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  • 1
    Online Resource
    Online Resource
    Graded expression of ceh-14 reporters in the hypodermis is induced by a gonadal signal
    Springer Science and Business Media LLC ; 2000
    In:  Development Genes and Evolution Vol. 210, No. 11 ( 2000-10-20), p. 564-569
    Details
    In: Development Genes and Evolution, Springer Science and Business Media LLC, Vol. 210, No. 11 ( 2000-10-20), p. 564-569
    Type of Medium: Online Resource
    ISSN: 0949-944X , 1432-041X
    URL: Article
    DOI: 10.1007/s004270000099
    Language: Unknown
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2000
    detail.hit.zdb_id: 1458990-4
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    VP16-activation of the C. elegans neural specification transcription factor UNC-86 suppresses mutations in downstream genes and causes defects in neural migration and axon outgrowth
    The Company of Biologists ; 1997
    In:  Development Vol. 124, No. 6 ( 1997-03-15), p. 1159-1168
    Details
    In: Development, The Company of Biologists, Vol. 124, No. 6 ( 1997-03-15), p. 1159-1168
    Abstract: The POU homeobox gene unc-86 specifies many neuroblast and neural fates in the developing C. elegans nervous system. Genes regulated by unc-86 are mostly unknown. Here we describe a genetic strategy for the identification of downstream pathways regulated by unc-86. We activate UNC-86 transcription activity by inserting the VP16 activation domain into an unc-86 genomic clone that bears all regulatory sequences necessary for normal expression in C. elegans. unc-86/VP16 complements unc-86 mutations in the specification of neuroblast and neural cell fates, but displays novel genetic activities: it can suppress non-null mutations in the downstream genes mec-3 and mec-7 that are necessary for mechanosensory neuron differentiation and function. These data suggest that UNC-86/VP16 increases the expression of mec-3 and mec-7 to compensate Nfor the decreased activities of mutant MEC-3 or MEC-7 proteins. The suppression of mutations in downstream genes by an activated upstream transcription factor should be a general strategy for the identification of genes in transcriptional cascades. unc-86/VP16 also causes neural migration and pathfinding defects and novel behavioral defects. Thus, increased or unregulated expression of genes downstream of unc-86 can confer novel neural phenotypes suggestive of roles for unc-86-regulated genes in neural pathfinding and function. Genetic suppression of these unc-86/VP16 phenotypes may identify the unc-86 downstream genes that mediate these events in neurogenesis.
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.124.6.1159
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1997
    detail.hit.zdb_id: 2007916-3
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  • 3
    Online Resource
    Online Resource
    Dominant gain-of-function mutations that lead to misregulation of the C. elegans heterochronic gene lin-14 , and the evolutionary implications of dominant mutations in pattern-formation genes
    The Company of Biologists ; 1991
    In:  Development Vol. 113, No. Supplement_1 ( 1991-01-01), p. 47-54
    Details
    In: Development, The Company of Biologists, Vol. 113, No. Supplement_1 ( 1991-01-01), p. 47-54
    Abstract: The heterochronic gene lin-14 controls the temporal sequence of developmental events in the C. elegans postembryonic cell lineage. It encodes a nuclear protein that is normally present in most somatic cells of late embryos and LI larvae but not in later larval stages or adults. Two lin-14 gain-of-function mutations cause an inappropriately high level of the lin-14 nuclear protein late in development. These mutations delete 3′ untranslated sequences from the lin-14 mRNAs and identify a negative regulatory element that controls the formation of the lin-14 protein temporal gradient. The 21 kb lin-14 gene contains 13 exons that are differentially spliced to generate two lin-14 protein products with variable N-terminal regions and a constant C-terminal region. No protein sequence similarity to any proteins in various databases was found. The temporal and cellular expression patterns of lin-14 protein accumulation is altered by mutations in the heterochronic genes lin-4 and lin-28. The lin-4 gene is required to down-regulate lin-14 protein levels during the mid-Ll stage. The lin-4 gene product could be the trans-acting factor that binds to the negative regulatory element in the lin-14 3′ untranslated region. In contrast, the lin-28 gene activity positively regulates lin-14 protein levels during early LI. Thus, these genes act antagonistically to regulate the lin-14 temporal switch. The normal down-regulation of lin-14 within 10 h of hatching is not determined by the passage of time per se, but rather is triggered when feeding induces post-embryonic development. Loss of lin-28 gene activity causes precocious down-regulation of lin-14 protein levels before feeding, whereas loss of lin-4 gene activity does not affect the level of lin-14 protein before feeding. These data suggest that to trigger the lin-14 temporal switch, the lin-4 gene is up-regulated after feeding which in turn down-regulates lin-14 via its 3’ untranslated region. We speculate on the evolutionary implications of dominant mutations in pattern-formation genes.
