Relevant bibliographies by topics / Egl-15

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  2. Dissertations / Theses

Academic literature on the topic 'Egl-15'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "Egl-15"

1

Schutzman, Jennifer L., Christina Z. Borland, John C. Newman, Matthew K. Robinson, Michelle Kokel, and Michael J. Stern. "The Caenorhabditis elegans EGL-15 Signaling Pathway Implicates a DOS-Like Multisubstrate Adaptor Protein in Fibroblast Growth Factor Signal Transduction." Molecular and Cellular Biology 21, no. 23 (December 1, 2001): 8104–16. http://dx.doi.org/10.1128/mcb.21.23.8104-8116.2001.

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ABSTRACT EGL-15 is a fibroblast growth factor receptor in the nematodeCaenorhabditis elegans. Components that mediate EGL-15 signaling have been identified via mutations that confer a Clear (Clr) phenotype, indicative of hyperactivity of this pathway, or a suppressor-of-Clr (Soc) phenotype, indicative of reduced pathway activity. We have isolated a gain-of-function allele of let-60 ras that confers a Clr phenotype and implicated bothlet-60 ras and components of a mitogen-activated protein kinase cascade in EGL-15 signaling by their Soc phenotype. Epistasis analysis indicates that the gene soc-1 functions in EGL-15 signaling by acting either upstream of or independently of LET-60 RAS. soc-1 encodes a multisubstrate adaptor protein with an amino-terminal pleckstrin homology domain that is structurally similar to the DOS protein in Drosophilaand mammalian GAB1. DOS is known to act with the cytoplasmic tyrosine phosphatase Corkscrew (CSW) in signaling pathways inDrosophila. Similarly, the C. elegans CSW ortholog PTP-2 was found to be involved in EGL-15 signaling. Structure-function analysis of SOC-1 and phenotypic analysis of single and double mutants are consistent with a model in which SOC-1 and PTP-2 act together in a pathway downstream of EGL-15 and the Src homology domain 2 (SH2)/SH3-adaptor protein SEM-5/GRB2 contributes to SOC-1-independent activities of EGL-15.
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Burdine, R. D., C. S. Branda, and M. J. Stern. "EGL-17(FGF) expression coordinates the attraction of the migrating sex myoblasts with vulval induction in C. elegans." Development 125, no. 6 (March 15, 1998): 1083–93. http://dx.doi.org/10.1242/dev.125.6.1083.

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During the development of the egg-laying system in Caenorhabditis elegans hermaphrodites, central gonadal cells organize the alignment of the vulva with the sex myoblasts, the progenitors of the egg-laying muscles. A fibroblast growth factor [EGL-17(FGF)] and an FGF receptor [EGL-15(FGFR)] are involved in the gonadal signals that guide the migrations of the sex myoblasts. Here we show that EGL-17(FGF) can act as an instructive guidance cue to direct the sex myoblasts to their final destinations. We find that egl-17 reporter constructs are expressed in the primary vulval cell and that EGL-17(FGF) expression in this cell correlates with the precise positioning of the sex myoblasts. We postulate that EGL-17(FGF) helps to coordinate the development of a functional egg-laying system, linking vulval induction with proper sex myoblast migration.
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Kuroyanagi, Hidehito, Genta Ohno, Shohei Mitani, and Masatoshi Hagiwara. "The Fox-1 Family and SUP-12 Coordinately Regulate Tissue-Specific Alternative Splicing In Vivo." Molecular and Cellular Biology 27, no. 24 (October 8, 2007): 8612–21. http://dx.doi.org/10.1128/mcb.01508-07.

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ABSTRACT Many pre-mRNAs are alternatively spliced in a tissue-specific manner in multicellular organisms. The Fox-1 family of RNA-binding proteins regulate alternative splicing by either activating or repressing exon inclusion through specific binding to UGCAUG stretches. However, the precise cellular contexts that determine the action of the Fox-1 family in vivo remain to be elucidated. We have recently demonstrated that ASD-1 and FOX-1, members of the Fox-1 family in Caenorhabditis elegans, regulate tissue-specific alternative splicing of the fibroblast growth factor receptor gene, egl-15, which eventually determines the ligand specificity of the receptor in vivo. Here we report that another RNA-binding protein, SUP-12, coregulates the egl-15 alternative splicing. By screening for mutants defective in the muscle-specific expression of our alternative splicing reporter, we identified the muscle-specific RNA-binding protein SUP-12. We identified juxtaposed conserved stretches as the cis elements responsible for the regulation. The Fox-1 family and the SUP-12 proteins form a stable complex with egl-15 RNA, depending on the cis elements. Furthermore, the asd-1; sup-12 double mutant is defective in sex myoblast migration, phenocopying the isoform-specific egl-15(5A) mutant. These results establish an in vivo model that coordination of the two families of RNA-binding proteins regulates tissue-specific alternative splicing of a specific target gene.
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Sundaram, M., J. Yochem, and M. Han. "A Ras-mediated signal transduction pathway is involved in the control of sex myoblast migration in Caenorhabditis elegans." Development 122, no. 9 (September 1, 1996): 2823–33. http://dx.doi.org/10.1242/dev.122.9.2823.

