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Ni, Xiaochun

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Xiaochun

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Ni, Xiaochun

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2017 - 20192

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Author's Publications: search.filters.isAuthorOfPublication.982bf3c4-96a1-4cdd-a0cc-f75d520c49a2

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    The Septate Junction Protein Tsp2A Restricts Intestinal Stem Cell Activity via Endocytic Regulation of aPKC and Hippo Signaling
    (Elsevier BV, 2019-01-15) Xu, Chiwei; Tang, Hong-Wen; Hung, Ruei-Jiun; Hu, Yanhui; Ni, Xiaochun; Housden, Benjamin; Perrimon, Norbert
    Hippo signaling and the activity of its transcriptional coactivator, Yorkie (Yki), are conserved and crucial regulators of tissue homeostasis. In the Drosophila midgut, after tissue damage, Yki activity increases to stimulate stem cell proliferation, but how Yki activity is turned off once the tissue is repaired is unknown. From an RNAi screen, we identified the septate junction (SJ) protein tetraspanin 2A (Tsp2A) as a tumor suppressor. Tsp2A undergoes internalization to facilitate the endocytic degradation of atypical protein kinase C (aPKC), a negative regulator of Hippo signaling. In the Drosophila midgut epithelium, adherens junctions (AJs) and SJs are prominent in intestinal stem cells or enteroblasts (ISCs or EBs) and enterocytes (ECs), respectively. We show that when ISCs differentiate toward ECs, Tsp2A is produced, participates in SJ assembly, and turns off aPKC and Yki-JAK-Stat activity. Altogether, our study uncovers a mechanism allowing the midgut to restore Hippo signaling and restrict proliferation once tissue repair is accomplished.
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    Activin Signaling Mediates Muscle-to-Adipose Communication in a Mitochondria Dysfunction-Associated Obesity Model
    (National Academy of Sciences, 2017-08-08) Song, Wei; Owusu-Ansah, Edward; Hu, Yanhui; Cheng, Daojun; Ni, Xiaochun; Zirin, Jonathan; Perrimon, Norbert
    Mitochondrial perturbation-associated dysregulation of one organ has been shown to nonautonomously affect the functions of other organs in both vertebrates and invertebrates. Using Drosophila as a genetic model organism, we characterized mitochondrial synchrony dysregulation across organs and uncovered that mitochondrial perturbation caused by complex I disruption in muscles remotely impairs mitochondrial function and lipid mobilization in the fat body, leading to obesity. We further identified that the TGF-β ligand Actβ, which is autonomously increased by muscular mitochondrial perturbation, mediates muscle-to-fat-body communication and synchronized mitochondrial dysregulation.