The Strip-Hippo Pathway Regulates Synaptic Terminal Formation by Modulating Actin Organization at the Drosophila Neuromuscular Synapses

Sakuma, Chisako; Saito, Yoshie; Umehara, Tomoki; Kamimura, Kazuo; Maeda, Nobuaki; Mosca, Timothy J.; Miura, Masayuki; Chihara, Takahiro

doi:10.1016/j.celrep.2016.07.066

Cited by 31 publications

(31 citation statements)

References 56 publications

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“…In the mouse embryo, loss of Strip1 arrests mesoderm migration after the gastrulation epithelial-to-mesenchymal transition (Bazzi et al, 2017). Indeed, STRIP1 has been shown to regulate cytoskeleton dynamics and cell migration on several occasions (Bai et al, 2011;Sakuma et al, 2015Sakuma et al, , 2016Suryavanshi et al, 2018). We discovered that the STRIPAK complex is an important and ancient regulator of plasticity of cell migration during both developmental processes and cancer metastasis (Madsen et al, 2015).…”

Section: Introductionmentioning

confidence: 82%

“…The accumulated findings have linked specific components of the complex to various biological functions including vesicular trafficking (Zhang et al, 2013;Lant et al, 2015), Golgi assembly (Kean et al, 2011), Hippo signaling (Ribeiro et al, 2010;Zheng et al, 2017), autophagy (Huang et al, 2017), cell migration (Madsen et al, 2015;Bazzi et al, 2017), and cell cycle control (Cornils et al, 2011;Frost et al, 2012;Kazmierczak-Baranska et al, 2015;Pandey et al, 2017). Substantiated by these findings, the STRIPAK complex is supervising embryogenesis and development (Lant et al, 2015;Madsen et al, 2015;Sakuma et al, 2015Sakuma et al, , 2016Bazzi et al, 2017;Pal et al, 2017;Zheng et al, 2017), circadian rhythms (Andreazza et al, 2015), type 2 diabetes (Chursa et al, 2017), and progression of cancer (Wong et al, 2014;Zhang et al, 2014;Madsen et al, 2015;Huang et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

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The STRIPAK Complex Regulates Response to Chemotherapy Through p21 and p27

Rodriguez-Cupello

Dam

Serini

et al. 2020

Front. Cell Dev. Biol.

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The STRIPAK complex has been linked to a variety of biological processes taking place during embryogenesis and development, but its role in cancer has only just started to be defined. Here, we expand on previous work indicating a role for the scaffolding protein STRIP1 in cancer cell migration and metastasis. We show that cell cycle arrest and decreased proliferation are seen upon loss of STRIP1 in MDA-MB-231 cells due to the induction of cyclin dependent kinase inhibitors, including p21 and p27. We demonstrate that p21 and p27 induction is observed in a subpopulation of cells having low DNA damage response and that the p21 high /γH2AX low ratio within single cells can be rescued by depleting MST3&4 kinases. While the loss of STRIP1 decreases cell proliferation and tumor growth, cells treated with low dosage of chemotherapeutics in vitro paradoxically escape therapy-induced senescence and begin to proliferate after recovery. This corroborates with already known research on the dual role of p21 and indicates that STRIP1 also plays a contradictory role in breast cancer, suppressing tumor growth, but once treated with chemotherapeutics, allowing for possible recurrence and decreased patient survival.

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Section: Introductionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

The STRIPAK Complex Regulates Response to Chemotherapy Through p21 and p27

Rodriguez-Cupello

Dam

Serini

et al. 2020

Front. Cell Dev. Biol.

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“…The roles of other STRIPAK components are less understood. An intact STRIPAK complex is required for negative regulation of Hippo signaling in distinct Drosophila cellular contexts, but the contribution of Mob4/Phocein has yet to be defined (Ribeiro et al, 2010;Schulte et al, 2010;Sakuma et al, 2016;Zheng et al, 2017;Neisch et al, 2017;Gil-Ranedo et al, 2019). Mob4/Phocein proteins have been shown to bind directly to STE20 kinases in both fly and mammalian cells (Ribeiro et al, 2010;Couzens et al, 2017;Chen et al, 2018), but it is unclear if Mob4/Phocein is required to recruit GCK-type STE20 kinases to the STRIPAK complex.…”

Section: The Stripak Complex Is a Negative Regulator Of Hippo Signalingmentioning

confidence: 99%

Mob Family Proteins: Regulatory Partners in Hippo and Hippo-Like Intracellular Signaling Pathways

Duhart

Raftery

2020

Front. Cell Dev. Biol.

