Dynactin is required to maintain nuclear position within postmitotic<i>Drosophila</i>photoreceptor neurons

Whited, Jessica L.; Cassell, Andre; Brouillette, Monique; Garrity, Paul

doi:10.1242/dev.01366

Cited by 63 publications

(64 citation statements)

References 57 publications

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“…CPs are thought to stabilize the barbed end of the Arp1 microfilament in the Dynactin complex, which is required for transport along microtubules (Schafer et al, 1994). cpa and cpb, like other Dynactin complex subunits, are required to maintain the position of nuclei in Drosophila photoreceptor neurons (Whited et al, 2004) (and data not shown). However, removal of kinesin heavy chain (khc), which counteracts Dynein/Dynactin-based transport, failed to rescue extrusion of cpa mutant cells in the wing disc (see Fig.…”

Section: Actin Capping Proteins Maintain Epithelial Integritymentioning

confidence: 97%

Actin capping protein α maintainsvestigial-expressing cells within theDrosophilawing disc epithelium

Janody

Treisman

2006

Development

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Tissue patterning must be translated into morphogenesis through cell shape changes mediated by remodeling of the actin cytoskeleton. We have found that Capping protein ␣ (Cpa) and Capping protein ␤ (Cpb), which prevent extension of the barbed ends of actin filaments, are specifically required in the wing blade primordium of the Drosophila wing disc. cpa or cpb mutant cells in this region, but not in the remainder of the wing disc, are extruded from the epithelium and undergo apoptosis. Excessive actin filament polymerization is not sufficient to explain this phenotype, as loss of Cofilin or Cyclase-associated protein does not cause cell extrusion or death. Misexpression of Vestigial, the transcription factor that specifies the wing blade, both increases cpa transcription and makes cells dependent on cpa for their maintenance in the epithelium. Our results suggest that Vestigial specifies the cytoskeletal changes that lead to morphogenesis of the adult wing.

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Section: Actin Capping Proteins Maintain Epithelial Integritymentioning

confidence: 97%

Actin capping protein α maintainsvestigial-expressing cells within theDrosophilawing disc epithelium

Janody

Treisman

2006

Development

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“…Moreover, in photoreceptor cells the nuclei fail to move apically toward the minus-end of microtubules, and instead remain at more basal locations. Informatively, this nuclear positioning phenotype can be suppressed by mutations in subunits of Kinesin, the plus-end directed microtubule motor (Whited et al, 2004). Finally, in green alga, post-mitotic nuclear migration is mediated in part by a Kinesin-1 protein (Holzinger and Lutz-Meindl, 2002).…”

Section: Proteins For Movingmentioning

confidence: 99%

Nuclear migration during retinal development

2008

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In this review we focus on the mechanisms, regulation, and cellular consequences of nuclear migration in the developing retina. In the nervous system, nuclear migration is prominent during both proliferative and post-mitotic phases of development. Interkinetic nuclear migration is the process where the nucleus oscillates from the apical to basal surfaces in proliferative neuroepithelia. Proliferative nuclear movement occurs in step with the cell cycle, with M-phase being confined to the apical surface and G1-, S-, and G2-phases occurring at more basal locations. Later, following cell cycle exit, some neuron precursors migrate by nuclear translocation. In this mode of cellular migration, nuclear movement is the driving force for motility. Following discussion of the key components and important regulators for each of these processes, we present an emerging model where interkinetic nuclear migration functions to distinguish cell fates among retinal neuroepithelia. Keywordsinterkinetic nuclear migration; nuclear translocation; nucleokinesis; neurogenesis; dynein; cell cycle; cell behavior OverviewNeuronal development is regulated by a complex array of intrinsic and extrinsic signals that act on progenitor neuroepithelial cells to ensure the correct cell type is generated in the right numbers and at the appropriate time of development (Donovan et al., 2005;Cayouette et al., 2006). In addition, multiple signaling cues are integrated in post-mitotic neuronal precursors to facilitate directed cell migration and correct laminar positioning (Malicki et al., 2004). This spatial and temporal regulation of neuronal cell-type fate commitment and histogenesis is dependent on the regulation of the mitotic cell cycle, and in particular at the level of cell cycle exit (Ohnuma and Harris, 2003). Recent data suggest that nuclear migration is a critical process for several aspects of neuronal development, including that of the neural retina. The focus of this review is on interkinetic nuclear migration and nuclear translocation during retinogenesis, although much of what we know is from observations in other regions of the developing nervous system. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript Interkinetic nuclear migrationInterkinetic nuclear migration is the proliferative cell behavior where the nuclei of neuroepithelial cells migrate in an apical-basal manner and in phase with the cell cycle (Frade 2002). Neuroepithelial cell divisions are confined to apical locations while S-phase occu...

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“…Other antibodies were obtained from DSHB (University of Iowa, IA, USA). Immunoblotting and immunohistochemistry were as described previously (Sears et al, 2003;Whited et al, 2004).…”

Section: Histology and Immunoblottingmentioning

confidence: 99%

Ptpmeg is required for the proper establishment and maintenance of axon projections in the central brain ofDrosophila

et al. 2007

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Ptpmeg is a cytoplasmic tyrosine phosphatase containing FERM and PDZ domains. Drosophila Ptpmeg and its vertebrate homologs PTPN3 and PTPN4 are expressed in the nervous system, but their developmental functions have been unknown. We found that ptpmeg is involved in neuronal circuit formation in the Drosophila central brain, regulating both the establishment and the stabilization of axonal projection patterns. In ptpmeg mutants, mushroom body (MB) axon branches are elaborated normally, but the projection patterns in many hemispheres become progressively abnormal as the animals reach adulthood. The two branches of MB ␣/␤ neurons are affected by ptpmeg in different ways; ptpmeg activity inhibits ␣ lobe branch retraction while preventing ␤ lobe branch overextension. The phosphatase activity of Ptpmeg is essential for both ␣ and ␤ lobe formation, but the FERM domain is required only for preventing ␣ lobe retraction, suggesting that Ptpmeg has distinct roles in regulating the formation of ␣ and ␤ lobes. ptpmeg is also important for the formation of the ellipsoid body (EB), where it influences the pathfinding of EB axons. ptpmeg function in neurons is sufficient to support normal wiring of both the EB and MB. However, ptpmeg does not act in either MB or EB neurons, implicating ptpmeg in the regulation of cell-cell signaling events that control the behavior of these axons.

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Dynactin is required to maintain nuclear position within postmitoticDrosophilaphotoreceptor neurons

Cited by 63 publications

References 57 publications

Actin capping protein α maintainsvestigial-expressing cells within theDrosophilawing disc epithelium

Actin capping protein α maintainsvestigial-expressing cells within theDrosophilawing disc epithelium

Nuclear migration during retinal development

Ptpmeg is required for the proper establishment and maintenance of axon projections in the central brain ofDrosophila

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