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.113.Supplement_1.47
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1991
    detail.hit.zdb_id: 2007916-3
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  • 4
    Online Resource
    Online Resource
    Regulation of ectodermal and excretory function by the C. elegans POU homeobox gene ceh-6
    The Company of Biologists ; 2001
    In:  Development Vol. 128, No. 5 ( 2001-03-01), p. 779-790
    Details
    In: Development, The Company of Biologists, Vol. 128, No. 5 ( 2001-03-01), p. 779-790
    Abstract: Caenorhabditis elegans has three POU homeobox genes, unc-86, ceh-6 and ceh-18. ceh-6 is the ortholog of vertebrate Brn1, Brn2, SCIP/Oct6 and Brn4 and fly Cf1a/drifter/ventral veinless. Comparison of C. elegans and C. briggsae CEH-6 shows that it is highly conserved. C. elegans has only three POU homeobox genes, while Drosophila has five that fall into four families. Immunofluorescent detection of the CEH-6 protein reveals that it is expressed in particular head and ventral cord neurons, as well as in rectal epithelial cells, and in the excretory cell, which is required for osmoregulation. A deletion of the ceh-6 locus causes 80% embryonic lethality. During morphogenesis, embryos extrude cells in the rectal region of the tail or rupture, indicative of a defect in the rectal epithelial cells that express ceh-6. Those embryos that hatch are sick and develop vacuoles, a phenotype similar to that caused by laser ablation of the excretory cell. A GFP reporter construct expressed in the excretory cell reveals inappropriate canal structures in the ceh-6 null mutant. Members of the POU-III family are expressed in tissues involved in osmoregulation and secretion in a number of species. We propose that one evolutionary conserved function of the POU-III transcription factor class could be the regulation of genes that mediate secretion/ osmoregulation.
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.128.5.779
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2001
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Analysis of xbx genes in C. elegans
    The Company of Biologists ; 2005
    In:  Development Vol. 132, No. 8 ( 2005-04-15), p. 1923-1934
    Details
    In: Development, The Company of Biologists, Vol. 132, No. 8 ( 2005-04-15), p. 1923-1934
    Abstract: Cilia and flagella are widespread eukaryotic subcellular components that are conserved from green algae to mammals. In different organisms they function in cell motility, movement of extracellular fluids and sensory reception. While the function and structural description of cilia and flagella are well established, there are many questions that remain unanswered. In particular, very little is known about the developmental mechanisms by which cilia are generated and shaped and how their components are assembled into functional machineries. To find genes involved in cilia development we used as a search tool a promoter motif, the X-box, which participates in the regulation of certain ciliary genes in the nematode Caenorhabditis elegans. By using a genome search approach for X-box promoter motif-containing genes(xbx genes) we identified a list of about 750 xbx genes(candidates). This list comprises some already known ciliary genes as well as new genes, many of which we hypothesize to be important for cilium structure and function. We derived a C. elegans X-box consensus sequence by in vivo expression analysis. We found that xbx gene expression patterns were dependent on particular X-box nucleotide compositions and the distance from the respective gene start. We propose a model where DAF-19, the RFX-type transcription factor binding to the X-box, is responsible for the development of a ciliary module in C. elegans, which includes genes for cilium structure, transport machinery, receptors and other factors.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.01775
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2005
    detail.hit.zdb_id: 2007916-3
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    Online Resource
  • 6
    Online Resource
    Online Resource
    Genetic identification of HSD-1, a conserved steroidogenic enzyme that directs larval development in Caenorhabditis elegans
    The Company of Biologists ; 2008
    In:  Development Vol. 135, No. 13 ( 2008-07-01), p. 2239-2249
    Details
    In: Development, The Company of Biologists, Vol. 135, No. 13 ( 2008-07-01), p. 2239-2249
