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Paradis Lab
Department of Biology
Lab Supplies & Receiving – Kalman
Brandeis University
415 South St.
Waltham, MA 02454

Suzanne Paradis, Ph.D.
Associate Professor
Department of Biology
Brandeis University
415 South St.
Waltham MA 02454

(781)736-5305 (office)
(781)736-3176/3177 (lab)
(781)736-3107 (fax)

E-mail | Faculty Profile
| Pubmed

Welcome to the Paradis Lab

Paradis Lab 2015
Paradis lab, c. 2015. Back row (left to right): Josiah Herzog, Leandro Royer, Sue Paradis, Dan Acker. Front row (left to right): Jackie McDermott, Mugdha Deshpande, Anna Moore, Katie Kimbrell, Katelyn (Kenny) Daman, Urann Chan

Our Research

Research in the Paradis laboratory seeks to define the genes that instruct neurons to establish and modify their connectivity, with the overall goal of understanding how neural network dysfunction contributes to neurological disorders. To this end, we pioneered an unbiased, forward genetic, RNAi-based screen in cultured primary neurons that revealed new genes which function to regulate synapse formation and dendritic morphology. Based on these findings, we identified the activity-regulated, small GTPase Rem2 as an important modulator of synapse formation and neuronal morphology both in vitro in cultured rodent neurons and in the optic tectum of Xenopus tadpoles. Our ongoing studies on Rem2 will reveal important insights into experience-dependent plasticity in an intact nervous system.

Another research focus of the lab is the molecular basis of inhibitory synapse formation, as this is an understudied area of synapse biology that has significant implications for human disease. We discovered that a class 4 Semaphorin, Sema4D, is required for the proper density of inhibitory, GABAergic synapses while having no affect on excitatory synapse formation. We also made the surprising discovery that Sema4D can drive GABAergic synapse formation on a rapid time scale (i.e. less than 30 minutes), and this effect is dependent on the presence of the its high affinity receptor, Plexin B1. Thus, Sema4D/Plexin B1 signaling is one of the few ligand/receptor pairs identified thus far that preferentially regulates inhibitory synapse formation. While we continue to investigate the mechanism of action of Sema4D in mediating GABAergic synapse formation, we are also investigating how we can harness the activity of Sema4D and other synaptogenic factors to drive inhibitory synapse formation in vivo as a potential therapeutic for neurodevelopmental disorders.