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Sex myoblast migration in the Caenorhabditis elegans hermaphrodite represents a simple, genetically amenable model system for studying how cell migration is regulated during development. Two separable components of sex myoblast guidance have been described: a gonad-independent mechanism sufficient for the initial anterior migration to the mid-body region, and a gonad-dependent mechanism required for precise final positioning (J. H. Thomas, M. J. Stern and H. R. Horvitz (1990) Cell 62, 1041–1052). Here, we demonstrate a role for a Ras-mediated signal transduction pathway in controlling sex myoblast migration. Loss-of-function mutations in let-60 ras, ksr-1, lin-45 raf, let-537/mek-2 or sur-1/mpk-1 cause defects in sex myoblast final positions that resemble those seen in gonad-ablated animals, while constitutively active let-60 ras(G13E) trans-genes allow fairly precise positioning to occur in the absence of the gonad. A mosaic analysis demonstrated that let-60 ras is required within the sex myoblasts to control proper positioning. Our results suggest that gonadal signals normally stimulate let-60 ras activity in the sex myoblasts, thereby making them competent to sense or respond to positional cues that determine the precise endpoint of migration. let-60 ras may have additional roles in sex myoblast guidance as well. Finally, we have also investigated genetic interactions between let-60 ras and other genes important for sex myoblast migration, including egl-15, which encodes a fibroblast growth factor receptor tyrosine kinase (D. L. DeVore, H. R. Horvitz and M. J. Stern (1995) Cell 83, 611–623). Since mutations reducing Ras pathway activity cause a different phenotype than those reducing egl-15 activity and since constitutive Ras activity only partially suppresses the migration defects of egl-15 mutants, we argue that let-60 ras and egl-15 do not act together in a single linear pathway.
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5

Desai, C., and H. R. Horvitz. "Caenorhabditis elegans mutants defective in the functioning of the motor neurons responsible for egg laying." Genetics 121, no. 4 (April 1, 1989): 703–21. http://dx.doi.org/10.1093/genetics/121.4.703.

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Abstract We have isolated and characterized 45 Caenorhabditis elegans mutants presumed to be defective in the functioning of the hermaphrodite-specific neurons (HSNs). Like hermaphrodites that lack the HSN motor neurons, these mutants are egg-laying defective and do not lay eggs in response to exogenous imipramine but do lay eggs in response to exogenous serotonin. Twenty of the 45 mutations define 10 new egl genes; the other 25 mutations are alleles of five previously defined genes, four of which are known to affect the HSNs. Seven mutations in three genes cause the HSNs to die in hermaphrodites, as they normally do in males. These genes appear to be involved in the determination of the sexual phenotype of the HSNs, and one of them (egl-41) is a newly identified gene that may function generally in sex determination. Five of the 15 genes are defined only by mutations that have dominant effects on egg laying. One gene egl(n1108), is defined by a temperature-sensitive allele that has a temperature-sensitive period after HSN development is complete, suggesting that egl(n1108) may be involved in HSN synaptic transmission. Four of the genes are defined by single alleles, which suggests that other such genes remain to be discovered. Mutations in no more than 4 of the 15 genes specifically affect the HSNs, indicating that there are few genes with functions needed only in this single type of nerve cell.
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6

Hoffmann, Michael, Christoph Segbert, Gisela Helbig, and Olaf Bossinger. "Intestinal tube formation in Caenorhabditis elegans requires vang-1 and egl-15 signaling." Developmental Biology 339, no. 2 (March 2010): 268–79. http://dx.doi.org/10.1016/j.ydbio.2009.12.002.

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7

Szewczyk, N. J. "Activated EGL-15 FGF receptor promotes protein degradation in muscles of Caenorhabditis elegans." EMBO Journal 22, no. 19 (October 1, 2003): 5058–67. http://dx.doi.org/10.1093/emboj/cdg472.

