Expression profile of the cadherin family in the developing <i>Drosophila</i> brain

Fung, Siaumin; Wang, Fay; Chase, Maretta; Godt, Dorothea; Hartenstein, Volker

doi:10.1002/cne.21539

Cited by 36 publications

(37 citation statements)

References 100 publications

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“…This makes glia a valuable tool to analyze the role of cadherins in cell migration in the nervous system. In contrast to previous reports (Fung et al, 2008;Iwai et al, 1997), we found that N-cad is expressed in peripheral glia and is required for their migration.…”

Section: N-cadherin and Glial Migrationcontrasting

confidence: 99%

“…The cadherin family of Ca 2+ dependent cell adhesion molecules are primarily involved in homophilic interactions (Arikkath and Reichardt, 2008;Giagtzoglou et al, 2009;Kiryushko et al, 2004) and are required for cell polarity, adhesion and motility (Harris and Tepass, 2010). In the vertebrate and in the Drosophila nervous systems, the most abundant classic cadherin is the neural (N)-cadherin (N-cad) (Fung et al, 2008;Stepniak et al, 2009), which promotes the formation of rather small adherens junctions (AJs) and is thought to provide the mechanical basis for static tissue organization (e.g. defined cell arrangement in polarized epithelium) as well as for plastic connections between cells.…”

Section: Introductionmentioning

confidence: 99%

“…Each member of this cell community is in contact with the neighboring cells, and glia-glia interactions tightly control migration extent, efficiency and coordination (Aigouy et al, 2004;Aigouy et al, 2008;(Berzsenyi et al, 2011). In Drosophila, N-cad controls growth cone guidance and axon bundle fasciculation (Iwai et al, 1997); however, it had been suggested that N-cad is not expressed in glia cells (Fung et al, 2008;Iwai et al, 1997). Here, we show that N-cad is dynamically and uniformly expressed in wing glial cells, and that it is necessary for the timely and efficient migration of the chain along the axon bundle.…”

Section: Introductionmentioning

confidence: 99%

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N-cadherin negatively regulates collective Drosophila glial migration via actin cytoskeleton remodeling

Kumar

Gupta

Berzsenyi

et al. 2015

Journal of Cell Science

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Cell migration is an essential and highly regulated process. During development, glia cells and neurons migrate over long distancesin most cases collectively -to reach their final destination and build the sophisticated architecture of the nervous system, the most complex tissue of the body. Collective migration is highly stereotyped and efficient, defects in the process leading to severe human diseases that include mental retardation. This dynamic process entails extensive cell communication and coordination, hence, the real challenge is to analyze it in the entire organism and at cellular resolution. We here investigate the impact of the Ncadherin adhesion molecule on collective glial migration, by using the Drosophila developing wing and cell-type specific manipulation of gene expression. We show that N-cadherin timely accumulates in glial cells and that its levels affect migration efficiency. N-cadherin works as a molecular brake in a dosage-dependent manner, by negatively controlling actin nucleation and cytoskeleton remodeling through a/b catenins. This is the first in vivo evidence for N-cadherin negatively and cell autonomously controlling collective migration.

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Section: N-cadherin and Glial Migrationcontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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N-cadherin negatively regulates collective Drosophila glial migration via actin cytoskeleton remodeling

Kumar

Gupta

Berzsenyi

et al. 2015

Journal of Cell Science

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“…In either case, Notch loss of function would disrupt cell adhesion and lead to the extrusion of epithelial cells. Subtypes of cadherins, such as DE-Cad, Cad99C, Fat, which we find preferentially expressed in the neuroepithelium (see also Fung et al, 2008), might be activated by Notch to maintain the neuroepithelium, and repressed by L'sc to promote neurogenesis. Notch mutant clones also upregulate expression of the neuroblast transcription factor Dpn (but not of L'sc), and divide asymmetrically only once they have delaminated from the epithelium.…”

Section: Research Articlementioning

confidence: 60%

Notch regulates the switch from symmetric to asymmetric neural stem cell division in the Drosophila optic lobe

2010

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SUMMARYThe proper balance between symmetric and asymmetric stem cell division is crucial both to maintain a population of stem cells and to prevent tumorous overgrowth. Neural stem cells in the Drosophila optic lobe originate within a polarised neuroepithelium, where they divide symmetrically. Neuroepithelial cells are transformed into asymmetrically dividing neuroblasts in a precisely regulated fashion. This cell fate transition is highly reminiscent of the switch from neuroepithelial cells to radial glial cells in the developing mammalian cerebral cortex. To identify the molecules that mediate the transition, we microdissected neuroepithelial cells and compared their transcriptional profile with similarly obtained optic lobe neuroblasts. We find genes encoding members of the Notch pathway expressed in neuroepithelial cells. We show that Notch mutant clones are extruded from the neuroepithelium and undergo premature neurogenesis. A wave of proneural gene expression is thought to regulate the timing of the transition from neuroepithelium to neuroblast. We show that the proneural wave transiently suppresses Notch activity in neuroepithelial cells, and that inhibition of Notch triggers the switch from symmetric, proliferative division, to asymmetric, differentiative division.

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“…2A,B) (Fung et al, 2008). The Fat pathway modulator lowfat is also expressed in NE (Mao et al, 2009).…”

Section: Expression Of Fat-hippo Pathway Components In the Brainmentioning

confidence: 99%

Influence of Fat-Hippo and Notch signaling on the proliferation and differentiation of Drosophila optic neuroepithelia

2010

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The Drosophila optic lobe develops from neuroepithelial cells, which function as symmetrically dividing neural progenitors. We describe here a role for the Fat-Hippo pathway in controlling the growth and differentiation of Drosophila optic neuroepithelia. Mutation of tumor suppressor genes within the pathway, or expression of activated Yorkie, promotes overgrowth of neuroepithelial cells and delays or blocks their differentiation; mutation of yorkie inhibits growth and accelerates differentiation. Neuroblasts and other neural cells, by contrast, appear unaffected by Yorkie activation. Neuroepithelial cells undergo a cell cycle arrest before converting to neuroblasts; this cell cycle arrest is regulated by Fat-Hippo signaling. Combinations of cell cycle regulators, including E2f1 and CyclinD, delay neuroepithelial differentiation, and Fat-Hippo signaling delays differentiation in part through E2f1. We also characterize roles for Jak-Stat and Notch signaling. Our studies establish that the progression of neuroepithelial cells to neuroblasts is regulated by Notch signaling, and suggest a model in which Fat-Hippo and Jak-Stat signaling influence differentiation by their acceleration of cell cycle progression and consequent impairment of Delta accumulation, thereby modulating Notch signaling. This characterization of Fat-Hippo signaling in neuroepithelial growth and differentiation also provides insights into the potential roles of Yes-associated protein in vertebrate neural development and medullablastoma.

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Expression profile of the cadherin family in the developing Drosophila brain

Cited by 36 publications

References 100 publications

N-cadherin negatively regulates collective Drosophila glial migration via actin cytoskeleton remodeling

N-cadherin negatively regulates collective Drosophila glial migration via actin cytoskeleton remodeling

Notch regulates the switch from symmetric to asymmetric neural stem cell division in the Drosophila optic lobe

Influence of Fat-Hippo and Notch signaling on the proliferation and differentiation of Drosophila optic neuroepithelia

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