The spatial and temporal expression pattern of sevenless is exclusively controlled by gene-internal elements.

Basler, Konrad; Siegrist, Patrick T.; Hafen, Ernst

doi:10.1002/j.1460-2075.1989.tb08367.x

Cited by 95 publications

(60 citation statements)

References 24 publications

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“…Our approach to investigating the functional role of each of the domains of CSW was to introduce domain-specific mutations into a construct that contained a csw cDNA expressed under the control of a hybrid sevenless enhancer/heat shock promoter transcriptional control element (16). This transcription unit (SE) directs constitutive expression in a subset of cells in the Drosphila eye, including the photoreceptor R7, R3, and R4 precursor cells and all four of the cone cell precursors.…”

Section: Resultsmentioning

confidence: 99%

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Mutational Analysis of the SRC Homology 2 Domain Protein-tyrosine Phosphatase Corkscrew

Allard¹,

Herbst²,

Carroll

et al. 1998

Journal of Biological Chemistry

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The SRC homology 2 (SH2) domain protein-tyrosine phosphatase, Corkscrew (CSW) is required for signaling by receptor tyrosine kinases, including the Sevenless receptor tyrosine kinase (SEV), which directs Drosophila R7 photoreceptor cell development. To investigate the role of the different domains of CSW, we constructed domain-specific csw mutations and assayed their effects on CSW function. Our results indicate that CSW SH2 domain function is essential, but either CSW SH2 domain can fulfill this requirement. We also found that CSW and activated SEV are associated in vivo in a manner that does not require either CSW SH2 domain function or tyrosine phosphorylation of SEV. In contrast, the interaction between CSW and Daughter of Sevenless, a CSW substrate, is dependent on SH2 domain function. These results suggest that the role of the CSW SH2 domains during SEV signaling is to bind Daughter of Sevenless rather than activated SEV. We also found that although CSW protein-tyrosine phosphatase activity is required for full CSW function, a catalytically inactive CSW is capable of providing partial function. In addition, we found that deletion of either the CSW proteintyrosine phosphatase insert or the entire CSW carboxyl terminus, which includes a conserved DRK/GRB2 SH2 domain binding sequence, does not abolish CSW function. Receptor tyrosine kinases (RTKs)1 regulate cellular growth and differentiation in response to extracellular signals. The binding of a specific ligand to the extracellular domain of an RTK leads to a well characterized series of biochemical events, including RTK dimerization, activation of the cytoplasmic tyrosine kinase domain, and phosphorylation of the RTK on specific tyrosine residues (reviewed in Ref. 1). The activated and phosphorylated RTK then regulates key cellular target proteins. Frequently, these targets contain either SRC homology 2 (SH2) domains or phosphotyrosine binding domains that bind to specific phosphorylated tyrosine residues of the RTK. The recruitment of such SH2-and phosphotyrosine binding domain-containing proteins regulates their function and leads to the activation of important intracellular signaling pathways. For example, the interaction of the SH2 domain-containing protein GRB2 with activated RTKs leads to the stimulation of the RAS pathways (2, 3).Among the key signaling proteins, the function of which is required during RTK signaling, is a class of protein-tyrosine phosphatases that includes SHP2 in mammals and Corkscrew (CSW) in Drosophila (reviewed in Ref. 4). In addition to their protein-tyrosine phosphatase (PTP) domains, these proteins are characterized by the presence of two SH2 domains at their amino terminus and a poorly conserved carboxyl-terminal "tail" region. In addition, CSW contains a domain of approximately 150 amino acids that interrupts its PTP domain and is not present in SHP2 (5). The first evidence that SHP2/CSW proteins were important for RTK signaling came from the identification of CSW as a maternally contributed, positively acting component du...

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Section: Resultsmentioning

confidence: 99%

“…The csw mutant cDNAs were subcloned into the transformation vector pKB267, which contains a hybrid promoter (SE) consisting of sevenless enhancers and the hsp70 promoter (16). This vector directs gene expression in a subset of cells in the eye, including R3, R4, and R7, as well as general expression in all cells following heat shock induction.…”

Section: Methodsmentioning

confidence: 99%

Mutational Analysis of the SRC Homology 2 Domain Protein-tyrosine Phosphatase Corkscrew

