<i>Drosophila</i> NAB (dNAB) is an orphan transcriptional co‐repressor required for correct CNS and eye development

Clements, Mark A.; Duncan, Dianne; Milbrandt, Jeffrey

doi:10.1002/dvdy.10209

Cited by 18 publications

(24 citation statements)

References 75 publications

(67 reference statements)

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“…klu encodes a zinc-finger protein but does not appear to interact directly with Nab (Clements et al, 2003), and we did not find evidence that nab and klu regulate each other. Surprisingly, we have found that nab misexpression rescues the phenotype of a lack of ABLKs observed in klu.…”

Section: A Genetic Cascade Involving Cas and Nab Specifies Ablk Neurocontrasting

confidence: 85%

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A genetic cascade involving klumpfuss, nab and castor specifies the abdominal leucokinergic neurons in the Drosophila CNS

et al. 2010

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SUMMARYIdentification of the genetic mechanisms underlying the specification of large numbers of different neuronal cell fates from limited numbers of progenitor cells is at the forefront of developmental neurobiology. In Drosophila, the identities of the different neuronal progenitor cells, the neuroblasts, are specified by a combination of spatial cues. These cues are integrated with temporal competence transitions within each neuroblast to give rise to a specific repertoire of cell types within each lineage. However, the nature of this integration is poorly understood. To begin addressing this issue, we analyze the specification of a small set of peptidergic cells: the abdominal leucokinergic neurons. We identify the progenitors of these neurons, the temporal window in which they are specified and the influence of the Notch signaling pathway on their specification. We also show that the products of the genes klumpfuss, nab and castor play important roles in their specification via a genetic cascade.

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Section: A Genetic Cascade Involving Cas and Nab Specifies Ablk Neurocontrasting

confidence: 85%

“…7F). In cas mutants, there is a complete loss of nab RNA and protein expression, with the exception of Nab midline expression (Baumgardt et al, 2009;Clements et al, 2003). We expressed nab in a cas mutant (elav-G4>UAS-nab cas D1 /cas D3 ), but found no evidence of rescue (Fig.…”

Section: Fig 5 Requirement For Notch Signaling In Ablk Specificatiomentioning

confidence: 92%

A genetic cascade involving klumpfuss, nab and castor specifies the abdominal leucokinergic neurons in the Drosophila CNS

et al. 2010

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“…NAB proteins comprise a family of transcriptional co-regulators implicated in various developmental processes in different organisms. Drosophila NAB was found to be required for determining specific neuronal fates in the embryonic CNS and for 1141 RESEARCH ARTICLE dNAB interacts with Brinker wing hinge patterning (Clements et al, 2003;Tsuji et al, 2008). Our work shows that dNAB induces cell elimination through induction of the JNK pathway, which in turn triggers Caspase-3-mediated apoptosis.…”

Section: Discussionmentioning

confidence: 70%

“…Through plasmid rescue of the mutagenic P-element and RNA in situ hybridization (Fig. 1B), we identified this insertion as a hypomorphic mutant allele of Drosophila nab (dnab) (Clements et al, 2003), a member of the NAB family of transcriptional co-repressors (Russo et al, 1995;Svaren et al, 1996). Complementation crosses with a known lethal deletion allele (dnab…”

Section: Dnab Is a Dpp Target In The Wing Discmentioning

confidence: 99%

The co-regulator dNAB interacts with Brinker to eliminate cells with reduced Dpp signaling

et al. 2009

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The proper development of tissues requires morphogen activity that dictates the appropriate growth and differentiation of each cell according to its position within a developing field. Elimination of underperforming cells that are less efficient in receiving/transducing the morphogenetic signal is thought to provide a general fail-safe mechanism to avoid developmental misspecification. In the developing Drosophila wing, the morphogen Dpp provides cells with growth and survival cues. Much of the regulation of transcriptional output by Dpp is mediated through repression of the transcriptional repressor Brinker (Brk), and thus through the activation of target genes. Mutant cells impaired for Dpp reception or transduction are lost from the wing epithelium. At the molecular level, reduced Dpp signaling results in Brk upregulation that triggers apoptosis through activation of the JNK pathway. Here we show that the transcriptional co-regulator dNAB is a Dpp target in the developing wing that interacts with Brk to eliminate cells with reduced Dpp signaling through the JNK pathway. We further show that both dNAB and Brk are required for cell elimination induced by differential dMyc expression, a process that depends on reduced Dpp transduction in outcompeted cells. We propose a novel mechanism whereby the morphogen Dpp regulates the responsiveness to its own survival signal by inversely controlling the expression of a repressor, Brk, and its co-repressor, dNAB.KEY WORDS: Brinker, Dpp survival signal, Wing development, dMyc (Dm)-induced cell competition, dNAB (Drosophila Nab)

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“…, cas , eagle-GAL4 , MZ360-eagle-GAL4 (Dittrich et al, 1997), worniu-GAL4 , pdm ED773 and UAS-pdm (Grosskortenhaus et al, 2006), nab SH143 and UAS-nab (Terriente Felix et al, 2007), nab G26 (Clements et al, 2003), sqz ie (Allan et al, 2003), sqz…”

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confidence: 99%

Neuroblast entry into quiescence is regulated intrinsically by the combined action of spatial Hox proteins and temporal identity factors

2008

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Neural stem cell quiescence is an important feature in invertebrate and mammalian central nervous system development, yet little is known about the mechanisms regulating entry into quiescence, maintenance of cell fate during quiescence, and exit from quiescence. Drosophila neural stem cells (called neuroblasts) provide an excellent model system for investigating these issues. Drosophila neuroblasts enter quiescence at the end of embryogenesis and resume proliferation during larval stages; however, no single neuroblast lineage has been traced from embryo into larval stages. Here, we establish a model neuroblast lineage, NB3-3, which allows us to reproducibly observe lineage development from neuroblast formation in the embryo, through quiescence, to the resumption of proliferation in larval stages. Using this new model lineage, we show a continuous sequence of temporal changes in the neuroblast, defined by known and novel temporal identity factors, running from embryonic through larval stages, and that quiescence suspends but does not alter the order of neuroblast temporal gene expression. We further show that neuroblast entry into quiescence is regulated intrinsically by two independent controls: spatial control by the Hox proteins Antp and Abd-A, and temporal control by previously identified temporal transcription factors and the transcription co-factor Nab.

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Drosophila NAB (dNAB) is an orphan transcriptional co‐repressor required for correct CNS and eye development

Cited by 18 publications

References 75 publications

A genetic cascade involving klumpfuss, nab and castor specifies the abdominal leucokinergic neurons in the Drosophila CNS

A genetic cascade involving klumpfuss, nab and castor specifies the abdominal leucokinergic neurons in the Drosophila CNS

The co-regulator dNAB interacts with Brinker to eliminate cells with reduced Dpp signaling

Neuroblast entry into quiescence is regulated intrinsically by the combined action of spatial Hox proteins and temporal identity factors

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