SPROUT Continues Growing Support for Brandeisian Innovators

Lil_Sprout_smallProgram Will Bestow Up to $100,000 to Promising Research Proposals

Could your research impact the world or do you have an idea that could create positive change? Need funding? SPROUT can help with that.

The popular SPROUT program, now in its sixth year, has announced increased funding for the 2016 round of proposals. SPROUT is funded by the Office of the Provost and run by Office of Technology Licensing. This year the Hassenfeld Family Innovation Center, recently created to support entrepreneurial and innovative collaborations happening across campus, contributed an additional $50,000 to be disbursed among the most promising requests.

Historically, the program has supported a diverse scope of lab-based innovations from all departments in the sciences  including Biology, Biochemistry, Physics, and Chemistry.  Past candidates have proposed projects ranging  from early‐stage research and development to patent‐ready projects ranging from treatments for diseases to lab tools.  Brandeis lab scientists have pitched their projects, including HIV vaccines (Sebastian Temme, Krauss lab),  neuroslicers (Yasmin Escobedo Lozoya, Nelson lab) and the use of carrot fiber as an anti-diabetic  (Michelle Landstrom, Hayes lab) to a panel of distinguished, outside judges. A SPROUT award can jumpstart your innovation and lead to continued opportunities. SPROUT awardees researching the use of carrot fiber as an anti-diabetic food agent were just awarded additional funding by the Massachusetts Innovation Commercialization Seed Fund program.

Other successful projects include “Enzymatic Reaction Recruits Chiral Nanoparticles to Inhibit Cancer Cells” led by Xuewen Du from the Xu lab, “Semaphorin4D: a disease‐modifying therapy for epilepsy” led by Daniel Acker of the Paradis lab, “X‐ray transparent Microfluidics for Protein Crystallization” led by Achini  Opathalage from the Fraden lab and “New and Rational Catalyst Development for Green Chemistry”  from the Thomas lab.  Those interested in learning more about past SPROUT winners are invited to read this recent Brandeis NOW article. A list of additional winners, along with their executive summaries, is available on the Brandeis OTL website.

Teams seeking support for scientific projects which require bench research, lab space, and/or lab equipment are encouraged to submit an abstract prior to the March 7 deadline. The competition is open to the entire Brandeis community including faculty, staff, and students. The Office of Technology Licensing will conduct information sessions on Thursday, February 25th 11:30 a.m.‐12:30 p.m. in Volen 201 and on Monday, February 29th 1:00 p.m.‐2:00 p.m. at the Shapiro Science Center, 1st Floor Library. Staff will address the application process as well as specific questions and interested applicants are highly encouraged to attend.

More details regarding the SPROUT awards, process and online application may be found at bit.ly/SPROUT16.

Mugdha Deshpande named Blazeman Postdoctoral Fellow

Assistant Professor of Biology Avital Rodal has received a grant from the Blazeman Foundation to study the traffic of growth signals in neurons in the animal models of ALS (Amyotrophic Lateral Sclerosis).  ALS, commonly known as ‘Lou Gehrig’s disease’, is a neurodegenerative disease that causes the loss of motor neurons. The Blazeman Foundation is a non-profit organization working to increase the awareness about this terminal disease and to support research towards finding treatments. Funding to the Rodal lab has enabled creation of the Blazeman Foundation Postdoctoral Fellowship for ALS Research, awarded to Mugdha Deshpande, Ph.D., who will use live imaging to examine and manipulate membrane traffic in fruit fly models of ALS, and who will also work with Dr. Suzanne Paradis to translate her findings to mammalian ALS models.

You can read more at BrandeisNOW.

Making new synapses with Sema4D

There are two main types of synaptic connections in the mammalian brain: excitatory glutamatergic synapses and inhibitory GABAergic synapses. The balance between excitatory and inhibitory inputs a neuron receives regulates the overall activity of neuronal networks; disruptions to this balance can cause epilepsy.

A new paper in J. Neuroscience from the Paradis lab shows that treatment of cultured neurons with the extracellular domain of the protein Sema4D causes a rapid increase (i.e. within 30 minutes) in the density of functional GABAergic synapses. Further, addition of Sema4D to neurons drives GABAergic synapse formation through a previously unappreciated mechanism: the splitting of pre-existing assemblies of the Gephyrin scaffolding protein. To our knowledge this is the fastest demonstration of synapse formation reported thus far and has significant implications for our understanding of the mechanisms of GABAergic synapse formation.

Screen Shot 2013-05-26 at 5.03.05 PMWhile the underlying mechanism of epileptogenesis is largely unknown, recurrent seizures emerge when there is an increase in network activity. One possible therapeutic treatment would be to restore normal network activity by increasing network inhibition. In an in vitro model of epilepsy, acute treatment with the protein Sema4D rapidly silences neuronal hyperexcitability, suggesting a possible use of Sema4D as a disease-modifying treatment for epilepsy.

Lead authors on the paper were Marissa Kuzirian, a grad student in the Neuroscience Ph.D. program, and Anna Moore, a Brandeis Neuroscience postdoctoral fellow.

NIH fellowships for Kuzirian and Ghiretti support neural development research

Marissa Kuzirian and Amy Ghiretti, graduate students in the lab of Dr. Suzanne Paradis, were each recently awarded Ruth L. Kirschstein National Research Service Awards for Individual Predoctoral Fellows (F31s) from the National Institutes of Health. Marissa’s 2.5-year award from the National Institute of Neurological Disorders and Stroke funds research to explore the role of Semaphorin4D and its receptor, PlexinB1, in regulating inhibitory synapse development and ultimately setting up proper neural connections in the mammalian CNS. Amy’s 2-year award from the National Institute on Drug Abuse funds a collaborative project between the Paradis, Lau, and Van Hooser labs here at Brandeis to elucidate the function of Rem2 in mediating experience-dependent changes in dendritic morphology in a living, intact animal system.