Allard¹,

Herbst²,

Carroll

et al. 1998

Journal of Biological Chemistry

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“…If tissue-specific RNAi knockdown produced PCP defects, we increased the phenotype by coexpressing UAS-dicer2 and/or, increasing transgene copy numbers or by elevating the temperature to enhance the activity of the GAL4/UAS system. Specific fly strains used: sev-GAL4 (Basler et al 1989), gift from K. Basler; Rh1-GFP, gift from F. Pichaud (Pichaud and Desplan 2001); UAS-dgo; sev-GAL4 (K. Gaengel and M. Mlodzik, unpub-lished results); UAS-pk sple , gift from D. Gubb, (Gubb et al 1999); Vang stbmX gift from Nuria Paricio; DrosDel deficiencies were received from Szeged (now distributed by the Bloomington Stock Center, Ryder et al 2007); Exelixis deficiencies (distributed by FlyBase, were from Harvard University/Exelixis) (Parks et al 2004); sev-Dsh (2x) and sev-Fz (Boutros et al 1998).…”

Section: Fly Stocks and Genetic Screenmentioning

confidence: 99%

Novel Regulators of Planar Cell Polarity: A Genetic Analysis in Drosophila

Weber

Gault²,

Olguı́n

et al. 2012

Genetics

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Planar cell polarity (PCP) is a common feature of many epithelia and epithelial organs. Although progress has been made in the dissection of molecular mechanisms regulating PCP, many questions remain. Here we describe a screen to identify novel PCP regulators in Drosophila. We employed mild gain-of-function (GOF) phenotypes of two cytoplasmic Frizzled (Fz)/PCP core components, Diego (Dgo) and Prickle (Pk), and screened these against the DrosDel genome-wide deficiency collection for dominant modifiers. Positive genomic regions were rescreened and narrowed down with smaller overlapping deficiencies from the Exelixis collection and RNAi-mediated knockdown applied to individual genes. This approach isolated new regulators of PCP, which were confirmed with loss-of-function analyses displaying PCP defects in the eye and/or wing. Furthermore, knockdown of a subset was also sensitive to dgo dosage or dominantly modified a dishevelled (dsh) GOF phenotype, supporting a role in Fz/PCP-mediated polarity establishment. Among the new "PCP" genes we identified several kinases, enzymes required for lipid modification, scaffolding proteins, and genes involved in substrate modification and/or degradation. Interestingly, one of them is a member of the Meckel-Gruber syndrome factors, associated with human ciliopathies, suggesting an important role for cell polarity in nonciliated cells.

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“…The sev enhancer directs expression within the R3, R4, R1, R6, Ready 1987). Thus it is likely that CBP is blocking an inhibitory signal, therefore committing the mystery cells and R7 photoreceptors and cone cells (Basler et al 1989;Bowtell et al 1991). Expression of the CBP to a photoreceptor cell fate.…”

Section: Generation Of Mosaic Clonesmentioning

confidence: 99%

CREB Binding Protein Functions During Successive Stages of Eye Development in Drosophila

et al. 2004

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During the development of the compound eye of Drosophila several signaling pathways exert both positive and inhibitory influences upon an array of nuclear transcription factors to produce a near-perfect lattice of unit eyes or ommatidia. Individual cells within the eye are exposed to many extracellular signals, express multiple surface receptors, and make use of a large complement of cell-subtype-specific DNA-binding transcription factors. Despite this enormous complexity, each cell will make the correct developmental choice and adopt the appropriate cell fate. How this process is managed remains a poorly understood paradigm. Members of the CREB binding protein (CBP)/p300 family have been shown to influence development by (1) acting as bridging molecules between the basal transcriptional machinery and specific DNA-binding transcription factors, (2) physically interacting with terminal members of signaling cascades, (3) acting as transcriptional coactivators of downstream target genes, and (4) playing a key role in chromatin remodeling. In a screen for new genes involved in eye development we have identified the Drosophila homolog of CBP as a key player in both eye specification and cell fate determination. We have used a variety of approaches to define the role of CBP in eye development on a cell-by-cell basis.T HE near-perfect ensemble of unit eyes or ommatidia tor followed by the stereotyped addition of the R2/5, R3/4, and R1/6 cell pairs. The R7 neuron is the last composing the compound eye of Drosophila melanogaster is the result of a carefully choreographed series of photoreceptor to be recruited and is then followed by the addition of accessory cone and pigment cells (Ready morphogenetic movements, cell-specific gene expression patterns, and cell-cell communications (Ready et al. 1976; Heberlein et al. 1993; Ma et al. 1993; Henuclear factors collectively termed the "eye specification berlein and Moses

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The spatial and temporal expression pattern of sevenless is exclusively controlled by gene-internal elements.

Cited by 95 publications

References 24 publications

Mutational Analysis of the SRC Homology 2 Domain Protein-tyrosine Phosphatase Corkscrew

Mutational Analysis of the SRC Homology 2 Domain Protein-tyrosine Phosphatase Corkscrew

Novel Regulators of Planar Cell Polarity: A Genetic Analysis in Drosophila

CREB Binding Protein Functions During Successive Stages of Eye Development in Drosophila

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