&lt;i&gt;Drosophila&lt;/i&gt; DOCK Family Protein Sponge Regulates the JNK Pathway during Thorax Development

Morishita, Kazushige; Ozasa, Fumito; Eguchi, Koichi; Yoshioka, Yasuhide; Yoshida, Hideki; Hayashi, Hiroshi; Yamaguchi, Masamitsu

doi:10.1247/csf.14008

Cited by 7 publications

(5 citation statements)

References 40 publications

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“…Spg also activates JNK pathway to promote thorax development (Morishita et al, 2014). In contrast, Zizknockdown exerted no apparent effect in photoreceptor cell differentiation (Fig.…”

Section: Discussionmentioning

confidence: 93%

“…Spg also plays a critical role in ASP development and tracheal cell viability that is mediated by the ERK signaling pathway (Morishita et al, 2017). In contrast, during thorax development, Spg positively regulates JNK pathway and this regulation is mediated by its association with Rac1 (Morishita et al, 2014). Spg also regulates development of the central nervous system (CNS) with ELMO during embryogenesis (Biersmith et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

<i>Drosophila</i> DOCK Family Protein Zizimin Involves in Pigment Cell Differentiation in Pupal Retinae

Ozasa

Morishita

Dang

et al. 2017

Cell Struct. Funct.

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“…Spg also activates JNK pathway to promote thorax development (Morishita et al, 2014). In contrast, Zizknockdown exerted no apparent effect in photoreceptor cell differentiation (Fig.…”

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

<i>Drosophila</i> DOCK Family Protein Zizimin Involves in Pigment Cell Differentiation in Pupal Retinae

Ozasa

Morishita

Dang

et al. 2017

Cell Struct. Funct.

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“…DOCKs, corresponding to the Dedicator of CytoKinesis family, are GEF proteins of RhoA/Rac/Cdc42 that regulate F-actin organization (for review [175]) and MT dynamics [176]. In fly, DOCK3/sponge positively regulates JNK via Rac1 [177]. A similar regulation seems to occur in mammals through DOCK7 [178] and through DOCK180/DOCK1 or DOCK5 associated to the JNKupstream regulator p130Cas ( [176], for review [179] and Section 5).…”

Section: Jnk and Septinsmentioning

confidence: 99%

Cytoskeleton and Associated Proteins: Pleiotropic JNK Substrates and Regulators

Benoit

Baillet

Poüs

2021

IJMS

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This review extensively reports data from the literature concerning the complex relationships between the stress-induced c-Jun N-terminal kinases (JNKs) and the four main cytoskeleton elements, which are actin filaments, microtubules, intermediate filaments, and septins. To a lesser extent, we also focused on the two membrane-associated cytoskeletons spectrin and ESCRT-III. We gather the mechanisms controlling cytoskeleton-associated JNK activation and the known cytoskeleton-related substrates directly phosphorylated by JNK. We also point out specific locations of the JNK upstream regulators at cytoskeletal components. We finally compile available techniques and tools that could allow a better characterization of the interplay between the different types of cytoskeleton filaments upon JNK-mediated stress and during development. This overview may bring new important information for applied medical research.

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“…Dock180/ELMO/Rac1 signaling acts downstream of the RTK PVR during thorax closure and border cell migration, and use of tissue-specific RNAi and a hypomorphic crk allele supports roles for Crk in both processes (Ishimaru et al , 2004; Geisbrecht et al , 2008). Another DOCK family GEF, the DOCK3 relative Sponge, acts in parallel to Mbc in both processes (Bianco et al , 2007; Morishita et al , 2014). Dock180/ELMO/Rac1 signaling also regulates the actin cytoskeleton during myoblast fusion, but despite clear evidence that Crk binds proteins essential for myoblast fusion, it is unclear whether Crk is required.…”

Section: Introductionmentioning

confidence: 99%

The Crk adapter protein is essential forDrosophilaembryogenesis, where it regulates multiple actin-dependent morphogenic events

Spracklen

Thornton-Kolbe

Bonner

et al. 2019

MBoC

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Small Src homology domain 2 (SH2) and 3 (SH3) adapter proteins regulate cell fate and behavior by mediating interactions between cell surface receptors and downstream signaling effectors in many signal transduction pathways. The CT10 regulator of kinase (Crk) family has tissue-specific roles in phagocytosis, cell migration, and neuronal development and mediates oncogenic signaling in pathways like that of Abelson kinase. However, redundancy among the two mammalian family members and the position of the Drosophila gene on the fourth chromosome precluded assessment of Crk’s full role in embryogenesis. We circumvented these limitations with short hairpin RNA and CRISPR technology to assess Crk’s function in Drosophila morphogenesis. We found that Crk is essential beginning in the first few hours of development, where it ensures accurate mitosis by regulating orchestrated dynamics of the actin cytoskeleton to keep mitotic spindles in syncytial embryos from colliding. In this role, it positively regulates cortical localization of the actin-related protein 2/3 complex (Arp2/3), its regulator suppressor of cAMP receptor (SCAR), and filamentous actin to actin caps and pseudocleavage furrows. Crk loss leads to the loss of nuclei and formation of multinucleate cells. We also found roles for Crk in embryonic wound healing and in axon patterning in the nervous system, where it localizes to the axons and midline glia. Thus, Crk regulates diverse events in embryogenesis that require orchestrated cytoskeletal dynamics.

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<i>Drosophila</i> DOCK Family Protein Sponge Regulates the JNK Pathway during Thorax Development

Cited by 7 publications

References 40 publications

<i>Drosophila</i> DOCK Family Protein Zizimin Involves in Pigment Cell Differentiation in Pupal Retinae

<i>Drosophila</i> DOCK Family Protein Zizimin Involves in Pigment Cell Differentiation in Pupal Retinae

Cytoskeleton and Associated Proteins: Pleiotropic JNK Substrates and Regulators

The Crk adapter protein is essential forDrosophilaembryogenesis, where it regulates multiple actin-dependent morphogenic events

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