Gilmartin Named Dean of Undergraduate Students

On July 1, 2016, Kevin Gilmartin, professor of English, will begin serving as Caltech's dean of undergraduate students.

In announcing Gilmartin's appointment, Joseph E. Shepherd, vice president for student affairs and the C. L. Kelly Johnson Professor of Aeronautics and Mechanical Engineering, described him as "an accomplished scholar and author who brings to this position twenty-five years of experience in teaching and mentoring our students, and who has shown a keen interest in the welfare of our undergraduate students in and outside of the classroom."

In his new role as dean of undergraduate students, Gilmartin will work on fostering academic and personal growth through counseling and support for student activities as well as acting as a liaison between students and faculty, says Shepherd.

A recipient the Feynman Prize, Caltech's highest teaching award, Gilmartin says he was attracted to the job of dean because "I have always found our students to be so interesting, and engaging. They are extraordinarily optimistic. They seem to have a positive attitude toward the world—they're curious, and they're open to new things. What more could you ask for?"

He says he sees his role as helping undergraduates develop and thrive. "I'm excited to work with students to help foster their intellectual and academic growth and their development as individuals," he says. "Our students are remarkably diverse and they have diverse interests. The Caltech curriculum is demanding, and focused, no doubt. But within it, and through it, our students do find so many opportunities."

He adds, "The dean's office provides essential support. But we can also encourage our students to do what they are inclined to do, to challenge themselves, to try new things."

Gilmartin received his undergraduate degree in English from Oberlin College in 1985. He received both his MS ('86) and PhD ('91) in English from the University of Chicago, joining the faculty of Caltech in 1991.

Barbara Green, who has served as the interim dean over the past year will return to her regular position as associate dean in July. In his announcement, Shepherd thanked Green "for her work with our students and service to the Institute [and for] being so willing and committed to the success of our undergraduate student body."

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On July 1, 2016, Kevin Gilmartin, professor of English, will begin serving as Caltech's dean of undergraduate students.

Oka Receives McKnight Award

Yuki Oka, assistant professor of biology, has been named one of six recipients of the 2016 McKnight Scholars Award. The McKnight Endowment Fund for Neuroscience awards $75,000 per year for three years to support young scientists who are establishing their own laboratories and research centers. The award is only available to researchers in the first four years of a tenure-track faculty position.

 

"A McKnight Scholar Award is one of the most prestigious early-career honors that a young neuroscientist can receive," said Anthony Movshon, chair of the awards committee and professor at New York University, in a press release. "This year's Scholars are a superbly talented group, with as much promise as any selected in the past. … Their work will help us to understand the brain's function in health and in disease, and will shape the neuroscience of the future."

 

Oka studies the neural mechanisms controlling thirst. These mechanisms help the body maintain a healthy balance of water and salt. He is attempting to isolate exactly which circuits in the brain regulate thirst and to determine how those circuits are triggered by external signals. Understanding these key brain functions may lead to new treatments for appetite-related disorders.

 

The McKnight Foundation of Minneapolis, Minnesota has supported neuroscience research since 1977. It created the Endowment Fund in 1986 in honor of William L. McKnight, an early leader of the 3M Company who had a personal interest in neurological diseases and wanted his legacy to help find cures. Previous awardees from Caltech include Athanossios Siapas, professor of computation and neural systems, and Kai Zinn, professor of biology.

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A Feeling Touch

Using funding from the BRAIN Initiative, Caltech biologists are developing neuroprosthetics to bring tactile sensations to the users of robotic arms.

Caltech biologist Richard Andersen is working to incorporate a sense of touch into the neural prosthetics he has been helping develop for years—devices implanted in the brain that allow a paralyzed patient to manipulate a robotic arm.

