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Tsai, Linus

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Tsai

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Linus

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Tsai, Linus

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2014 - 20172

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Author's Publications: search.filters.isAuthorOfPublication.49bf199e-3b1f-4cd8-867a-b30ddc1550b6

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    A Molecular Census of Arcuate Hypothalamus and Median Eminence Cell Types
    (2017) Campbell, John; Macosko, Evan; Fenselau, Henning; Pers, Tune H.; Lyubetskaya, Anna; Tenen, Danielle; Goldman, Melissa; Verstegen, Anne; Resch, Jon; McCarroll, Steven; Rosen, Evan; Lowell, Bradford; Tsai, Linus
    The hypothalamic arcuate-median eminence complex (Arc-ME) controls energy balance, fertility, and growth through molecularly distinct cell types, many of which remain unknown. To catalog cell types in an unbiased way, we profiled gene expression in 20,921 individual cells in and around the adult mouse Arc-ME using Drop-seq. We identify 50 transcriptionally distinct Arc-ME cell populations, including a rare tanycyte population at the Arc-ME diffusion barrier, a novel leptin-sensing neuronal population, multiple AgRP and POMC subtypes, and an orexigenic somatostatin neuronal population. We extended Drop-seq to detect dynamic expression changes across relevant physiological perturbations, revealing cell type-specific responses to energy status, including distinctly responsive subtypes of AgRP and POMC neurons. Finally, integrating our data with human GWAS data implicates two previously unknown neuronal subtypes in the genetic control of obesity. This resource will accelerate biological discovery by providing insights into molecular and cell type diversity from which function can be inferred.
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    Identification of nuclear hormone receptor pathways causing insulin resistance by transcriptional and epigenomic analysis
    (2014) Kang, Sona; Tsai, Linus; Zhou, Yiming; Evertts, Adam; Xu, Su; Griffin, Michael J.; Issner, Robbyn; Whitton, Holly J.; Garcia, Benjamin A.; Epstein, Charles B.; Mikkelsen, Tarjei S.; Rosen, Evan
    Summary Insulin resistance is a sine qua non of Type 2 diabetes (T2D) and a frequent complication of multiple clinical conditions, including obesity, aging, and steroid use, among others. How such a panoply of insults can result in a common phenotype is incompletely understood. Furthermore, very little is known about the transcriptional and epigenetic basis of this disorder, despite evidence that such pathways are likely to play a fundamental role. Here, we compare cell autonomous models of insulin resistance induced by the cytokine tumor necrosis factor-α (TNF) or by the steroid dexamethasone (Dex) to construct detailed transcriptional and epigenomic maps associated with cellular insulin resistance. These data predict that the glucocorticoid receptor and vitamin D receptor are common mediators of insulin resistance, which we validate using gain- and loss-of-function studies. These studies define a common transcriptional and epigenomic signature in cellular insulin resistance enabling the identification of pathogenic mechanisms.