    Abstract: In C. elegans, steroid hormones function in conjunction with insulin/IGF-1-like signaling in promoting reproductive development over entry into the diapausal dauer stage. The NCR-1 and -2 (NPC1-related) intracellular cholesterol transporters function redundantly in preventing dauer arrest,presumably by regulating the availability of substrates for steroid hormone synthesis. We have identified hsd-1 as a new component of this cholesterol trafficking/processing pathway, using an ncr-1 enhancer screen. HSD-1 is orthologous to 3β-hydroxysteroid dehydrogenase/Δ5-Δ4 isomerases(3β-HSDs), which are key steroidogenic enzymes in vertebrates, and is exclusively expressed in two neuron-like XXX cells that are crucial in preventing dauer arrest, suggesting that it is involved in biosynthesis of dauer-preventing steroid hormones. The hsd-1 null mutant displays defects in inhibiting dauer arrest: it forms dauers in the deletion mutant backgrounds of ncr-1 or daf-28/insulin; as a single mutant,it is hypersensitive to dauer pheromone. We found that hsd-1 defects can be rescued by feeding mutant animals with several steroid intermediates that are either downstream of or in parallel to the 3β-HSD function in the dafachronic acid biosynthetic pathway, suggesting that HSD-1 functions as a 3β-HSD. Interestingly, sterols that rescued hsd-1 defects also bypassed the need for the NCR-1 and/or -2 functions, suggesting that HSD-1-mediated steroid hormone production is an important functional output of the NCR transporters. Finally, we found that the HSD-1-mediated signal activates insulin/IGF-I signaling in a cell non-autonomous fashion, suggesting a novel mechanism for how these two endocrine pathways intersect in directing development.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.016972
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2008
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    The C. elegans POU-domain transcription factor UNC-86 regulates the tph-1 tryptophan hydroxylase gene and neurite outgrowth in specific serotonergic neurons
    The Company of Biologists ; 2002
    In:  Development Vol. 129, No. 16 ( 2002-08-15), p. 3901-3911
    Details
    In: Development, The Company of Biologists, Vol. 129, No. 16 ( 2002-08-15), p. 3901-3911
    Abstract: A fundamental question in developmental neurobiology is how a common neurotransmitter is specified in different neuronal types?. We describe cell-specific regulation of the serotonergic phenotype by the C. elegans POU-transcription factor UNC-86. We show that unc-86 regulates particular aspects of the terminal neuronal identity in four classes of serotonergic neurons, but that the development of the ADF serotonergic neurons is regulated by an UNC-86-independent program. In the NSM neurons, the role of unc-86 is confined in late differentiation; the neurons are generated but do not express genes necessary for serotonergic neurotransmission. unc-86-null mutations affect the expression in NSM of tph-1, which encodes the serotonin synthetic enzyme tryptophan hydroxylase, and cat-1, which encodes a vesicular transporter that loads serotonin into synaptic vesicles, suggesting that unc-86 coordinately regulates serotonin synthesis and packaging. However, unc-86-null mutations do not impair the ability of NSM to reuptake serotonin released from the ADF serotonergic chemosensory neurons and this serotonin reuptake is sensitive to the serotonin reuptake block drugs imipramine and fluoxetine, demonstrating that serotonin synthesis and reuptake is regulated by distinct factors. The NSM neurons in unc-86-null mutants also display abnormal neurite outgrowth, suggesting a role of unc-86 in regulating this process as well.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.129.16.3901
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2002
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Hormonal Signal Amplification Mediates Environmental Conditions during Development and Controls an Irreversible Commitment to Adulthood
    Public Library of Science (PLoS) ; 2012
    In:  PLoS Biology Vol. 10, No. 4 ( 2012-4-10), p. e1001306-
    Details
    In: PLoS Biology, Public Library of Science (PLoS), Vol. 10, No. 4 ( 2012-4-10), p. e1001306-
    Type of Medium: Online Resource
    ISSN: 1545-7885
    URL: Article
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    DOI: 10.1371/journal.pbio.1001306
    DOI: 10.1371/journal.pbio.1001306.g001
    DOI: 10.1371/journal.pbio.1001306.g002
    DOI: 10.1371/journal.pbio.1001306.g003
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    DOI: 10.1371/journal.pbio.1001306.s001
    DOI: 10.1371/journal.pbio.1001306.s002
    DOI: 10.1371/journal.pbio.1001306.s003
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    DOI: 10.1371/journal.pbio.1001306.s007
    DOI: 10.1371/journal.pbio.1001306.s008
