Golgi-dependent reactivation and regeneration of Drosophila quiescent neural stem cells

Gujar, Mahekta R; Gao, Yang; Teng, Xiang; Deng, Qiannan; Lin, Kun-Yang; Tan, Yan; Toyama, Yusuke; Wang, Hongyan

doi:10.1016/j.devcel.2023.07.010

Cited by 6 publications

(21 citation statements)

References 69 publications

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“…The microtubule minus-end binding protein Patronin is critical for NSC reactivation As microtubule regulators are involved in quiescent NSC reactivation (Deng et al, 2021;preprint: Gujar et al, 2022;Gujar et al, 2023), we investigated whether Patronin plays a role in NSC reactivation. At 24 h ALH, the vast majority of wild-type NSCs were reactivated and incorporated with EdU and only 11.5% of NSCs were quiescent and negative for EdU (Fig 1A -C).…”

Section: Resultsmentioning

confidence: 99%

“…The Golgi apparatus has emerged as potential acentrosomal MTOCs in several cell types, such as neurons, epithelial, and muscle cells (De Camilli et al , 1986 ; Horton et al , 2005 ; Ori‐McKenney et al , 2012 ; Zhou et al , 2014 ; Yang & Wildonger, 2020 ). We showed recently that Golgi acts as the acentrosomal MTOC in quiescent NSCs (preprint: Gujar et al , 2022 ; Gujar et al , 2023 ). Remarkably, quiescent NSC cellular protrusions can be regenerated upon injury by laser severing, and this regeneration relies on Golgi and microtubule growth in quiescent NSCs (preprint: Gujar et al , 2022 ; Gujar et al , 2023 ).…”

Section: Introductionmentioning

confidence: 99%

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Patronin/CAMSAP promotes reactivation and regeneration of Drosophila quiescent neural stem cells

Gujar

Gao

Teng³

et al. 2023

EMBO Reports

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The ability of stem cells to switch between quiescent and proliferative states is crucial for maintaining tissue homeostasis and regeneration. Drosophila quiescent neural stem cells (qNSCs) extend a primary protrusion that is enriched in acentrosomal microtubules and can be regenerated upon injury. Arf1 promotes microtubule growth, reactivation (exit from quiescence), and regeneration of qNSC protrusions upon injury. However, how Arf1 is regulated in qNSCs remains elusive. Here, we show that the microtubule minus‐end binding protein Patronin/CAMSAP promotes acentrosomal microtubule growth and quiescent NSC reactivation. Patronin is important for the localization of Arf1 at Golgi and physically associates with Arf1, preferentially with its GDP‐bound form. Patronin is also required for the regeneration of qNSC protrusion, likely via the regulation of microtubule growth. Finally, Patronin functions upstream of Arf1 and its effector Msps/XMAP215 to target the cell adhesion molecule E‐cadherin to NSC‐neuropil contact sites during NSC reactivation. Our findings reveal a novel link between Patronin/CAMSAP and Arf1 in the regulation of microtubule growth and NSC reactivation. A similar mechanism might apply to various microtubule‐dependent systems in mammals.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Patronin/CAMSAP promotes reactivation and regeneration of Drosophila quiescent neural stem cells

Gujar

Gao

Teng³

et al. 2023

EMBO Reports

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“…Proximity ligation assay (PLA) was performed as described ([58], Adopted from Duolink PLA, Merck). Mouse neural progenitor cells were transfected with the following constructs including control-GFP, control-myc, Arl2-GFP and Cdk5rap2-myc using Lipofectamine Transfection reagent (Invitrogen).…”

Section: Methodsmentioning

confidence: 99%

Arl2 Associates with Cdk5rap2 to Regulate Cortical Development via Microtubule Organization

Ma,

Lin,

Divya

et al. 2024

Preprint

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ADP ribosylation factor-like GTPase 2 (Arl2) is crucial for controlling mitochondrial fusion and microtubule assembly in various organisms. Arl2 regulates the asymmetric division of neural stem cells in Drosophila via microtubule growth. However, the function of mammalian Arl2 during cortical development was unknown. Here, we demonstrate that mouse Arl2 plays a new role in corticogenesis via regulating microtubule growth, but not mitochondria functions. Arl2 knockdown leads to impaired proliferation of neural progenitor cells (NPCs) and neuronal migration. Arl2 knockdown in mouse NPCs significantly diminishes centrosomal microtubule growth and delocalization of centrosomal proteins Cdk5rap2 and γ-tubulin. Moreover, Arl2 physically associates with Cdk5rap2 by in silico prediction using AlphaFold Multimer and in vitro binding assays. Remarkably, Cdk5rap2 overexpression significantly rescues the neurogenesis defects caused by Arl2 knockdown. Therefore, Arl2 plays an important role in mouse cortical development through microtubule growth via the centrosomal protein Cdk5rap2.

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“…For instance, myoblast reposition their GA from a perinuclear position to an even distributed configuration as they differentiate into myotubes, with the repositioning being actin-dependent and driven by Myosin VI (Lu et al 2001 ; Percival and Froehner 2007 ). Similarly, neural stem cells initially have perinuclear GA. During development, radial glial cells (RG) undergo apical-basal repositioning in various contexts, including Drosophila quiescent neural stem cells reactivation (Gujar et al 2023 ) and neurogenesis from induced pluripotent stem cell (iPSC) (Scharaw et al 2023 ). These dynamic changes in GA positioning and morphology raise intriguing questions about their potential role in stem cell contributions to wound healing.…”

Section: The Function Of Ga Fragmentation Stem Cell Activation and Wo...mentioning

confidence: 99%

“…Their reactivation relies on an evolutionarily conserved insulin growth factor (IGF) signaling pathway and microtubule-rich extensions. Recent studies suggest that the GA and its outposts (GOP) can act as a microtubule-organizing center (MTOC) in quiescent NSCs (Valenzuela et al 2020 ), with Golgi-resident GTPase ARF1 and its guanine nucleotide exchange factor (GEF) Sec71 playing a pivotal role in promoting NSC reactivation and regeneration (Gujar et al 2023 ). These findings highlight the essential role of GA in regeneration after injury in vivo.…”

Section: The Function Of Ga Fragmentation Stem Cell Activation and Wo...mentioning

confidence: 99%

Reevaluating Golgi fragmentation and its implications in wound repair

Wijaya,

2024

Cell Regen

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The Golgi Apparatus (GA) is pivotal in vesicle sorting and protein modifications within cells. Traditionally, the GA has been described as a perinuclear organelle consisting of stacked cisternae forming a ribbon-like structure. Changes in the stacked structure or the canonical perinuclear localization of the GA have been referred to as “GA fragmentation”, a term widely employed in the literature to describe changes in GA morphology and distribution. However, the precise meaning and function of GA fragmentation remain intricate. This review aims to demystify this enigmatic phenomenon, dissecting the diverse morphological changes observed and their potential contributions to cellular wound repair and regeneration. Through a comprehensive analysis of current research, we hope to pave the way for future advancements in GA research and their important role in physiological and pathological conditions.

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Golgi-dependent reactivation and regeneration of Drosophila quiescent neural stem cells

Cited by 6 publications

References 69 publications

Patronin/CAMSAP promotes reactivation and regeneration of Drosophila quiescent neural stem cells

Patronin/CAMSAP promotes reactivation and regeneration of Drosophila quiescent neural stem cells

Arl2 Associates with Cdk5rap2 to Regulate Cortical Development via Microtubule Organization

Reevaluating Golgi fragmentation and its implications in wound repair

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