Diverse populations of neurons and glia emerge during development in a coordinated series of steps that balance proliferation of neural progenitor cells with their sequential differentiation into distinct cell types. A fundamental question motivating our work is understanding how neural progenitor cells integrate the multitude of signals to which they are exposed into precise programs of gene expression that guide the adoption of cell fate. In the developing brain, calcium represents a point of convergence linking environmental cues with intrinsic genetic programs. Mutations in calcium channels and proteins involved in decoding calcium signals have also been reproducibly linked to psychiatric disorders of developmental origin. Our previous and current studies in both mouse and human cortical cells suggest that normal differentiation involves precise regulation of intracellular calcium and that mutations linked to developmental disorders perturb this process. This in turn causes a failure to properly transduce developmental cues into specific cellular events, which cascades through development and manifests as cellular phenotypes observed in the context of neurodevelopmental disease. In this presentation, I will share published and unpublished work from our lab focusing on two aspects of calcium signaling in the embryonic cerebral cortex: ion channels that initiate calcium entry and molecular pathways that propagate calcium signals into long-term changes in cellular behavior.
I am a cellular, molecular and developmental neuroscientist focused on understanding the precise mechanisms by which neural stem cells integrate intrinsic and extrinsic signals to generate the diversity of cell types in the brain. These interests initially manifested in research conducted at Memorial Sloan Kettering Cancer Center, where we published a series of papers investigating the specification and in vivo integration of pluripotent stem cell derivatives in normal or diseased brain states. Using this background as a springboard, during my doctoral work at Stanford I initiated a novel research direction demonstrating a role for electrically-evoked calcium signals through a psychiatric disease-relevant calcium channel on the regulation of genetic programs specifying neuronal identity. Based on the broad implications of this work, I was selected to bypass postdoctoral training and launch my independent research program as a Sandler Faculty Fellow at the University of California, San Francisco. As an independent investigator, I have established a research team that is integrating a variety of complementary approaches to interrogate the roles of calcium signaling, electrical activity and ion channel splicing in sculpting brain development, with an eye towards understanding how these fundamental mechanisms are altered to give rise to neurodevelopmental disorders and co-opted in neurodegeneration and brain tumor formation.
 Panagiotakos et al. eLife 2019;8:e51037. DOI: https://doi.org/10.7554/eLife.51037
 Braun S*, Petrova R*, Tang J, Miller E, Tang Y, and Panagiotakos G¶, Crabtree GR¶. BAF subunit switching regulates chromatin accessibility to control cell cycle exit in the developing mammalian cortex. Preprint bioRxiv 910794; cover article, Genes & Development, 35(5-6): 335-353. 2021 Mar 1. PMID: 33602870.