John Lisman (1944-2017)

Chair of Biology Piali Sengupta wrote:

It is with great sadness that I am writing to let you know that John Lisman passed away last night. He passed away peacefully surrounded by his family. John was an influential and creative scientist and a very good friend to all of us in Biology and Neuroscience. We are glad that we had the opportunity to honor him and hear from him at the Volen Retreat last week. He will be much missed.

John’s talk at the Volen Retreat earlier this month, delivered by video conference, is available here: The critical role of CaMKII in memory storage: 6 key physiological and behavioral tests

The family has asked that in lieu of flowers people consider contributing to the John Lisman Memorial Scholarship

Update: The Memorial Service, taking place at 2 p.m. Thu Oct 26, will be live streamed. Brandeis community members can watch the live streaming in real time in Gerstenzang 121 as well as the Shapiro Science Center level 1 library. There will be a reception at the Brandeis Faculty Club at 3:30 open to the community.

We also wanted to share some tweets from past students and colleagues:

We also received this longer tribute from Michael Kahana:

I was greatly saddened to hear the news that John Lisman passed away this weekend. I spoke with him just a few weeks ago and was greatly looking forward to his upcoming visit to Penn. Although he told me of his illness, I was hoping to have a little more time with my good colleague and friend. Upon learning of his passing, I wanted to write down a few memories to share with friends and colleagues who knew John well.

I vividly recall when I first met John, at an evening gathering at his home that I attended just prior to joining the faculty at Brandeis (this may have been a precursor to the famous Boston Hippocampus meetings that John helped organize). The meeting was teaming with energy, and John welcomed me warmly, introducing me to other scientists in the room. John had recently become very interested in human memory, and as a newly minted PhD working on memory, John took me under his wings, teaching me about neurophysiology and quizzing me enthusiastically about the psychology of memory, a field that John was keen to master as quickly as possible.

John was a polymath, bursting with creative energy, and capable of seeing connections between diverse fields. Over the subsequent decade at Brandeis, John had an enormous influence on my career and research direction, introducing me to theta and gamma rhythms, and teaching me about countless topics in neurophysiology. On a typical day in the Volen Center, John would rush into my lab eager to share a new discovery or ask me a question about a study of memory that he had just learned about. He had this incredibly-infectious scientific curiosity, and he was always abundantly generous with his time, both with me and my students.

I particularly remember the early days when John was developing the LIJ (Lisman-Idiart-Jensen) model, and trying to learn as much as he could about the Sternberg task and other related phenomena in the field of human memory. Although I frequently challenged John on this front, he kept at it, continuing to refine the model together with Ole Jensen until they were able to answer many of the most serious objections. I just saw that the original paper was cited more than 1,200 times, and several of the follow up papers are well into the many hundreds of citations. This is arguably the most creative neurophysiological model of a cognitive function, and the best example of an attempt to link detailed physiological measurements to behavioral measures of human memory.

We have all lost a great friend, colleague, and mentor, and the field of neuroscience has lost one of its shining stars. I want to share my deepest sympathies with all of you who knew and loved John.

May his family be comforted among the mourners of Zion and Jerusalem.
Mike Kahana

Thomas Reese shared his thoughts:

John, your intellect and spirit lighted more than 30 summers my life at the MBL in Woods Hole.  You were a reference point for neurobiology there, holding court at your favorite table at the Kidd, at the far end of the dock.  A cherished invitation to lunch at exactly 12:00, with interesting synapse people passing though, or to hear a deluge of you new ideas about how a synapse is, or should be, put together.  Occasionally an invitation to dinner outside, behind your house with talk of many things…..joined by the delightful Natashia and other interesting people….discussing well into the night.

If Woods Hole is a little scientific Athens, you were our Socrates, lurking on Milfield. questioning in your disarming, open open way…bringing out the truth.  You were our Dogenes. searching Gardner Road for a man with the honest truth.

John, ,…John..it will seem empty there without you…you
will be very much missed..Tom Reese.     NIH

Rodal lab find surprising new link between inflammation and Lowe Syndrome

Could a disease with symptoms in the brain, eyes, and kidneys actually be caused by problems with immune cells? A team of scientists from the Rodal Lab, co-first authored by Steven Del Signore and Sarah Biber and including three Brandeis undergraduates (Katy Lehmann ‘16, Stephanie Heimler ‘17, and Ben Rosenfeld ’18), think this just might be the case with Lowe Syndrome, in a new paper published Oct 13th in PLOS Genetics.

Patients with Lowe Syndrome suffer from kidney failure, congenital cataracts, and several neurological problems including intellectual disability and seizures. Scientists have known for some time that the disease is caused by mutations in a gene called OCRL, but remain unsure how its loss causes such a diverse array of symptoms. A big problem has been that OCRL appears to do many different jobs inside cells, including controlling how they divide, how they sense their surroundings, and how they store and transport materials inside small packages called endosomes.

Fly immune cells showing the tracks of moving endosomes. Single tracks represent the path of individual endosomes over time.

