Lori J Lorenz PhD
|Institution||University of Massachusetts Medical School|
|Department||Program in Molecular Medicine|
|Address||University of Massachusetts Medical School|
373 Plantation Street
Worcester MA 01605
ACADEMIC BACKGROUND: Lori Lorenz received a B.S. in Biochemistry and Molecular Biology from Purdue University, and earned a Ph.D. in Biology with an NIH predoctoral fellowship to study circadian rhythms with Michael Rosbash at Brandeis University. She explored Drosophila genetics with Norbert Perrimon at Harvard Medical School through an NIH postdoctoral award, and became Instructor of Cell Biology with funding from the Taplin Foundation. In 2002, she came to the University of Massachusetts Medical School with a grant from the Whitehall Foundation to investigate mRNA translation in the nervous system. SCIENCE/TRANSLATION: We identified a gene that affects axon growth in Drosophila and found that the encoded protein, Neuroguidin, contains eIF4E-binding domains similar to those in proteins that inhibit mRNA translation (Jung et al., 2006). We found that Neuroguidin preferentially inhibits translation through a cytoplasmic polyadenylation element-binding site for the translation factor, CPEB. We also found that Neuroguidin regulates mRNA translation and synaptic plasticity in the rodent brain (Udagawa et al., 2012). SCIENCE/BEHAVIOR: Drosophila locomotor activity patterns entrain to light/dark environments similarly to humans, with higher levels during the day and lower levels at night. Genes controlling circadian rhythms vary in expression transcriptionally and continue to drive rhythmic behavior in subsequent darkness. Through transgenic GAL4/UAS and RNAi techniques, we find that homologs of Neuroguidin and CPEB (Orb) influence rest/activity patterns during entrainment, suggesting a role for translation in the generation of sleep/wake behavior or arousal. Hyper-excitability is common in autistic individuals upon silencing of the fragile X mental retardation gene, fmr1. Infertility due to loss of dfmr in flies is rescued by reduced orb (Costa et al., 2005). We find that reduced CPEB relieves electrophysiologic, developmental, and behavioral defects in a mouse model of fragile X syndrome (Udagawa et al., 2013), implicating an important role for translational homeostasis in normal brain function.
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