Andersen and colleagues first reported success of their original implant in early 2015. The team, led by Andersen, placed their prosthesis in the posterior parietal cortex, an area that controls the intent to move rather than controlling movement directly as previous experiments had done. This allowed Erik Sorto, a 35-year-old man who has been paralyzed from the neck down for more than 10 years, to use a robotic arm placed next to his body to perform a fluid hand-shaking gesture, play rock-paper-scissors, and even grasp a bottle of beer and bring it to his mouth for a sip—something he had long dreamed of doing.

This research on how to make a robotic arm move resulted in a 2015 National Science Foundation grant to Andersen from President Obama's Brain Research through Advancing Innovative Neurotechnology—or BRAIN—Initiative, as well as seed money from the California Blueprint for Research to Advance Innovations in Neuroscience (Cal-BRAIN) program, the California complement to the federal initiative, which gave out its first-ever monetary awards last year to a group of researchers that included Andersen.

Andersen is now using those Cal-BRAIN funds—designed to bring together interdisciplinary teams of scientists and engineers from diverse fields for fundamental brain research—to take his team's work to the next level. His hope is to enable people using robotic arms to literally regain their sense of touch—their ability to feel an object in their "hands."

For more on Andersen's work, read A Feeling Touch on E&S+

 

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Caltech biologists are developing neuroprosthetics to bring tactile sensations to the users of robotic arms.

DNA Origami: Folded DNA as a Building Material for Molecular Devices

Living things use DNA to store the genetic information that makes each plant, bacterium, and human being unique. The reproduction of this information is made possible because DNA's nucleotides—A's and T's, G's and C's—fit together perfectly, like matching jigsaw puzzle pieces. Engineers can take advantage of the matching between long strands of DNA nucleotides to use DNA as a kind of molecular origami, folding it into everything from nanoscale smiley face artwork to serious drug-delivery devices.

On Wednesday, May 25, at 8 p.m. in Beckman Auditorium, Paul Rothemund (BS '94), the inventor of the DNA origami technique, will explain how his group and groups around the world are using DNA origami in applications ranging from potential cancer treatments to devices for computing. Rothemund is research professor of bioengineering, computing and mathematical sciences, and computation and neural systems in the Division of Engineering and Applied Science at Caltech. Admission is free.

What do you do?

I use DNA and RNA as building materials to create shapes and patterns with a resolution of just a few nanometers. The smallest features in the DNA structures we make are about 20,000 times smaller than the pixels in the fanciest computer displays, which are each about 80 microns across. A large part of our work over the last 20 years has been just figuring out how to get DNA or RNA strands to fold themselves into a desired computer-designed shape. As we've mastered the ability to make whatever shape or pattern we desire, we've moved on to using these shapes as "pegboards" for arranging other nano-sized objects, such as protein enzymes, carbon-nanotube transistors, and fluorescent molecules.

Why is this important?

Every task in your body, from digesting food to moving your muscles to sensing light, is powered by tiny nanometer-scale biological machines, all built from the "bottom up" via the self-folding of molecules such as proteins and RNAs. The billions of transistors that make up the chips in our cell phones and computers are tens of nanometers in size, but they are built in a "top down" fashion using fancy printing processes in billion-dollar factories. Our goal is to learn how to build complex artificial devices the way biology builds natural ones—that is, starting from self-folding molecules that assemble together into larger more complex structures. In addition to vastly cheaper devices, this will enable completely new applications, such as man-made molecular machines that can make complex therapeutic decisions and apply drugs only where needed.

How did you get into this line of work?

As an undergraduate at Caltech, I had great difficulty trying to decide how to combine my diverse interests in computer science, chemistry, and biology. Fortunately, the late Jan L. A. van de Snepscheut introduced his computer science class to the hypothetical idea of building a DNA Turing machine—a very simple machine which can nevertheless run every possible computer program. He challenged us, suggesting that someone who knew about both biochemistry and computer science could come up with a concrete way to build such a DNA computer. For a project class in information theory with Yaser Abu-Mostafa, a professor of electrical engineering and computer science, I came up with a pretty inefficient, yet possible, way to do this. At the time, I couldn't interest any Caltech professors in building my DNA computer, but shortly after, USC professor Len Adleman published a paper on a more practical DNA computer in Science. I joined Adleman's lab at USC as a graduate student, and I've been trying to use DNA to build computers or other complex devices ever since. I returned to Caltech as a postdoc in 2001 and became a research professor in 2008.

