Journal articles: 'Egl-15'

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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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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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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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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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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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11

Li, Yanyan, Ji Feng, Hailong Liu, Lin Wang, Tom Hsiang, Xihong Li, and Junbin Huang. "Genetic Diversity and Pathogenicity of Ralstonia solanacearum Causing Tobacco Bacterial Wilt in China." Plant Disease 100, no. 7 (July 2016): 1288–96. http://dx.doi.org/10.1094/pdis-04-15-0384-re.

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Bacterial wilt caused by Ralstonia solanacearum is the most serious soilborne disease of tobacco (Nicotiana tabacum) in China. In this study, 89 strains were collected in 2012 to 2014 from across the four major tobacco-growing areas in China. The strains were identified as phylotype I by multiplex polymerase chain reaction and further divided into seven sequevars based on polymorphisms in the endoglucanase (egl) gene. Among the seven sequevars, four (15, 17, 34, and 44) have been previously described as pathogens of tobacco and two (13 and 14), which are reported here on tobacco, were previously found only on other plants. In addition, a new sequevar named 54 was identified. Strains from tobacco from different regions showed different levels of genetic diversity based on partial egl gene sequences. The farther north the distribution, the lower the gene diversity found. Pathogenicity of 27 representative strains was assessed by inoculation onto three tobacco cultivars of varying susceptibility. Through cluster analysis of area under the disease progress curve values, the 27 strains were classified into different pathotypes based on virulence; however, no obvious associations were found between sequevar and pathotype. These results will assist in determining geographical distribution of strains, and provide the foundation for breeding and integrated management programs in China.

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12

Goodman, S. J. "Alternative splicing affecting a novel domain in the C. elegans EGL-15 FGF receptor confers functional specificity." Development 130, no. 16 (August 15, 2003): 3757–66. http://dx.doi.org/10.1242/dev.00604.

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Díaz-Balzac, Carlos A., María I. Lázaro-Peña, Gibram A. Ramos-Ortiz, and Hannes E. Bülow. "The Adhesion Molecule KAL-1/anosmin-1 Regulates Neurite Branching through a SAX-7/L1CAM–EGL-15/FGFR Receptor Complex." Cell Reports 11, no. 9 (June 2015): 1377–84. http://dx.doi.org/10.1016/j.celrep.2015.04.057.

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Bolvar, J., J. R. Huynh, H. Lpez-Schier, C. Gonzlez, D. St Johnston, and A. Gonzlez-Reyes. "Centrosome migration into the Drosophila oocyte is independent of BicD and egl, and of the organisation of the microtubule cytoskeleton." Development 128, no. 10 (May 15, 2001): 1889–97. http://dx.doi.org/10.1242/dev.128.10.1889.

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During early Drosophila oogenesis, one cell from a cyst of 16 germ cells is selected to become the oocyte, and accumulates oocyte-specific proteins and the centrosomes from the other 15 cells. Here we show that the microtubule cytoskeleton and the centrosomes follow the same stepwise restriction to one cell as other oocyte markers. Surprisingly, the centrosomes still localise to one cell after colcemid treatment, and in BicD and egl mutants, which abolish the localisation of all other oocyte markers and the polarisation of the microtubule cytoskeleton. In contrast, the centrosomes fail to migrate in cysts mutant for Dynein heavy chain 64C, which disrupts the fusome. Thus, centrosome migration is independent of the organisation of the microtubule cytoskeleton, and seems to depend instead on the polarity of the fusome.

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Theurkauf, W. E., B. M. Alberts, Y. N. Jan, and T. A. Jongens. "A central role for microtubules in the differentiation of Drosophila oocytes." Development 118, no. 4 (August 1, 1993): 1169–80. http://dx.doi.org/10.1242/dev.118.4.1169.

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Drosophila oocytes develop within cysts containing 16 cells that are interconnected by cytoplasmic bridges. Although the cysts are syncytial, the 16 cells differentiate to form a single oocyte and 15 nurse cells, and several mRNAs that are synthesized in the nurse cells accumulate specifically in the oocyte. To gain insight into the mechanisms that generate the cytoplasmic asymmetry within these cysts, we have examined cytoskeletal organization during oocyte differentiation. Shortly after formation of the 16 cell cysts, a prominent microtubule organizing center (MTOC) is established within the syncytial cytoplasm, and at the time the oocyte is determined, a single microtubule cytoskeleton connects the oocyte with the remaining 15 cells of each cyst. Recessive mutations at the Bicaudal-D (Bic-D) and egalitarian (egl) loci, which block oocyte differentiation, disrupt formation and maintenance of this polarized microtubule cytoskeleton. Microtubule assembly-inhibitors phenocopy these mutations, and prevent oocyte-specific accumulation of oskar, cyclin B and 65F mRNAs. We propose that formation of the polarized microtubule cytoskeleton is required for oocyte differentiation, and that this structure mediates the asymmetric accumulation of mRNAs within the syncytial cysts.

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Huang, Jichang, Zhen Wu, and Xumin Zhang. "Short-Term Mild Temperature-Stress-Induced Alterations in the C. elegans Phosphoproteome." International Journal of Molecular Sciences 21, no. 17 (September 3, 2020): 6409. http://dx.doi.org/10.3390/ijms21176409.