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8

Stern, M. J., and H. R. Horvitz. "A normally attractive cell interaction is repulsive in two C. elegans mesodermal cell migration mutants." Development 113, no. 3 (November 1, 1991): 797–803. http://dx.doi.org/10.1242/dev.113.3.797.

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In wild-type Caenorhabditis elegans hermaphrodites, two bilaterally symmetric sex myoblasts (SMs) migrate anteriorly to flank the precise center of the gonad, where they divide to generate the muscles required for egg laying (J. E. Sulston and H. R. Horvitz (1977) Devl Biol. 56, 110–156). Although this migration is largely independent of the gonad, a signal from the gonad attracts the SMs to their precise final positions (J. H. Thomas, M. J. Stern and H. R. Horvitz (1990) Cell 62, 1041–1052). Here we show that mutations in either of two genes, egl-15 and egl-17, cause the premature termination of the migrations of the SMs. This incomplete migration is caused by the repulsion of the SMs by the same cells in the somatic gonad that are the source of the attractive signal in wild-type animals.
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9

Li, Menghui, Shuzhen Wang, Shuli Guo, and Zhenyu Zhang. "Endoscopic Groin Lymphadenectomy With a Thigh Approach to Gynecologic Malignancies: A Retrospective Study With 5-Year Experience." International Journal of Gynecologic Cancer 25, no. 2 (February 2015): 325–30. http://dx.doi.org/10.1097/igc.0000000000000348.

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ObjectivesThe objective of this study was to report a safe and feasible technique with endoscopic groin lymphadenectomy (EGL) through thigh approach in the treatment of different gynecologic malignancies.Study DesignConsecutive gynecological malignant patients proceeded to groin lymphadenectomy were treated by this technique over a 5-year period (2005 to 2010). Data regarding the surgical perioperative complications were recorded.ResultsEleven patients with 21 EGL were performed. Procedures included bilateral groin lymphadenectomy (n = 10) and left groin lymphadenectomy (n = 1). The median patient age and body mass index were 61 years and 25.2, respectively. The median operational time, which includes the dissection of both groins and the other procedures, was 210 minutes. The median blood loss was 200 mL. The median number of retrieved lymph nodes was 13 (range, 8–26), and all of these are histologically negative. No intraoperative complications occurred. One patient was noted in cutaneous cellulitis on the right side of the patient with clinical resolution 15 days after surgery. There were no perioperative mortalities. All the cutaneous scars were healed without wound breakdown. There were no perioperative mortalities. At the latest follow-up, all patients were completely satisfied with the cosmetic results.ConclusionsIn this study, we first report EGL with a thigh approach in gynecologic malignancies; it is a safe and feasible technique, for groin nodal dissection, with low risks of morbidity of the skin and legs. A larger prospective study with long-term and survival analyses is warranted.
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10

Polanska, Urszula M., Laurence Duchesne, Janet C. Harries, David G. Fernig, and Tarja K. Kinnunen. "N-Glycosylation Regulates Fibroblast Growth Factor Receptor/EGL-15 Activity in Caenorhabditis elegans in Vivo." Journal of Biological Chemistry 284, no. 48 (October 2, 2009): 33030–39. http://dx.doi.org/10.1074/jbc.m109.058925.

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Dissertations / Theses on the topic "Egl-15"

1

Kim, Shinhye. "Molecular mechanism of the Fibroblast Growth Factor Receptor, egl-15, and α-integrin receptor, ina-1, in gland cell migration during embryonic development of the Caenorhabditis elegans pharynx." 2015. http://hdl.handle.net/1993/30238.

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Caenorhabditis elegans is a powerful tool to study cellular migration and morphogenesis during organ development. During pharynx development, the dorsal gland cell, g1p, is born in the anterior aspect of the pharyngeal primordium and undergoes a form of morphogenesis called retrograde extension. egl-15, the single Fibroblast Growth Factor Receptor (FGFR) in C. elegans and ina-1, one of two α-integrin receptors, are both required for the proper extension or migration of g1p cell. Mutations in either egl-15 or ina-1 show similar gland cell over-migration defects where the gland cell body migrates past the terminal bulb and is located in proximity of the intestine. The kinase domain of EGL-15 was found to be required for migration and transgenic rescue strategies were used to determine the tissue of EGL-15 function. RNA interference was used to determine if egl-15 and ina-1 are functioning in the same pathway to regulate gland cell migration.
February 2015
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