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A preview of Paul Rothemund's upcoming Watson Lecture.

Seven from Caltech Elected to National Academy of Sciences

Three Caltech professors and four Caltech alumni have been elected to the prestigious National Academy of Sciences (NAS). The announcement was made Tuesday, May 3.

Raymond Deshaies is a professor of biology, investigator at the Howard Hughes Medical Institute, and executive officer for molecular biology. Deshaies's work focuses on understanding the basic biology of protein homeostasis, the mechanisms that maintain a normal array of functional proteins within cells and organisms. He is the founder of Caltech's Proteome Exploration Laboratory to study and sequence proteomes, which are all of the proteins encoded by a genome.

John Eiler is the Robert P. Sharp Professor of Geology and professor of geochemistry, as well as the director of the Caltech Microanalysis Center. Eiler uses geochemistry to study the origin and evolution of meteorites and the earth's rocks, atmosphere, and interior. Recently, his team published a paper detailing how dinosaurs' body temperatures can be deduced from isotopic measurements of their eggshells.

Ares Rosakis is the Theodore von Kármán Professor of Aeronautics and Mechanical Engineering in the Division of Engineering and Applied Science. His research interests span a wide spectrum of length and time scales and range from the mechanics of earthquake seismology, to the physical processes involved in the catastrophic failure of aerospace materials, to the reliability of micro-electronic and opto-electronic structures and devices.

Deshaies, Eiler, and Rosakis join 70 current Caltech faculty and three trustees as members of the NAS. Also included in this year's new members are four alumni: Ian Agol (BS '92), Melanie S. Sanford (PhD '01), Frederick J. Sigworth (BS '74), and Arthur B. McDonald (PhD '70).

The National Academy of Sciences is a private, nonprofit organization of scientists and engineers dedicated to the furtherance of science and its use for the general welfare. It was established in 1863 by a congressional act of incorporation signed by Abraham Lincoln that calls on the academy to act as an official adviser to the federal government, upon request, in any matter of science or technology.

A full list of new members is available on the academy website at: http://www.nasonline.org/news-and-multimedia/news/may-3-2016-NAS-Electio...

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Three faculty members and four alumni have been elected to the National Academy of Sciences.

When Beneficial Bacteria Knock But No One is Home

The community of beneficial bacteria that live in our intestines, known as the gut microbiome, are important for the development and function of the immune system. There has been growing evidence that certain probiotics—therapies that introduce beneficial bacteria into the gut—may help alleviate some of the symptoms of intestinal disorders such as Crohn's disease. By studying the interplay between genetic risk factors for Crohn's and the bacteria that populate the gut, researchers at Caltech have discovered a new potential cause for this disorder in some patients—information that may lead to advances in probiotic therapies and personalized medicine.

The results were published online in the May 5 edition of the journal Science.

Previously, scientists had found that patients with Crohn's disease often exhibit alterations in both their genome and their gut microbiome—the diverse collection of bacteria that reside in the intestine. More than 200 genes have been implicated as having a role in the susceptibility to Crohn's. For years, researchers in the field have believed that these are genes that normally function by sensing pathogenic bacteria and deploying an immune response to kill the unwanted microbes; when these genes are defective, the pathogenic bacteria survive, multiply in the gut, and lead to disease.

"While we believe that all of that is true, in this study we were curious to see if some of the genes that are important in sensing pathogenic bacteria may also be important in sensing beneficial bacteria to promote immune health," says the study's first author, Hiutung Chu, a postdoctoral scholar in biology and biological engineering at Caltech. "Typically, the signals from these beneficial commensal microbes promote anti-inflammatory responses that dampen inflammation in the gut. However, mutations in genes that sense and respond to pathogenic bacteria would also impair the response to the beneficial ones. So it's kind of a new spin on the existing dogma."