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Exposure to mild early-life stresses can slow down aging, and protein phosphorylation might be an essential regulator in this process. However, the mechanisms of phosphorylation-based signaling networks during mild early-life stress remain elusive. Herein, we systematically analyzed the phosphoproteomes of Caenorhabditis elegans, which were treated with three mild temperatures (15 °C, 20 °C, and 25 °C) in two different short-term groups (10 min and 60 min). By utilizing an iTRAQ-based quantitative phosphoproteomic approach, 18,187 phosphosites from 3330 phosphoproteins were detected in this study. Volcano plots illustrated that the phosphorylation abundance of 374 proteins and 347 proteins, were significantly changed at 15 °C and 25 °C, respectively. Gene ontology, KEGG pathway and protein-protein interaction network analyses revealed that these phosphoproteins were primarily associated with metabolism, translation, development, and lifespan determination. A motif analysis of kinase substrates suggested that MAPK, CK, and CAMK were most likely involved in the adaption processes. Moreover, 16 and 14 aging-regulated proteins were found to undergo phosphorylation modifications under the mild stresses of 15 °C and 25 °C, respectively, indicating that these proteins might be important for maintaining long-term health. Further lifespan experiments confirmed that the candidate phosphoproteins, e.g., EGL-27 and XNP-1 modulated longevity at 15 °C, 20 °C, and 25 °C, and they showed increased tolerance to thermal and oxidative stresses. In conclusion, our findings offered data that supports understanding of the phosphorylation mechanisms involved in mild early-life stresses in C. elegans. Data are available via ProteomeXchange with identifier PXD021081.

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Dinkova, Tzvetanka D., Brett D. Keiper, Nadejda L. Korneeva, Eric J. Aamodt, and Robert E. Rhoads. "Translation of a Small Subset of Caenorhabditis elegans mRNAs Is Dependent on a Specific Eukaryotic Translation Initiation Factor 4E Isoform." Molecular and Cellular Biology 25, no. 1 (January 1, 2005): 100–113. http://dx.doi.org/10.1128/mcb.25.1.100-113.2005.

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ABSTRACT The mRNA cap-binding protein eukaryotic translation initiation factor 4E (eIF4E) participates in protein synthesis initiation, translational repression of specific mRNAs, and nucleocytoplasmic shuttling. Multiple isoforms of eIF4E are expressed in a variety of organisms, but their specific roles are poorly understood. We investigated one Caenorhabditis elegans isoform, IFE-4, which has homologues in plants and mammals. IFE-4::green fluorescent protein (GFP) was expressed in pharyngeal and tail neurons, body wall muscle, spermatheca, and vulva. Knockout of ife-4 by RNA interference (RNAi) or a null mutation produced a pleiotropic phenotype that included egg-laying defects. Sedimentation analysis demonstrated that IFE-4, but not IFE-1, was present in 48S initiation complexes, indicating that it participates in protein synthesis initiation. mRNAs affected by ife-4 knockout were determined by DNA microarray analysis of polysomal distribution. Polysome shifts, in the absence of total mRNA changes, were observed for only 33 of the 18,967 C. elegans mRNAs tested, of which a disproportionate number were related to egg laying and were expressed in neurons and/or muscle. Translational regulation was confirmed by reduced levels of DAF-12, EGL-15, and KIN-29. The functions of these proteins can explain some phenotypes observed in ife-4 knockout mutants. These results indicate that translation of a limited subset of mRNAs is dependent on a specific isoform of eIF4E.

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Liu, Huanli, Shuping Zhang, Mark A. Schell, and Timothy P. Denny. "Pyramiding Unmarked Deletions in Ralstonia solanacearum Shows That Secreted Proteins in Addition to Plant Cell-Wall-Degrading Enzymes Contribute to Virulence." Molecular Plant-Microbe Interactions® 18, no. 12 (December 2005): 1296–305. http://dx.doi.org/10.1094/mpmi-18-1296.

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Ralstonia solanacearum, like many phytopathogenic bacteria, makes multiple extracellular plant cell-wall-degrading enzymes (CWDE), some of which contribute to its ability to cause wilt disease. CWDE and many other proteins are secreted to the milieu via the highly conserved type II protein secretion system (T2SS). R. solanacearum with a defective T2SS is weakly virulent, but it is not known whether this is due to absence of all the CWDE or the loss of other secreted proteins that contribute to disease. These alternatives were investigated by creating mutants of wild-type strain GMI1000 lacking either the T2SS or up to six CWDE and comparing them for virulence on tomato plants. To create unmarked deletions, genomic regions flanking the target gene were polymerase chain reaction (PCR)-amplified, were fused using splice overlap extension PCR, were cloned into a suicide plasmid harboring the sacB counter-selectable marker, and then, were site-specifically introduced into the genome. Various combinations of five deletions (δpehA, δpehB, δpehC, δpme, and δegl) and one inactivated allele (cbhA::aphA-3) resulted in 15 mutants missing one to six CWDE. In soil-drench inoculation assays, virulence of mutants lacking only pectic enzymes (PehA, PehB, PehC, and Pme) was not statistically different from GMI1000, but all the mutants lacking one or both cellulolytic enzymes (Egl or CbhA) wilted plants significantly more slowly than did the wild type. The GMI-6 mutant that lacks all six CWDE was more virulent than the mutant lacking only its two cellulolytic enzymes, and both were significantly more virulent than the T2SS mutant (GMI-D). Very similar results were observed in wounded-petiole inoculation assays, so GMI-6 and GMI-D appear to be less capable of colonizing tomato tissues after invasion. Because the T2SS mutant was much less virulent than the sixfold CWDE mutant, we conclude that other secreted proteins contribute substantially to the ability of R. solanacearum GMI1000 to systemically colonize tomato plants.

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Journal articles on the topic 'Egl-15'

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