From neutrinos to fly vision to follicle regeneration, university researchers talked about a wide array of research at the Yale Science and Engineering Forum on May 3.

The Yale Quantum Institute hosted the event, which has taken place annually since 1995. Professor A. Douglas Stone, who has been one of the principal organizers of the event since it began, said the intent is to give Yale faculty members a chance to see what their colleagues have been working on.

Over the years, many people who have spoken at this have gone on to become leaders in their field, and various collaborations have come out of it, said Stone, the Carl A. Morse Professor of Applied Physics and professor of physics, who serves as director of Yales Division of Physical Sciences.

Although the presentations are aimed at scientists, theyre also designed to be accessible to researchers from all disciplines. That means Stone will occasionally break into a presenters talk to ask that a particularly jargon-laden sentence be rephrased. Others in the audience are also encouraged to speak up if they lose the thread of the discussion.

The event was broken into three sessions quantitative biology and biophysics, physics of the visible and invisible, and regenerative biology and featured a diverse roster of speakers:

Damon Clark, assistant professor of molecular, cellular, and developmental biology, discussed how flies sense motion a process that involves putting the insects on tiny spherical treadmills and how they ably elude the swatter despite having relatively low-resolution vision.

Jonathon Howard, the Eugene Higgins Professor of Molecular Biophysics and Biochemistry and professor of physics, discussed a family of motor proteins known as kinesin and how they travel along microtubules.

Peter Rakich, assistant professor of applied physics, discussed how the power of sound can be used to amplify light waves on a silicon microchip and the new applications this could lead to (navigational sensors, and low-noise lasers, for instance).

Karsten Heeger, professor of physics and director of the Wright Laboratory, presented his research on neutrinos, dark matter, and other mysteries of the universe.

Josien van Wolfswinkel, assistant professor of molecular cellular and developmental biology, discussed a group of flatworms known as planaria that have the capability to regenerate any missing body region.

Valerie Horsley, the Maxine F. Singer '57 Associate Professor of Molecular, Cellular, and Developmental Biology and associate professor of dermatology, discussed adipocytes cells that store energy as fat and their role in the regrowth of hair follicles and the healing of skin wounds.

We try to get to a good mix that would appeal to a wide range of scientists, said one of the events organizers, Thomas Pollard, Sterling Professor of Molecular, Cellular, and Developmental Biology, and professor of cell biology and of molecular biophysics and biochemistry. Its just a chance for the science community at Yale to enjoy the excitement of their colleagues work. Were all so busy during the rest of the year that we dont get much of a chance to hear our colleagues speak.

The event does more than just satisfy scientific curiosity; its been known to kick start cross-disciplinary collaborations. Audience member Richard Prum, the William Robertson Coe Professor of Ornithology of Ecology and Evolutionary Biology, recalled his talk at the event in 2005 on his research into the optics of bird feathers.

We had made some very important general progress, but we were still far from an analytical solution, he said. Attendee Eric Dufresne, then a professor in Yales chemical engineering department, suggested that one of Prums images looked like a spinodal decomposition and was perhaps part of a phase separation process.

I said, Ive got no idea what youre talking about, but lets have lunch. They did, and it turned out Dufresnes intuition was correct. More than 12 years later, the collaboration continues, and has brought in more faculty members from engineering and physics. Its an example of why events such as Wednesdays forum are so important, Prum said.

Its hard to get scientists out of their own labs, he said, so this is absolutely necessary to bring people out of their silos.

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Researchers catch up on each other's work at forum - Yale News

Cell death, caused due to lack of glucose in which cells die in an unexpected manner, follows a process similar to what we would expect from an immune response, a new study found.

Are you one of those who starve yourselves for losing weight? You might want to think that again. According to a new study, researchers have characterized the cell death process due to starvation, in which the endoplasmic reticulum plays a leading role.

The study got published in journal Molecular and Cellular Biology.

Usually, programmed cell death -- also called apoptosis -- follows a biochemical pathway related to the permeabilization of mitochondria; However, we observed that in cases of cell death due to lack of glucose, cells die in an unexpected way, following a process similar to what we would expect from an immune response, stated Dr. Cristina Muoz-Pinedo, studys lead author.

The study finds that in cell-death-related treatments such as chemotherapy, the mitochondrial pathway is activated. Instead, when starved, cells activate the so-called death receptors on their membrane, which are normally used by the lymphocytes of the immune system to attack and destroy infected cells.

Starving yourself to losing weight may not be the bet options, the study found.

The researchers have been able to relate the activation of these membrane receptors to the endoplasmic reticulum, a cellular organelle involved in protein synthesis and lipid metabolism, as well as intracellular transport.

Feeling the stress produced by the lack of nutrients, the reticulum send an alarm signal that triggers the appearance of death receptors in the membrane, said Dr Muoz-Pinedo.

According to our in vitro results, we assume that this is how the tumour cells located in the centre of a tumour -- the so-called necrotic core -- die, because there are never enough nutrients in those areas. On the other hand, in ischemia, besides the lack of oxygen there is also cell death due to lack of glucose, so this process could also be related to the activity of the endoplasmic reticulum at a biochemical level, added the IDIBELL researcher.

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Starvation leads to 'cell death' which isn't good for the body - Hindustan Times

Professor Jodi Nunnari, chair of the department of molecular and cellular biology in the College of Biological Sciences at UC Davis, has been elected as a member of the National Academy of Sciences.

Nunnari studies mitochondria, tiny structures that provide energy to living cells and that are implicated in a wide range of diseases, including heart disease, stroke and inherited conditions.