To figure this out, Chu and her colleagues in the laboratory of Sarkis Mazmanian, the Luis B. and Nelly Soux Professor of Microbiology, designed several experiments to study how genetic mutations might interrupt the immune-enhancing effects of a known beneficial bacterium, Bacteroides fragilis. The researchers tested their new theory by using B. fragilis to treat mice that had nonfunctional versions of two genes known to play a role in Crohn's disease risk, called ATG16L1 and NOD2.

The researchers found that if just one of these two genes was absent, the mice were unable to develop disease-protective immune cells called regulatory T cells in response to B. fragilis—and that even after treatment with B. fragilis, symptoms in an ATG16L1-deficient mouse model of intestinal disease remained unchanged.

Chu and Mazmanian then obtained blood samples from both healthy patients and patients with Crohn's disease at the Cedars-Sinai Medical Center in Los Angeles. "We could see that certain patients' immune cells responded to Bacteroides fragilis, while immune cells from other patients didn't respond at all," Chu says. "Because the cells from Cedars had already been genotyped, we were able to match up our results with the patients' genotypes: immune cells from individuals with the protective version of ATG16L1 responded to the treatment, but cells from patients who had the mutated version of the gene showed no anti-inflammatory response to B. fragilis."

Mazmanian says the results suggest that the faulty versions of these genes may cause Crohn's disease in two different ways: by being unable to assist in destroying pathogenic bacteria and by preventing the beneficial immune signals usually elicited by "good" bacteria. "What Hiutung has shown is that there are specific bacteria in the human microbiome that appear to utilize the pathways that are encoded by these genes—genes normally involved in killing bacteria—to send beneficial signals to the host," he says.

This work reveals the important relationship between the genome and the microbiome—and it may also one day be used to improve the use of probiotics in clinical trials, Mazmanian says. "For example, our previous work has suggested using B. fragilis as a probiotic treatment for certain disorders. What this new study suggests is that there are certain populations that wouldn't benefit from this treatment because they have this genetic predisposition," he notes. "Right now, clinical trials don't do a good job of identifying which patients might respond best to treatment, but our experiments in mouse models suggest that, conceptually, you could design clinical trials that are more effective."

The research described in the paper, "Gene-Microbiota Interactions Contribute to the Pathogenesis of Inflammatory Bowel Disease," was funded by the National Institutes of Health, the Cedars-Sinai F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, the Lupus Research Institute, the European Union, the Crohn's and Colitis Foundation of America, the Leona M. and Harry B. Helmsley Charitable Trust, and the Heritage Medical Research Institute.

In addition to Chu and Mazmanian, other Caltech coauthors include former graduate students Arya Khosravi (PhD '14) and Yue Shen (PhD '12); research technician assistants Indah Kusumawardhani and Alice Kwon; and Wei-Li Wu, a postdoctoral scholar in biology and biological engineering. Coauthors from other institutions include: Anilton Vasconcelos and Peter Ernst from UC San Diego; Larissa Cunha and Douglas Green from St. Jude Children's Research Hospital in Memphis; Anne Mayer, Amal Kambal, and Herbert Virgin from the Washington University School of Medicine in St. Louis; Stephan Targan and Dermot McGovern from Cedars-Sinai Medical Center; and Ramnik Xavier from Harvard Medical School.

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Wednesday, May 11, 2016
Noyes 147 (J. Holmes Sturdivant Lecture Hall) – Arthur Amos Noyes Laboratory of Chemical Physics

Administrative Contact Information Session

American Academy of Arts and Sciences Elects Two from Caltech

The American Academy of Arts and Sciences has elected two Caltech professors—Hirosi Ooguri and Rob Phillips—as fellows. The American Academy is one of the nation's oldest honorary societies; this class of members is its 236th, and it includes a total of 213 scholars and leaders representing such diverse fields as academia, business, public affairs, the humanities, and the arts.

