Andrea Guerrero and Gina Turrigiano Receive 2020 Gilliam Fellowship

Gina Turrigiano & Andrea Guerrero

Andrea Guerrero (left) and Gina Turrigiano (right)

Andrea Guerrero, a Neuroscience PhD student working in the Turrigiano lab, a 2020 Gilliam Fellowships for Advanced Study recipient. The Gilliam Fellowship is awarded to the student and dissertation adviser, therefore Gina Turrigiano will also participate in this fellowship. Turrigiano said, “I am really pleased that Andrea was awarded this fellowship, which recognizes her potential to become a scientific leader.  I am also really excited at the opportunity to improve my mentoring skills that this terrific program provides to me as her PhD advisor.”

The purpose of the Gilliam Fellowship is to increase diversity among scientists who are preparing for leadership roles, particularly as college and university faculty members.  Fellows receive up to three years of support for dissertation research, typically in years three, four, and five of their PhD study. The Gilliam Fellowship is part of HHMI.

In response to receiving the award Guerrero said, “I am honored and excited to be selected as a 2020 HHMI Gilliam Fellowship recipient as it will aid my own advancement in an academic-track career and will importantly promote diversity and inclusion within the Brandeis science community.”

Andrea describes her research as follows:

“The human Shank3 gene is strongly associated with Autism Spectrum Disorder (ASD). Shank3 protein functions as a scaffold that plays a crucial role in synapse formation and maintenance. Prior work in our lab supports the idea that differential Shank3 phosphorylation alters its activity. Phosphomimetic and phosphodeficient mutants show dysfunction in the mechanisms that normally maintain brain circuitry homeostasis. In order to understand how Shank3 is able to do this, I will investigate how the phosphorylation state of Shank3 changes its synaptic localization, protein binding interactions, and cellular signaling pathways in vitro. Additionally, I will assess the effects of overexpression of Shank3 phosphorylation mutants on synaptic plasticity within the rodent primary visual cortex. My research project has the potential to uncover novel cellular pathways that can be targeted for ASD therapeutic development.”

 

 

Applied Mathematics and AI meet Law and Social Justice

Jonathan Touboul

For the past two years, Applied Mathematics Professor Jonathan Touboul and his team has been working in collaboration with Law Professor Samuel Dahan at Queen’s University (Canada) in modeling legal decisions and predicting court decisions on Canadian labor law. Their academic work covers the determination of a worker’s status or the calculation of a severance package (paper appearing in a forthcoming issue of the McGill Law Journal). With the COVID-19 crisis and nearly 2 million Canadian jobs lost in 2 months, Touboul, Dahan, Prof. Maxime Cohen (McGill) and their colleagues realized that their research could be applied to assist more people, and serve to help democratize legal services, particularly towards those who lack proper access to law and legal information.

Joining their efforts with a team of law and computer science students at Queen’s University, Jonathan Touboul and his team provided modeling and data science expertise to develop predictive algorithms that helped launch MyOpenCourt.org. This is a free AI powered platform that offers easy access to their research and algorithms to provide personalized predictions, explanations, list of most similar situations from the case law, and offers the option to connect the user with a network of pro-bono lawyers for a free consultation.

Learn more:

• “Championing AI for social justice”, Queens University
• “Conflict Analytics Lab launches app for workers laid off during the pandemic”, McGill University

Susan Lovett elected to the American Academy of Arts and Sciences

Susan LovettSusan Lovett, the Abraham S. and Gertrude Burg Professor of Microbiology, has been elected to the American Academy of Arts and Sciences. She was among the 276 outstanding individuals that were elected to the Academy in 2020 and announced on April 23. Brandeis University Professor, Anita Hill, joins Professor Lovett as a 2020 member of AAAS.

The Lovett lab studies the fundamental mechanisms by which cells preserve genetic information by the study of DNA damage repair and mutation avoidance in the model organism Escherichia coli. Additionally, they research how cell cycle events including DNA replication and chromosome segregation are coupled to cellular physiology and to the status of the chromosome.

Lovett joins other Brandeis science faculty members: Jeff Gelles, Gina Turrigiano, James Haber, Michael Rosbash, Eve Marder, David Derosier, Gregory Petsko, Stanley Deser, and Edgar Brown, Jr.

Founded in 1780, the Academy recognizes the outstanding achievements of individuals in academia, the arts, business, government, and public affairs.

Read more: BrandeisNow

DNA molecules tell nanoparticles how to self-assemble

Nature uses self-assembly to make a diversity of complex structures, such as biomolecules, virus shells, and cytoskeletal filaments. Today a key challenge is to translate this assembly process to artificial systems. DNA-coated nanoparticles provide a particularly promising approach to realizing this vision, since the base sequences can be designed to encode the formation of a chosen structure.

