

“The good news is that knowing what the problem is, we can think about ways to solve it,” he added. “This kinked amino acid is where we want to look.”

The research offers clues to pharmaceutical companies, which could develop ways to prevent formation of the kink or get the repair enzyme to work better; or by designing a cap that would prevent fibrils from growing.

Clarke said beta amyloid and a much larger protein tau — with more than 750 amino acids — make a devastating one-two punch that forms fibrils and spreads them to many neurons throughout the brain. All humans have both beta amyloid and tau. Researchers say it appears that beta amyloid produces fibrils that can lead to tau aggregates, which can spread the toxicity to other brain cells. However, exactly how beta amyloid and tau work together to kill neurons is not yet known.

In this study, Warmack produced crystals, both the normal and kinked types, in 15 of beta amyloid’s amino acids. She used a modified type of cryo-electron microscopy to analyze the crystals. Cryo-electron microscopy, whose development won its creators the 2017 Nobel Prize in chemistry, enables scientists to see large biomolecules in extraordinary detail. Professor Tamir Gonen pioneered the modified microscopy, called microcrystal electron diffraction, which enables scientists to study biomolecules of any size.

Eisenberg is UCLA’s Paul D. Boyer Professor of Molecular Biology and a Howard Hughes Medical Institute investigator. Other researchers are co-author Gonen, a professor of biological chemistry and physiology at the UCLA David Geffen School of Medicine and a Howard Hughes Medical Institute investigator; and Jose Rodriguez, assistant professor of chemistry and biochemistry who holds the Howard Reiss Career Development Chair.

The research was funded by the National Science Foundation, National Institutes of Health, Howard Hughes Medical Institute, and the UCLA Longevity Center’s Elizabeth and Thomas Plott Chair in Gerontology, which Clarke held for five years.

This article originally appeared in the UCLA Newsroom.