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Studies in yeast first delineated the function of Mob proteins in kinase pathways that regulate cell division and shape; in multicellular eukaryotes Mobs regulate tissue growth and morphogenesis. In animals, Mobs are adaptors in Hippo signaling, an intracellular signal-transduction pathway that restricts growth, impacting the development and homeostasis of animal organs. Central to Hippo signaling are the Nuclear Dbf2-Related (NDR) kinases, Warts and LATS1 and LATS2, in flies and mammals, respectively. A second Hippo-like signaling pathway has been uncovered in animals, which regulates cell and tissue morphogenesis. Central to this emergent pathway are the NDR kinases, Tricornered, STK38, and STK38L. In Hippo signaling, NDR kinase activation is controlled by three activating interactions with a conserved set of proteins. This review focuses on one co-activator family, the highly conserved, non-catalytic Mps1binder-related (Mob) proteins. In this context, Mobs are allosteric activators of NDR kinases and adaptors that contribute to assembly of multiprotein NDR kinase activation complexes. In multicellular eukaryotes, the Mob family has expanded relative to model unicellular yeasts; accumulating evidence points to Mob functional diversification. A striking example comes from the most sequence-divergent class of Mobs, which are components of the highly conserved Striatin Interacting Phosphatase and Kinase (STRIPAK) complex, that antagonizes Hippo signaling. Mobs stand out for their potential to modulate the output from Hippo and Hippo-like kinases, through their roles both in activating NDR kinases and in antagonizing upstream Hippo or Hippo-like kinase activity. These opposing Mob functions suggest that they coordinate the relative activities of the Tricornered/STK38/STK38L and Warts/LATS kinases, and thus have potential to assemble nodes for pathway signaling output. We survey the different facets of Mobdependent regulation of Hippo and Hippo-like signaling and highlight open questions that hinge on unresolved aspects of Mob functions.

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“…The mammalian adaptive immune system is also influenced by the activation of the Hippo signaling pathway (Yamauchi & Moroishi, ). Even during the development of the nervous system, the Hippo pathway is responsible for the proliferation of neuronal progenitors (Cao, Pfaff, & Gage, ), their differentiation (Lin et al, ), migration (Fry et al, ), myelination (Deng et al, ), dendritic arborization (Emoto, ), and successful neural connectivity formation (Sakuma et al, ). Although less explored, the Hippo signaling pathway is getting a lot of attention in recent days for its latent biological importance.…”

Section: Biological Functions Of the Hippo Signaling Pathwaymentioning

confidence: 99%

The emerging role of Hippo signaling in neurodegeneration

Sahu

Mondal

2019

J of Neuroscience Research

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Neurodegeneration refers to the complex process of progressive degeneration or neuronal apoptosis leading to a set of incurable and debilitating conditions. Physiologically, apoptosis is important in proper growth and development. However, aberrant and unrestricted apoptosis can lead to a variety of degenerative conditions including neurodegenerative diseases. Although dysregulated apoptosis has been implicated in various neurodegenerative disorders, the triggers and molecular mechanisms underlying such untimely and faulty apoptosis are still unknown. Hippo signaling pathway is one such apoptosis‐regulating mechanism that has remained evolutionarily conserved from Drosophila to mammals. This pathway has gained a lot of attention for its tumor‐suppressing task, but recent studies have emphasized the soaring role of this pathway in inflaming neurodegeneration. In addition, strategies promoting inactivation of this pathway have aided in the rescue of neurons from anomalous apoptosis. So, a thorough understanding of the relationship between the Hippo pathway and neurodegeneration may serve as a guide for the development of therapy for various degenerative diseases. The current review focuses on the mechanism of the Hippo signaling pathway, its upstream and downstream regulatory molecules, and its role in the genesis of numerous neurodegenerative diseases. The recent efforts employing the Hippo pathway components as targets for checking neurodegeneration have also been highlighted.

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The Strip-Hippo Pathway Regulates Synaptic Terminal Formation by Modulating Actin Organization at the Drosophila Neuromuscular Synapses

Cited by 31 publications

References 56 publications

The STRIPAK Complex Regulates Response to Chemotherapy Through p21 and p27

The STRIPAK Complex Regulates Response to Chemotherapy Through p21 and p27

Mob Family Proteins: Regulatory Partners in Hippo and Hippo-Like Intracellular Signaling Pathways

The emerging role of Hippo signaling in neurodegeneration

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