Hirosi Ooguri is the director of the Walter Burke Institute for Theoretical Physics and the Fred Kavli Professor of Theoretical Physics and Mathematics in the Division of Physics, Mathematics and Astronomy. He works on quantum field theory and superstring theory, aiming to invent new theoretical tools to solve fundamental questions in physics.

Rob Phillips is the Fred and Nancy Morris Professor of Biophysics and Biology and has appointments in the Division of Engineering and Applied Science and the Division of Biology and Biological Engineering. He focuses on the physical biology of the cell using biophysical theory as well as single-molecule and single-cell experiments.

Ooguri and Phillips join 86 current Caltech faculty as members of the American Academy. Also included in this year's list are two Caltech trustees, David Lee (PhD '74) and Ron Linde (MS '62, PhD '64); as well as three additional alumni: Gerard Fuller (MS '77, PhD '80), Melanie Sanford (PhD '01), and Robert Schoelkopf (PhD '95).

Founded in 1780 by John Adams, James Bowdoin, John Hancock, and other scholar-patriots, the academy aims to serve the nation by cultivating "every art and science which may tend to advance the interest, honor, dignity, and happiness of a free, independent, and virtuous people." The academy has elected as fellows and foreign honorary members "leading thinkers and doers" from each generation, including George Washington and Ben Franklin in the 18th century, Daniel Webster and Ralph Waldo Emerson in the 19th, and Albert Einstein and Woodrow Wilson in the 20th. This year's class of fellows includes novelist Colm Tóibín, La Opinión publisher and CEO Monica Lozano, jazz saxophonist Wayne Shorter, former Botswanan president Festus Mogae, and autism author and spokesperson Temple Grandin.

A full list of new members is available on the academy website at www.amacad.org/members.

The new class will be inducted at a ceremony on October 8, 2016, in Cambridge, Massachusetts.

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Hirosi Ooguri and Rob Phillips have been elected as members of the American Academy of Arts and Sciences.

Mapping Neurons to Improve the Treatment of Parkinson's

Because billions of neurons are packed into our brain, the neuronal circuits that are responsible for controlling our behaviors are by necessity highly intermingled. This tangled web makes it complicated for scientists to determine exactly which circuits do what. Now, using two laboratory techniques pioneered in part at Caltech, Caltech researchers have mapped out the pathways of a set of neurons responsible for the kinds of motor impairments—such as difficulty walking—found in patients with Parkinson's disease.

The work—from the laboratory of Viviana Gradinaru (BS '05), assistant professor of biology and biological engineering—was published on April 20 in the journal Neuron.

In patients with Parkinson's disease, gait disorders and difficulty with balance are often caused by the degeneration of a specific type of neuron—called cholinergic neurons—in a region of the brainstem called the pedunculopontine nucleus (PPN). Damage to this same population of neurons in the PPN is also linked to reward-based behaviors and disorders, such as addiction.

Previously, researchers had not been able to untangle the neural circuitry originating in the PPN to understand how both addictions and Parkinson's motor impairments are modulated within the same population of cells. Furthermore, this uncertainty created a barrier to treating those motor symptoms. After all, deep brain stimulation—in which a device is inserted into the brain to deliver electrical pulses to a targeted region—can be used to correct walking and balance difficulties in these patients, but without knowing exactly which part of the PPN to target, the procedure can lead to mixed results.

"The circuits responsible for controlling our behaviors are not nicely lined up, where this side does locomotion and this side does reward," Gradinaru says, and this disordered arrangement arises from the way neurons are structured. Much as a tree extends into the ground with long roots, neurons are made up of a cell body and a long string-like axon that can diverge and project elsewhere into different areas of the brain. Because of this shape, the researchers realized they could follow the neuron's "roots" to an area of the brain less crowded than the PPN. This would allow them to more easily look at the two very different behaviors and how they are implemented.