A recent publication from the Rogers Lab shows that interactions between DNA-coated particles can be encoded using DNA oligomers dispersed in solution that bind the particles together.  By changing the linker sequences in solution, Ph.D. students Janna Lowensohn and Alex Hensley showed that the same set of components can be directed to form a variety of different crystal structures. Going forward, this approach may be used to create programmable materials that can sense and respond to their environment.

 

DNA instructions

Paper: Self-Assembly and Crystallization of DNA-Coated Colloids via Linker-Encoded Interactions. Lowensohn J, Hensley A, Perlow-Zelman M, Rogers WB. Langmuir. 2020 Feb 18. doi: 10.1021/acs.langmuir.9b03391. (PubMed abstract)

Shinji Rho named 2020 Goldwater Scholar

Shinji Rho, Brandeis UndergraduateCongratulations to Shinji Rho who has been named a 2020 Goldwater Scholar.  The Goldwater Scholarship is a national scholarship designed to encourage outstanding students in their sophomore and junior year to pursue research careers in the fields of mathematics, the natural sciences, and engineering.

Shinji is currently a junior. Her project at Brandeis is on a transcriptional activator Gal4, which binds to upstream activating sequence (UAS) sites in the yeast genome to promote transcription. Previous studies have shown that dwell time of Gal4 on the UAS is significantly longer in purified systems than in cells. She is interested in finding the reason for this dwell time difference using single-molecule light microscopy. The findings of her project will provide a more realistic view of how transcription activation system behaves when nuclear proteins are present. 

Shinji plans to obtain a PhD degree in cancer biology, ultimately conducting research on developing more accurate and easily accessible breast cancer diagnosis methods.

Her mentor is Jeff Gelles, Aron and Imre Tauber Professor of Biochemistry and Molecular Pharmacology.

 

Autism-linked Gene Keeps Brains in Balance

Mutations in the human Shank3 gene – so called “Shankopathies” – are strongly associated with Autism-spectrum disorders and intellectual disability, and appear to increase risk for a number of other disorders such as bipolar disorder and epilepsy. How it is that loss of function of this single gene generates pervasive disfunction within the neural circuits that underlie cognition and behavior is not understood. Now a recent report from the Turrigiano lab at Brandeis (Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent V1. Neuron. 2020 Mar 10. ) sheds light into this process, by showing how Shank3 loss disables mechanisms that normally act to keep brain circuitry in balance. Much as your body maintains a constant temperature through the use of internal thermostats and negative feedback mechanisms, brain circuits maintain balanced activity – neither too low and unresponsive, nor too high and hyperactive – by using a set of so-called “homeostatic” plasticity mechanisms to keep circuit excitability within an ideal range. This process is especially important during childhood and adolescence, because developing circuits can easily get out of balance as brain circuitry changes as a result of normal developmental processes.

Using mouse and rat models of human Shankopathies, the team, led by Research Associate Vedakumar Tatavarty, found that loss of Shank3 disables these homeostatic plasticity mechanisms and prevents brain circuits from compensating for changes to sensory drive. These defects in homeostatic plasticity are due to acute loss of Shank3 within individual neurons, meaning they are not an indirect effect of messed-up circuit wiring caused by loss of the gene throughout development. This finding suggests that Shank3 is a fundamental part of the cellular machinery that normally mediates homeostatic plasticity. The team went on to show that homeostatic plasticity could be restored after Shank3 loss by treatment with Lithium – a drug with a long history of use to treat neuropsychiatric disorders such as bipolar disorder – and that Lithium was also able to reduce a repetitive grooming behavior in mice that lack Shank3. These mice normally groom to excess, even to the point of self-injury, but a week of lithium treatment was able to reduce grooming to normal levels.

So do these findings suggest that Lithium might be useful in treating human Shankopathies? While Lithium remains the frontline treatment for some human disorders such as bipolar disorder, it is not well-tolerated, says Turrigiano, “and of course we cannot extrapolate from findings in mice directly to humans. Instead, we hope to use Lithium as a tool to reveal the pathways that can restore homeostatic plasticity in Shankopathies, which in the long term may allow us to design better, more specific interventions”. Defects in homeostatic plasticity have been implicated in a wide range of human brain disorders ranging from Autism spectrum disorders to Alzheimer’s disease, so these studies are likely to have important implications for overall brain health.

Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent V1. Tatavarty V, Torrado Pacheco A, Groves Kuhnle C, Lin H, Koundinya P, Miska NJ, Hengen KB, Wagner FF, Van Hooser SD, Turrigiano GG. Neuron. 2020 Mar 10. pii: S0896-6273(20)30184-7. doi: 10.1016/j.neuron.2020.02.033.

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