    DOI: 10.1371/journal.pbio.1001306.s009
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2012
    detail.hit.zdb_id: 2126773-X
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  • 9
    Online Resource
    Online Resource
    Rictor/TORC2 regulates fat metabolism, feeding, growth, and life span in Caenorhabditis elegans
    Cold Spring Harbor Laboratory ; 2009
    In:  Genes & Development Vol. 23, No. 4 ( 2009-02-15), p. 496-511
    Details
    In: Genes & Development, Cold Spring Harbor Laboratory, Vol. 23, No. 4 ( 2009-02-15), p. 496-511
    Abstract: Rictor is a component of the target of rapamycin complex 2 (TORC2). While TORC2 has been implicated in insulin and other growth factor signaling pathways, the key inputs and outputs of this kinase complex remain unknown. We identified mutations in the Caenorhabditis elegans homolog of rictor in a forward genetic screen for increased body fat. Despite high body fat, rictor mutants are developmentally delayed, small in body size, lay an attenuated brood, and are short-lived, indicating that Rictor plays a critical role in appropriately partitioning calories between long-term energy stores and vital organismal processes. Rictor is also necessary to maintain normal feeding on nutrient-rich food sources. In contrast to wild-type animals, which grow more rapidly on nutrient-rich bacterial strains, rictor mutants display even slower growth, a further reduced body size, decreased energy expenditure, and a dramatically extended life span, apparently through inappropriate, decreased consumption of nutrient-rich food. Rictor acts directly in the intestine to regulate fat mass and whole-animal growth. Further, the high-fat phenotype of rictor mutants is genetically dependent on akt-1 , akt-2 , and serum and glucocorticoid-induced kinase-1 ( sgk-1 ). Alternatively, the life span, growth, and reproductive phenotypes of rictor mutants are mediated predominantly by sgk-1 . These data indicate that Rictor/TORC2 is a nutrient-sensitive complex with outputs to AKT and SGK to modulate the assessment of food quality and signal to fat metabolism, growth, feeding behavior, reproduction, and life span.
    Type of Medium: Online Resource
    ISSN: 0890-9369 , 1549-5477
    URL: Article
    DOI: 10.1101/gad.1775409
    RVK:
    WA 15000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2009
    detail.hit.zdb_id: 1467414-2
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    MUT-16 promotes formation of perinuclear Mutator foci required for RNA silencing in the C. elegans germline
    Cold Spring Harbor Laboratory ; 2012
    In:  Genes & Development Vol. 26, No. 13 ( 2012-07-01), p. 1433-1444
    Details
    In: Genes & Development, Cold Spring Harbor Laboratory, Vol. 26, No. 13 ( 2012-07-01), p. 1433-1444
    Abstract: RNA silencing can be initiated by endogenous or exogenously delivered siRNAs. In Caenorhabditis elegans, RNA silencing guided by primary siRNAs is inefficient and therefore requires an siRNA amplification step involving RNA-dependent RNA polymerases (RdRPs). Many factors involved in RNA silencing localize to protein- and RNA-rich nuclear pore-associated P granules in the germline, where they are thought to surveil mRNAs as they exit the nucleus. Mutator class genes are required for siRNA-mediated RNA silencing in both germline and somatic cells, but their specific roles and relationship to other siRNA factors are unclear. Here we show that each of the six mutator proteins localizes to punctate foci at the periphery of germline nuclei. The Mutator foci are adjacent to P granules but are not dependent on core P-granule components or other RNAi pathway factors for their formation or stability. The glutamine/asparagine (Q/N)-rich protein MUT-16 is specifically required for the formation of a protein complex containing the mutator proteins, and in its absence, Mutator foci fail to form at the nuclear periphery. The RdRP RRF-1 colocalizes with MUT-16 at Mutator foci, suggesting a role for Mutator foci in siRNA amplification. Furthermore, we demonstrate that genes that yield high levels of siRNAs, indicative of multiple rounds of siRNA amplification, are disproportionally affected in mut-16 mutants compared with genes that yield low levels of siRNAs. We propose that the mutator proteins and RRF-1 constitute an RNA processing compartment required for siRNA amplification and RNA silencing.
    Type of Medium: Online Resource
    ISSN: 0890-9369 , 1549-5477
    URL: Article
    DOI: 10.1101/gad.193904.112
    RVK:
    WA 15000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2012
    detail.hit.zdb_id: 1467414-2
    SSG: 12
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