Cheng Xiao, a senior research scientist at Caltech and first author on the study, began by mapping the projections of the cholinergic neurons in the PPN of a rat using a technique developed by the Gradinaru lab called Passive CLARITY Technique, or PACT. In this technique, a solution of chemicals is applied to the brain; the chemicals dissolve the lipids in the tissue and render that region of the brain optically transparent—see-through, in other words—and able to take up fluorescent markers that can label different types of neurons. The researchers could then follow the path of the PPN neurons of interest, marked by a fluorescent protein, by simply looking through the rest of the brain.

Using this method, Gradinaru and Xiao were able to trace the axons of the PPN neurons as they extended into two regions of the midbrain: the ventral substantia nigra, a landmark area for Parkinson's disease that had been previously associated with locomotion; and the ventral tegmental area, a region of the brain that had been previously associated with reward.

Next, the researchers used an electrical recording technique to keep track of the signals sent by PPN neurons—confirming that these neurons do, in fact, communicate with their associated downstream structures in the midbrain. Then, the scientists went on to determine how this specific population of neurons affects behavior. To do this, they used a technique that Gradinaru helped develop called optogenetics, which allows researchers to manipulate neural activities—in this case, by either exciting or inhibiting the PPN neural projections in the midbrain—using different colors of light.

Using the optogenetic approach in rats, the researchers found that exciting the neuronal projections in the ventral substantia nigra would stimulate the animal to walk around its environment; by contrast, they could stop the animal's movement by inhibiting these same projections. Furthermore, they found that they could stimulate reward-seeking behavior by exciting the neuronal projections in the ventral tegmental area, but could cause aversive behavior by inhibiting these projections.

"Our results show that the cholinergic neurons from the PPN indeed have a role in controlling both behaviors," Gradinaru says. "Although the neurons are very densely packed and intermingled, these pathways are, to some extent, dedicated to very specialized behaviors." Determining which pathways are associated with which behaviors might also improve future treatments, she adds.

"In the past it's been difficult to target treatment to the PPN because the specific neurons associated with different behaviors are intermingled at the source—the PPN. Our results show that you could target the axonal projections in the substantia nigra for movement disorders and projections in the ventral tegmental area for reward disorders, as addiction is," Gradinaru says. In addition, she notes, these projections in the midbrain are much easier to access surgically than their source in the PPN.

Although this new information could inform clinical treatments for Parkinson's disease, the PPN is only one region of the brain and there are many more important examples of connectivity that need to be explored, Gradinaru says. "These results highlight the need for brain-wide functional and anatomical maps of these long-range neuronal projections; we've shown that tissue clearing and optogenetics are enabling technologies in the creation of these maps."

These results are published in a paper titled, "Cholinergic mesopontine signals govern locomotion and reward through dissociable midbrain pathways." In addition to Gradinaru and Xiao, other Caltech coauthors include Jounhong Ryan Cho, Chunyi Zhou, Jennifer Treweek, Ken Chan, Sheri McKinney, and Bin Yang. The work was supported by the National Institutes of Health, the Heritage Medical Research Institute, the Pew Charitable Trust, the Michael J. Fox Foundation, and the Sloan Foundation; the Beckman Institute supports the Resource Center on CLARITY, Optogenetics, and Vector Engineering (CLOVER) for technology development and broad dissemination.

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Mapping Neurons to Improve Parkinson's
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Caltech researchers have mapped out a circuit of neurons responsible for motor impairment in patients with Parkinson's disease.

Midnight Blue: A New System for Color Vision

The swirling skies of Vincent Van Gogh's Starry Night illustrate a mystery that has eluded biologists for more than a century—why do we perceive the color blue in the dimly lit night sky? A newly discovered mechanism of color vision in mice might help answer this question, Caltech researchers say.