To try to solve this mystery, a team of researchers from the Rodal lab used the fruit fly, which has its own version of the OCRL gene and allowed the investigators to perform powerful genetic experiments to figure out precisely what OCRL is doing, and where. To do this, the group created a fly missing its OCRL gene. They were surprised to find that, rather than eye or neurological defects, loss of OCRL hyper-activated cells of the innate immune system. The innate immune system is the first line of defense against infection in humans (and the only defense in fruit flies), when cells release inflammatory signals that mobilize specialized cells to attack invading pathogens.

The team determined that OCRL is required in one of these specialized immune cells in the fly, and that the immune-cell activation was caused by problems in a particular step of intracellular transport. Every cell of the body has its own postal service, which is used to pack and ship signals that tell the cell or its neighbors to grow, divide, or jump into action (see movie here to watch endosomes moving inside living fly immune cells). The OCRL mutant immune cells had a problem in a key step that controls whether signals get thrown in the trash or shipped outside the cell, and this caused the immune activation.

How do these findings relate to Lowe Syndrome? The authors think these results suggest a possible cause for the seizures that patients experience. When similar immune-like cells in the brain release excessive inflammatory signals, it can cause several forms of epilepsy. Further, OCRL has been linked to at least one mouse model of epilepsy. Going forward, the researchers will try to identify which immune signals are responsible, and how these findings translate to human cells.

Del Signore SJ (*), Biber SA (*), Lehmann KS, Heimler SR, Rosenfeld BH, Eskin TL, Sweeney ST, Rodal AA. dOCRL maintains immune cell quiescence by regulating endosomal traffic. Plos Genet. 2017;13(10):e1007052.

 

 

Rosbash, Hall & Young Awarded Nobel Prize

Michael Rosbash, Nobel Laureate

Brandeis researchers Michael Rosbash, the Peter Gruber Endowed Chair in Neuroscience, and Professor Emeritus of Biology Jeffrey C. Hall have received this year’s Nobel Prize in Physiology or Medicine, together with Michael Young from The Rockefeller University,  for their pioneering work on the molecular mechanisms controlling circadian rhythm.

More about Michael

More about Jeff

More about Drosophila

 

Sebastian Kadener Returns to Brandeis as Associate Professor

Sebastian Kadener

From 2002 to 2008, Sebastian Kadener was a postdoc working in the Michael Rosbash laboratory. He is returning to Brandeis as an Associate Professor of Biology. Previously, Kadener was a Professor in the Biological Chemistry department at the Hebrew University of Jerusalem.

The Kadener laboratory studies how molecular processes in the brain determines behavior with a special emphasis on RNA metabolism. Additionally, they study the role of circular RNAs (circRNAs) at the molecular and neural levels as well as the mechanisms underlying circadian clocks.

Kadener’s paper, “Translation of CircRNAs”, appeared in Molecular Cell in April 2017. It was reviewed in Nature Reviews Genetics and Science Daily.

Judith Tsipis Steps Down as Director of Genetic Counseling Program

Tsipis dinner

After 25 years at the helm of the Brandeis Genetic Counseling program, Judith Tsipis has handed over the leadership reins to Gretchen Schneider.

On June 3rd, close to 100 people gathered in the Levin Ballroom at Brandeis to honor and celebrate Judith’s illustrious career as a pioneer in the field of training genetic counselors. Attendees included over 40 alumni, former and present faculty members, family and close friends.

Highlights and memories were shared by: Beth Rosen-Sheidley, an alum from the first graduating class in 1994; Kathryn Spitzer Kim, the first Assistant Director from the Program; Gretchen Schneider; Judith’s son Yanni and husband, Kosta; and two additional alumni, Christa Haun and Jason Carmichael.

Judith created the master’s program in response to her own family’s experience with Canavan disease, a recessive degenerative disorder that causes progressive damage to nerve cells in the brain. Brandeis admitted its first class in 1992 and is proud to have over 200 alumni.

Judith will continue to be involved with the program in various capacities: coordinating journal club, serving as a thesis advisor and member of the Advisory Board.

 

 

 

Amy Lee Named 2017 Searle Scholar

Figure from Amy Lee

Assistant Professor of Biology Amy Si-Ying Lee was named a 2017 Searle Scholar, receiving $300,000 in flexible funding to support her work over the next three years. Lee’s research is focused on discovering how gene regulation occurs through novel mechanisms of mRNA translation. Specifically, her lab studies how non-canonical translation pathways shape cell growth and differentiation, and why defects in mRNA translation lead to developmental disorders and cancer.

Lee, who came to Brandeis in Summer 2016, has a PhD form Harvard and did her postdoc at UC Berkeley. She has also been awarded a 2017 Sloan Research Fellowship and in January won the Charles H. Hood Foundation Child Health Research Award. Lee’s lab is up and running and recruiting postdocs and PhD students (through the Molecular & Cell Biology and Biochemistry & Biophysics graduate programs). In Fall 2017, Lee will teach BIOL 105, Molecular Biology.

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