YAP and TAZ Regulate Cc2d1b and Purβ in Schwann Cells

Belin, Sophie; Herron, Jacob; VerPlank, Jordan J. S.; Park, Yungki; Feltri, L; Poitelon, Yannick

doi:10.3389/fnmol.2019.00177

Cited by 10 publications

(9 citation statements)

References 74 publications

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“…Overexpression of Yap/Taz in naïve adult nerves leads to an increase in Schwann cell proliferation (Mindos et al, 2017 ; Wu et al, 2018 ). Yap/Taz initiate the expression of DNA binding proteins like Tead1 (Lopez-Anido et al, 2016 ), Cc2d1b, and Purβ (Sophie et al, 2019 ) to promote Schwann cell proliferation and myelination.…”

Section: Schwann Cells: Understanding Development To Engineer Repairmentioning

confidence: 99%

Insights Into the Role and Potential of Schwann Cells for Peripheral Nerve Repair From Studies of Development and Injury

Balakrishnan

Belfiore

Chu

et al. 2021

Front. Mol. Neurosci.

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Peripheral nerve injuries arising from trauma or disease can lead to sensory and motor deficits and neuropathic pain. Despite the purported ability of the peripheral nerve to self-repair, lifelong disability is common. New molecular and cellular insights have begun to reveal why the peripheral nerve has limited repair capacity. The peripheral nerve is primarily comprised of axons and Schwann cells, the supporting glial cells that produce myelin to facilitate the rapid conduction of electrical impulses. Schwann cells are required for successful nerve regeneration; they partially “de-differentiate” in response to injury, re-initiating the expression of developmental genes that support nerve repair. However, Schwann cell dysfunction, which occurs in chronic nerve injury, disease, and aging, limits their capacity to support endogenous repair, worsening patient outcomes. Cell replacement-based therapeutic approaches using exogenous Schwann cells could be curative, but not all Schwann cells have a “repair” phenotype, defined as the ability to promote axonal growth, maintain a proliferative phenotype, and remyelinate axons. Two cell replacement strategies are being championed for peripheral nerve repair: prospective isolation of “repair” Schwann cells for autologous cell transplants, which is hampered by supply challenges, and directed differentiation of pluripotent stem cells or lineage conversion of accessible somatic cells to induced Schwann cells, with the potential of “unlimited” supply. All approaches require a solid understanding of the molecular mechanisms guiding Schwann cell development and the repair phenotype, which we review herein. Together these studies provide essential context for current efforts to design glial cell-based therapies for peripheral nerve regeneration.

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Section: Schwann Cells: Understanding Development To Engineer Repairmentioning

confidence: 99%

Insights Into the Role and Potential of Schwann Cells for Peripheral Nerve Repair From Studies of Development and Injury

Balakrishnan

Belfiore

Chu

et al. 2021

Front. Mol. Neurosci.

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“…47 In contrast to the CNS, in the PNS, many aspects of the development of the myelinating glia, Schwann cells, rely heavily on YAP/TAZ, including proliferation, differentiation, and myelination. [92][93][94][95][96][97] YAP/TAZ, therefore, seem to play an important role in the development of glial cells as well as neurons.…”

Section: Effectmentioning

confidence: 99%

The role of Hippo‐YAP/TAZ signaling in brain development

Terry

Kim

2022

Developmental Dynamics

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In order for our complex nervous system to develop normally, both precise spatial and temporal regulation of a number of different signaling pathways is critical. During both early embryogenesis and in organ development, one pathway that has been repeatedly implicated is the Hippo-YAP/TAZ signaling pathway. The paralogs YAP and TAZ are transcriptional co-activators that play an important role in cell proliferation, cell differentiation, and organ growth.Regulation of these proteins by the Hippo kinase cascade is therefore important for normal development. In this article, we review the growing field of research surrounding the role of Hippo-YAP/TAZ signaling in normal and atypical brain development. Starting from the development of the neural tube to the development and refinement of the cerebral cortex, cerebellum, and ventricular system, we address the typical role of these transcriptional co-activators, the functional consequences that manipulation of YAP/TAZ and their upstream regulators have on brain development, and where further research may be of benefit.

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“…Additionally, fibrillary collagens, which are reduced in Gli1 nulls, normally confer mechanical stability to peripheral nerves (Ushiki and Ide, 1986). Loss of these ECM components may alter nerve stiffness in the Gli1 nulls, impacting mechanical signaling that regulates SC differentiation (Belin et al, 2019). Finally, there is a rich array of paracrine signals released by EFs, whose expression is affected by nerve injury (Toma et al, 2020), that may likewise be altered in the Gli1 nulls and impact SC development.…”

Section: Reciprocal Intercellular Signaling During Pns Developmentmentioning

confidence: 99%

Gli1 Regulates the Postnatal Acquisition of Peripheral Nerve Architecture

et al. 2021

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Peripheral nerves are organized into discrete compartments. Axons, Schwann cells (SCs), and endoneurial fibroblasts (EFs) reside within the endoneurium and are surrounded by the perineurium, a cellular sheath comprised of layers of perineurial glia (PNG). SC secretion of Desert Hedgehog (Dhh) regulates this organization. In Dhh nulls, the perineurium is deficient and the endoneurium is subdivided into small compartments termed minifascicles. Human Dhh mutations cause a neuropathy with similar defects.Here we examine the role of Gli1, a canonical transcriptional effector of hedgehog signaling, in regulating peripheral nerve organization in mice of both genders. We identify PNG, EFs, and pericytes as Gli1-expressing cells by genetic fate mapping. Although expression of Dhh by SCs and Gli1 in target cells is coordinately regulated with myelination, Gli1 expression unexpectedly persists in Dhh null EFs. Thus, Gli1 is expressed in EFs noncanonically (i.e., independent of hedgehog signaling). Gli1 and Dhh also have nonredundant activities. Unlike Dhh nulls, Gli1 nulls have a normal perineurium. Like Dhh nulls, Gli1 nulls form minifascicles, which we show likely arise from EFs. Thus, Dhh and Gli1 are independent signals: Gli1 is dispensable for perineurial development but functions cooperatively with Dhh to drive normal endoneurial development. During development, Gli1 also regulates endoneurial extracellular matrix production, nerve vascular organization, and has modest, nonautonomous effects on SC sorting and myelination of axons. Finally, in adult nerves, induced deletion of Gli1 is sufficient to drive minifascicle formation. Thus, Gli1 regulates the development and is required to maintain the endoneurial architecture of peripheral nerves.

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YAP and TAZ Regulate Cc2d1b and Purβ in Schwann Cells

Cited by 10 publications

References 74 publications

Insights Into the Role and Potential of Schwann Cells for Peripheral Nerve Repair From Studies of Development and Injury

Insights Into the Role and Potential of Schwann Cells for Peripheral Nerve Repair From Studies of Development and Injury

The role of Hippo‐YAP/TAZ signaling in brain development

Gli1 Regulates the Postnatal Acquisition of Peripheral Nerve Architecture

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