Regulation of Glia Number in Drosophila by Rap/Fzr, an Activator of the Anaphase-Promoting Complex, and Loco, an RGS Protein

Kaplow, Margarita; Korayem, Adam H.; Venkatesh, Tadmiri

doi:10.1534/genetics.107.086397

Cited by 16 publications

(19 citation statements)

References 82 publications

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“…3A; Kaplow et al 2008). Drosophila Cdh1 mutants have a significantly higher number of glial cells in the brain.…”

Section: Control Of Neurogenesis and Gliogenesis By Cdh1-apcmentioning

confidence: 99%

“…Conversely, Cdh1 overexpression in flies markedly reduces the number of glial cells. The protein Loco, a regulator of G-protein signaling, has been identified as a substrate of Cdh1-APC in the regulation of gliogenesis (Kaplow et al 2008). Cdh1 interacts with Loco in the Drosophila larva brain, leading to its ubiquitination and consequent degradation.…”

Section: Control Of Neurogenesis and Gliogenesis By Cdh1-apcmentioning

confidence: 99%

“…Cdh1 interacts with Loco in the Drosophila larva brain, leading to its ubiquitination and consequent degradation. Loss-offunction Loco mutant flies harbor a reduced number of glial cells (Kaplow et al 2008). Whether Cdh1-APC suppresses gliogenesis in the mammalian nervous system remains to be determined.…”

Section: Control Of Neurogenesis and Gliogenesis By Cdh1-apcmentioning

confidence: 99%

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A decade of the anaphase-promoting complex in the nervous system

Huang

Bonni

2016

Genes Dev.

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Control of protein abundance by the ubiquitin-proteasome system is essential for normal brain development and function. Just over a decade ago, the first post-mitotic function of the anaphase-promoting complex, a major cell cycle-regulated E3 ubiquitin ligase, was discovered in the control of axon growth and patterning in the mammalian brain. Since then, a large number of studies have identified additional novel roles for the anaphase-promoting complex in diverse aspects of neuronal connectivity and plasticity in the developing and mature nervous system. In this review, we discuss the functions and mechanisms of the anaphase-promoting complex in neurogenesis, glial differentiation and migration, neuronal survival and metabolism, neuronal morphogenesis, synapse formation and plasticity, and learning and memory. We also provide a perspective on future investigations of the anaphase-promoting complex in neurobiology.Protein degradation regulates diverse biological processes in the developing and mature nervous system. Spatial and temporal control of protein turnover and abundance influences distinct stages of neural development and function from neurogenesis and neuronal morphogenesis to synapse formation and pruning to plasticity and learning (Hegde and Upadhya 2007;Yi and Ehlers 2007;Segref and Hoppe 2009;Yamada et al. 2013). Protein degradation by the proteasome requires ubiquitination, which is mediated by the sequential action of an E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, and E3 ubiquitin ligase (Hershko and Ciechanover 1992;Scheffner et al. 1995;Ciechanover 2005;Hershko 2005;Weissman et al.

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“…3A; Kaplow et al 2008). Drosophila Cdh1 mutants have a significantly higher number of glial cells in the brain.…”

Section: Control Of Neurogenesis and Gliogenesis By Cdh1-apcmentioning

confidence: 99%

Section: Control Of Neurogenesis and Gliogenesis By Cdh1-apcmentioning

confidence: 99%

Section: Control Of Neurogenesis and Gliogenesis By Cdh1-apcmentioning

confidence: 99%

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A decade of the anaphase-promoting complex in the nervous system

Huang

Bonni

2016

Genes Dev.

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“…For example, murine CDH1 coordinates lens differentiation by targeting the transcriptional corepressor SnoN for degradation on TGF-␤ signaling (40). In Drosophila, FZR contributes to glial-neuron cell fate by targeting loco for degradation (41). Similarly, CCS52A2 function could promote the QC and/or stem cell fate.…”

Section: Apc/c Cdh1/fzr/ccs52a Complex As Cell Cycle Regulator or Dirmentioning

confidence: 99%

APC/C ^CCS52A complexes control meristem maintenance in the Arabidopsis root

Vanstraelen

Baloban

Ines

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

164

178

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Plant organs originate from meristems where stem cells are maintained to produce continuously daughter cells that are the source of different cell types. The cell cycle switch gene CCS52A, a substrate specific activator of the anaphase promoting complex/ cyclosome (APC/C), controls the mitotic arrest and the transition of mitotic cycles to endoreduplication (ER) cycles as part of cell differentiation. Arabidopsis, unlike other organisms, contains 2 CCS52A isoforms. Here, we show that both of them are active and regulate meristem maintenance in the root tip, although through different mechanisms. The CCS52A1 activity in the elongation zone of the root stimulates ER and mitotic exit, and contributes to the border delineation between dividing and expanding cells. In contrast, CCS52A2 acts directly in the distal region of the root meristem to control identity of the quiescent center (QC) cells and stem cell maintenance. Cell proliferation assays in roots suggest that this control involves CCS52A2 mediated repression of mitotic activity in the QC cells. The data indicate that the CCS52A genes favor a low mitotic state in different cell types of the root tip that is required for meristem maintenance, and reveal a previously undescribed mechanism for APC/C mediated control in plant development.CDH1 ͉ cell differentiation ͉ endoreduplication ͉ quiescent center ͉ stem cells P lant growth and development depend on the persistent activity of meristems, allowing continuous postembryonic organogenesis. In the root tip, meristem maintenance is controlled by different mechanisms that involve the maintenance of stem cells in the root meristem (RM) and spatial control over mitotic exit at the RM-elongation zone (EZ) border.In the distal RM, stem cells are maintained in an undifferentiated state by the quiescent center (QC) cells (1). The QC represents a center of mitotic inactive cells resting in an extended G 1 phase (2). The stem cells around the QC divide according to strict spatial rules, and provide cell progenies that detach from the QC and differentiate into different root cell types (3). The auxin-PLETHORA (PLT) pathway provides positional information to set up the QC and surrounding stem cells whose activities depend on WOX5 and SHORT ROOT (SHR)-SCARECROW (SCR) transcription factors (4-7).As cells reach the RM-EZ border, they start to expand and terminally differentiate. Recently, it has been demonstrated that the spatial boundary of the RM and EZ is controlled by the rate of meristematic cell differentiation at this border (8). The transition involves exit from the mitotic cycle to the endocycle (9). In eukaryotes, endoreduplication (ER) onset requires inhibition of mitotic cyclin-dependent kinase (cdk) activities (10-12). This inhibition can be achieved by multiple mechanisms, but mostly by the degradation of mitotic cyclins by the anaphase promoting complex/cyclosome (APC/C) (13-15). The APC/C is an ubiquitin ligase that regulates cell cycle progression from metaphase to S phase by targeted degradation of numerous ce...

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“…Considering that Loco is required at various developmental stages, including as neuroblast division, glial differentiation, blood-brain barrier formation and reproductive systems, 14,15,17,[29][30][31] the changes of loco expression during embryonic development may cause detrimental consequences, such as lethality of loco homozygous mutant flies. 17,31 Future studies that investigate adult-specific regulation of loco expression will reveal more levels are reduced.…”

Section: O N O T D I S T R I B U T Ementioning

confidence: 99%