The work, which was done in the laboratory of Markus Meister, Anne P. and Benjamin F. Biaggini Professor of Biological Sciences, will be published on April 14 in the print edition of the journal Nature.

In humans, vision is enabled by two types of light-sensitive photoreceptor cells called rods and cones. When these photoreceptors detect light, they send a signal to specialized neurons in the retina called retinal ganglion cells, or RGCs, which then transmit visual information to the brain by firing electrical pulses along the optic nerve.

A standard biology textbook would likely explain that vision in dim light is enabled by rods—sensitive light detectors that are only capable of producing black and white vision. Color vision, on the other hand, is enabled by cones, which are active in bright light. Humans have three types of cones, and each cone contains a different light-sensitive chemical, or pigment, that reacts to different colors, or wavelengths, of light. We have red-, green-, and blue-sensitive cones, and the brain perceives color by comparing the different signals it receives from nearby cones of each type.

To explore whether or not there were other modes of color vision, Meister and his team studied another mammal: the mouse. Previous behavioral studies indicated that mice are indeed capable of some form of color vision. As in humans, that vision is dependent on light signals picked up by cones. Mice have two types of cones—one that is sensitive to medium-wavelength green light and one that is sensitive to short-wavelength ultraviolet light (UV).

"The odd thing about the mouse is that these two kinds of cones are actually located in different parts of the retina," Meister says. "Mice look at the upper part of the visual field with their UV cones and the lower part with their green cones. We wanted to know how a mouse perceives color when any given part of the image is analyzed with only one cone or the other cone—meaning the brain can't compare the two cone signals to determine a color."

The researchers discovered that a certain type of neuron in the mouse retina, called a JAMB retinal ganglion cell (J-RGC), was critical. These J-RGCs can signal color to the brain because they fire faster in response to green light and stop firing in response to ultraviolet light. Curiously, the J-RGCs were turned on by green light even in the upper part of the visual field, which contained no green cones.

Through additional experiments, Meister and his team discovered how the J-RGC compares signals from the ultraviolet cones to signals from rods, which are also sensitive in the green part of the spectrum. This revealed, for the first time, an essential antagonistic relationship between the rods and the cones of the retina. Rods excite a neuron called a horizontal cell, which then inhibits the ultraviolet cones.

Meister and his colleague, first author Maximilian Joesch from Harvard University, wanted to determine how this color vision system would be helpful to a mouse in its natural environment. To find out, they fitted a camera with filters that would replicate the wavelengths detected by the mouse rods and cones and used it to take images of plants and materials that a mouse might encounter in nature.

Their photographic scavenger hunt yielded two materials—seeds and mouse urine—that were much more visible through the mouse's green and ultraviolet system than through human color vision. The researchers speculate that because mice need seeds for sustenance and use urine for social communication—via "urine posts," a form of territorial marking—they might use this mechanism to find food and spot neighbors.

Meister says there is reason to believe that this same pathway—from rods to horizontal cells to cones—is responsible for the human perception of the color blue in dim light. In the human retina, the horizontal cell preferentially inhibits the red and green cones, but not the blue cones.

"In really dim light, our cones don't receive enough photons to work, but they continue to emit a low-level baseline signal to the rest of the retina that is independent of light," he explains. "The rods are active, however, and through the horizontal cell they inhibit both the red and green cones. Because this baseline signal from the red and green cones is suppressed, it looks like the blue cones are more active. To the rest of the retina, it seems like everything in the field of vision is blue."  

So, perhaps Van Gogh's color choice for the night sky was a biological decision as well as an artistic one. "Color has intrigued scientists, artists, and poets throughout human civilization. Our paper adds to the understanding of how this quality of the world is perceived," Meister says.

Meister's work was published in a paper titled "A neuronal circuit for color vision based on rod-cone opponency." Funding for the work was provided by the National Institutes of Health and The International Human Frontier Science Program Organization.

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A newly discovered mechanism of color vision in mice might help answer why the dimly lit night sky has a bluish cast.

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