The basis for Marissa and Amy’s work comes from research into neurodevelopmental disorders such as Autism Spectrum Disorders (ASDs), as well as drug abuse and addiction. Proteins that regulate neurodevelopmental processes such as synapse development and dendritic morphology are important in both neurological disorders and drug addiction. Proper communication between neurons depends on the precise assembly and development of synaptic connections. The transmembrane protein Semaphorin4D (Sema4D) is necessary for proper GABAergic synapse formation, as knockdown of expression in the postsynaptic neuron by RNAi leads to a decrease in GABAergic synaptic density in cultured neurons (Paradis et al 2007). Marissa’s work will further explore this role of Sema4D in GABAergic synapse development.

Inhibitory synapses are identified in white along dendrites of a rat hippocampal neuron. Synapses are defined as sites of overlap between the postsynaptic protein GABAA receptor subunit γ2 (red) and the presynaptic protein GAD65 (blue) visualized by immunostaining. Neurons are visualized by immunostaining for MAP2 (green).

Marissa’s preliminary results demonstrate that adding the soluble, extracellular domain of Sema4D to cultured hippocampal neurons is sufficient to drive GABAergic synapse formation. This increase depends on the expression of Sema4D’s receptor, PlexinB1. Thus, Marissa’s work defines PlexinB1 as a novel receptor mediating GABAergic synapse formation in response to Sema4D in the mammalian CNS. The goal of Marissa’s project is to elucidate the role of Sema4D and its receptor, PlexinB1, in GABAergic synapse development. In experiments she proposed, she hypothesizes that Sema4D acts to initiate assembly of GABAergic synaptic proteins such as GABAA receptors and gephyrin through its receptor PlexinB1. This will be tested using a variety of imaging techniques in cultured hippocampal neurons, including confocal and time-lapse imaging, to measure the mobility and accumulation of GABAergic synaptic proteins in neurons after treatment with soluble Sema4D. The experiments will not only greatly expand our understanding of a novel receptor-ligand pair in GABAergic synapse development, it will inform as to some of the basic mechanisms underlying GABAergic synaptogenesis.

Molecular mechanisms, such as the Sema4D-PlexB1 interaction described above, are critical for the ability of the central nervous system (CNS) to respond to extracellular stimuli and make corresponding changes in the structure and function of a neuron. At the behavioral level, this plasticity allows an organism to respond to a changing environment appropriately in order to survive. At the level of individual neurons, this is reflected in changes in gene expression that occur in response to a variety of stimuli, including alterations in neuronal network activity. The goal of Amy’s work is to characterize a direct molecular link between changes in neuronal activity and changes in dendritic morphology.

A neuron in the optic tectum of a Xenopus tadpole; Green Fluorescent Protein expression allows the dendrites to be visualized.

Amy has previously implicated the protein Rem2, a type of signaling molecule known as a GTPase, as a mediator of such neurodevelopmental processes as excitatory synapse formation and dendritic morphology (Ghiretti & Paradis 2011). The expression of Rem2 in individual neurons is upregulated following increased neuronal activity, suggesting that it may serve as a direct link between changes in activity and corresponding changes in the structure and function of neurons. Her recently funded work will utilize Xenopus laevis tadpoles to study the effects of visual experience (by exposing the tadpoles to a light stimulus) on Rem2 expression, and in turn, how Rem2 mediates experience-dependent changes in the morphology of neurons in a region of the brain known as the optic tectum, where visual processing takes place. Ultimately, a full understanding of how Rem2 functions to shape the morphology of neurons in an intact system may help to inform knowledge of how the human brain changes as a result of neurological disorders or drug abuse, and aid in the development of more effective treatments to prevent these changes from occurring.

Wolman ’10 named HHMI Medical Research Fellow

Dylan Wolman ’10 talks about the merits of taking a year out of medical school to do intense lab research at the Howard Hughes Medical Institute’s Janelia Farm Research Campus as part of the HHMI Medical Research Fellows Program in a story on the HHMI News website. Wolman explains

“A year of research provides an avenue to practice what should be an essential skill in any scientific field: questioning ‘why.’ “

While at Brandeis, Wolman, a Bio/Neuro double major, did undergraduate research in the Paradis lab. His thesis on “Involvement of USP12 and USP46 ubiquitin proteases in synaptic glutamate receptor accumulation” earned him high honors in Neuroscience. Wolman is currently a medical student at Tufts University School of Medicine.

 

Brandeis Undergrads Gain Awards at SACNAS

On October 29th, 2011, Brandeis undergrads Lamia Harper (’12), Charity Frempomaa (’12), Sadrach Pierre (’13) and Carlos Pérez (’13) from our local SACNAS chapter represented Brandeis at the Annual Conference of the Society for Advancing Chicanos and Native Americans in Science (SACNAS) in San José, California.  Lamia and Sadrach both received awards for their research poster presentations. Lamia, who works in the Paradis lab, won an award in the Cellular and Molecular Biology category for her poster: Gene Discovery: Protein Kinases that Affect Synapse Development in the Mammalian CNS. Sadrach, who works in the Thomas lab in Chemistry, was awarded under the Biochemistry category for his poster: Sulfoamide Boronic Acids as Inhibitors of Beta-Lactamase.

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