Jodi Nunnari. Courtesy photo

Beginning as a postdoctoral researcher, Jodi has made discoveries that have transformed her field and helped demystify the genesis of a broad range of diseases, said Ralph Hexter, interim chancellor of UCD.

Her pioneering work is a prime example of our universitys commitment to fundamental research to improve the human condition. I could not be happier to see her receive this much-deserved recognition.

Nunnaris lab studies the behavior of mitochondria which have their own DNA, separate from the cell nucleus inside cells. Her work looks at the mechanisms through which mitochondria divide and fuse together, and at how mitochondrial DNA is organized and transmitted.

Nunnari is among 84 new members and 21 foreign associates elected to the academy this year. She is one of 27 current or retired UCD faculty who are members or foreign associates of the academy.

Election to the National Academies of Sciences is among the highest honors a scientist can receive in recognition of their distinguished scholarly contributions, said Mark Winey, dean of the College of Biological Sciences.

Jodis election is very well deserved for her groundbreaking work on mitochondria. As powerhouses of the cell, mitochondrial failure is linked to a variety of inherited diseases, as well as neurological disorders and aging.

Nunnari earned her bachelors degree from the College of Wooster in Ohio and her doctorate, in pharmacology, from Vanderbilt University. She carried out her postdoctoral research in the laboratory of Peter Walter at UC San Francisco, where she discovered that mitochondria form a dynamic network with the cell. This concept has led her to fundamental insights into how mitochondria grow, divide and function.

The National Academy of Sciences is a private, nonprofit institution that was established under a congressional charter signed by President Abraham Lincoln in 1863. Together with the National Academy of Engineering and the National Academy of Medicine, it provides advice on science, engineering, and health policy to the federal government and other organizations.

UC Davis News

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UCD's Jodi Nunnari elected to National Academy of Sciences - Davis Enterprise

May 4, 2017

10x Genomics, a company focused on enabling the mastery of biology by accelerating genomic discovery, today announced publication of an article in the journal Nature of a collaborative research study with researchers at the Stanford University School of Medicine. The article entitled, "Non-equivalence of Wnt and R-spondin ligands during Lgr5+ intestinal stem-cell self-renewal," utilizes the 10x Genomics' Single Cell 3' Solution for single-cell RNA-seq (scRNA-seq) to unravel the priming and self-renewal mechanisms of intestinal stem cells (ISCs).

The renewal and differentiation of Lgr5+ ISCs is critical to the continuous regeneration of the epithelial lining of the gut, which enables us to absorb nutrients and provides a barrier to protect us from the external environment. Disruptions in this process can lead to or worsen human intestinal disorders such as inflammatory bowel disease (IBD), gastrointestinal cancer and Celiac disease.

This carefully regulated process occurs within a stem-cell niche called the intestinal crypt, and depends on Wnt signaling, which can be turned up by Wnt and R-spondin (RSPO) ligands. The authors sought to identify the unique functional roles of Wnt and RSPO ligands for regulating Lgr5+ ISCs and the relative contributions of both ligands to in vivo Wnt signaling and stem-cell biology.

The authors were able to show using in vivo experiments that Wnt and RSPO are not redundant signals. RSPO was shown to expand stem cell number. Although Wnt was needed to maintain Lgr5+ ISCs in the presence of RSPO, Wnt was not sufficient to induce additional numbers of Lgr5+ ISCs above a certain threshold, demonstrating that RSPO, and not Wnt, establishes the set point for Lgr5+ ISC number. The authors performed single-cell RNA-seq to definitively show that the signaling contributions of Wnt and RSPO elicited distinct effects on ISCs, by fully characterizing the expression profile for each unique cellular subtype on a cell-by-cell basis upon perturbation of those signals in vivo.

By characterizing gene expression from 13,102 single cells, Yan and colleagues were able to show that Lgr5- control cells represented differentiated cell types of the small intestinal lineages, including Paneth, goblet, enteroendocrine, enterocyte, pre-enterocyte, and tuft cells. The Lgr5+ cells consisted of three cellular sub-populations, corresponding to cycling stem cells, non-cycling stem cells, and transit amplifying cells. The authors were able to further show that these three distinct sub-populations of Lgr5+ cells were each uniquely affected by perturbations in Wnt and RSPO signaling, conclusively demonstrating that Wnts are priming factors that enable stem cells to be competent by expressing RSPO receptors on their cell surface, whereas RSPOs are actual self-renewal factors that expand stem cell number.

"Single-cell analysis provided conclusive evidence for the unique roles of Wnt and RSPO signaling to their respective function, either co-operatively priming Lgr5+ cells for competency, or for RSPO-mediated self-renewal," said Grace Zheng, Ph.D., research scientist at 10x Genomics. "This powerfully illustrates the utility of single-cell RNA-seq to monitor discrete stem-cell states and their dynamic perturbation. To do this with any other technology would have been extremely cumbersome, if not impossible."

"We are very excited about this result, and it opens up the possibility that analogous multi-tiered regulation by priming and self-renewal factors may be a generalized property of stem cells across other organ systems, either through Wnt and RSPO or functionally equivalent stem-cell niche components," said Ben Hindson, Ph.D., president, co-founder, and chief scientific officer of 10x Genomics. "This could have wide-reaching implications for stem-cell research and potentially yield new insight towards therapeutic applications in the future."

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New study uses 10x Genomics' Single Cell 3' Solution to unravel stem cell self-renewal mechanism - News-Medical.net