Gloria Choi

Gloria Bohyun Choi is an American neuroscientist and neuroimmunologist and the Samuel A. Goldblith Career Development Professor in the Picower Institute for Learning and Memory at the Massachusetts Institute of Technology. Choi is known for elucidating the role of the immune system in the development of autism spectrum disorder-like phenotypes. Her lab currently explores how sensory experiences drive internal states and behavioural outcomes through probing the olfactory system as well as the neuroimmune system.

Early life and education Choi was born in South Korea and immigrated to America in her teenage years. Her family settled in Southern California, where Choi developed a liking and interest in math and science because these subjects were easier to grasp while she was adjusting to the language barrier.

Since Choi had an early interest in applications of her studies, she joined the lab of Richard Harland to conduct laboratory research in molecular and cellular biology. Though she was just an undergraduate researcher, Choi became second author on a paper published in 2001 showing that the neural plate specifies somite size in the developing frog. Early into her graduate career, Choi explored the fate specification and differentiation of cells of the central nervous system in development. Her first paper in which she was co-first author highlighted the finding that the transcription factor, Olig2, sequentially defines motor neuron and oligodendrocyte fate specification. However, Choi and her colleagues were curious about the differentiation and specification of astrocytes in the central nervous system. Accordingly, they probed the roles of Olig1 and Olig2 transcription factors in astroglial specification and found that just as Olig1/2 promote motor neuron specification and suppress interneuron specification in the neurogenic phase, Olig1/2 promote oligodendrocyte specification and suppress astroglial specification in the later phase. This work has changed the way scientists think about the "logic" or "decision tree" that governs the differentiation of multipotent neural stems cells into neurons, astrocytes, and oligodendrocytes as they showed that cell subtype is fate restricted prior to restricting the overall neuronal or glial fate.

Choi then led some of the first projects in Anderson's lab exploring the neural circuits underlying innate behaviours. All animals possess the innate ability to detect social stimuli of another animal and exhibit either defensive or reproductive behaviours in response. Continuing to study olfaction, Choi explored how the piriform cortex encodes olfactory stimuli and drives behaviour. She discovered in 2011, that the piriform cortex does not spatially encode odors. To elucidate this finding, Choi stimulated random ensembles of piriform neurons, using optogenetics, and paired stimulation with an unconditioned stimulus, either shock or reward. At MIT, where she later moved to The Picower Institute, Choi's lab focuses on exploring how sensory stimuli drive distinct internal states as well as behavioural responses. With her extensive training in exploring the neural circuits involved in olfaction, Choi uses the olfactory system as a tool to explore the connections between sensory inputs and behavioural outcomes, how neuromodulators shape and modify circuits, and how these circuits maintain plasticity. Due to this knowledge, Choi and her team explored the role of oxytocin in social behaviours driven by olfactory cues. The experimental model for this clinical observation is known as Maternal Immune Activation (or MIA) which Choi used to examine which immune cell population is implicated in driving ASD-like behaviours. They found that maternal intestinal bacteria promote T cell differentiation in T helper 17 cells which release IL-17a and mediate the development of cortical abnormalities. They found that the dysgranular zone of the primary somatosensory cortex was the site of abnormalities and that inhibiting this region reduced ASD-like behavioural abnormalities in offspring of mothers with MIA. The administration of LPS, which induces IL-17a, rescued the behavioural phenotypes in MIA models while direct administration of IL-17a into the primary somatosensory cortex was required to reduce behavioural abnormalities in monogenic ASD models. 2021 Carol and Gene Ludwig Award for Early Career Research 2018 Peter Gruss Young Investigator Award Winner 2017 Simons Foundation Autism Research Initiative Pilot Awardee 2014 Cell's 40th Anniversary 40 under 40 2014 Sloan Research Fellowship

Publications

IL-17a promotes sociability in mouse models of neurodevelopmental disorder. Michael Douglas Reed, Yeong Shin Yim, Ralf D. Wimmer, Hyunju Kim, Changhyeon Ryu, Gwyneth Margaret Welch, Matias Andina, Hunter Oren King, Ari Waisman, Michael M. Halassa, Jun R. Huh* & Gloria B. Choi*. Nature 2019 December 18; I Can't Watch: A Genetic and Circuit-Level Investigation of Observational Fear Learning. Michael Douglas Reed, Gloria B. Choi. Neuron 2018 May 2; Reversing behavioural abnormalities in mice exposed to maternal inflammation. Yeong Shin Yim, Ashley Park, Janet Berrios, Mathieu Lafourcade, Leila M. Pascual, Natalie Soares, Joo Yeon Kim, Sangdoo Kim, Hyunju Kim, Ari Waisman, Dan R. Littman, Ian R. Wickersham, Mark T. Harnett, Jun R. Huh* & Gloria B. Choi*. Nature 2017 September 13; The maternal interleukin-17a pathway in mice promotes autism-like phenotypes in offspring. Gloria B. Choi, Yeong S. Yim, Helen Wong, Sangdoo Kim, Hyunju Kim, Sangwon V. Kim, Charles A. Hoeffer, Dan R. Littman, Jun R. Huh. Science. 2016 Jan 28; pp. Lhx6 delineates a pathway mediating innate reproductive behaviors from the amygdala to the hypothalamus. Choi, G.B., Dong, H.W., Murphy, A., Eichele, G., Yancopoulos, G.D., Valenzuela, D.M., Swanson, L., and Anderson D.J. Neuron. 2005 May 19;46(4):647-60. The neural plate specifies somite size in the Xenopus laevis gastrula. Mariani, F.V., Choi, G.B., and Harland, R.M. Dev Cell. 2001 Jul;1(1):115-26.