scholarly journals Identification of genes that interact with glp-1, a gene required for inductive cell interactions in Caenorhabditis elegans

Development ◽  
1989 ◽  
Vol 106 (1) ◽  
pp. 133-143 ◽  
Author(s):  
E.M. Maine ◽  
J. Kimble
Keyword(s):  
Body Shape ◽  
Suppressor Gene ◽  
Temperature Sensitive ◽  
Cellular Interactions ◽  
C Elegans ◽  
Germline Proliferation ◽  
Mutant Phenotypes ◽  
Mitosis And Meiosis ◽  
Ts Mutations ◽  
Molecular Nature

The glp-1 gene functions in two inductive cellular interactions and in development of the embryonic hypodermis of C. elegans. We have isolated six mutations as recessive suppressors of temperature-sensitive (ts) mutations of glp-1. By mapping and complementation tests, we found that these suppressors are mutations of known dumpy (dpy) genes; dpy genes are required for development of normal body shape. Based on this result, we asked whether mutations previously isolated in screens for mutants defective in body shape could also suppress glp-1(ts). From these tests, we learned that unselected mutations of eight genes required for normal C. elegans morphogenesis, including the four already identified, suppress glp-1(ts). All of these suppressors rescue all three mutant phenotypes of glp-1(ts) (defects in embryonic induction of pharyngeal tissue, in embryonic hypodermis development, and in induction of germline proliferation). However, they do not rescue putative glp-1 null mutants and therefore do not bypass the requirement for glp-1 in development. In the light of current ideas about the molecular nature of the glp-1 and suppressor gene products, we propose an interaction between the glp-1 protein and components of the extracellular matrix and speculate that this interaction may impose spatial constraints on the decision between mitosis and meiosis in the germline.

scholarly journals Characterization of Seven Genes Affecting Caenorhabditis elegans Hindgut Development

Genetics ◽  
1999 ◽  
Vol 153 (2) ◽  
pp. 731-742 ◽  
Author(s):  
Helen M Chamberlin ◽  
Keith B Brown ◽  
Paul W Sternberg ◽  
James H Thomas
Keyword(s):  
Caenorhabditis Elegans ◽  
Regional Identity ◽  
Cell Types ◽  
Postembryonic Development ◽  
Temperature Sensitive ◽  
Mesodermal Cell ◽  
C Elegans ◽  
Blast Cells ◽  
Mutant Phenotypes ◽  
Male Specific

Abstract We have identified and characterized 12 mutations in seven genes that affect the development of the Caenorhabditis elegans hindgut. We find that the mutations can disrupt the postembryonic development of the male-specific blast cells within the hindgut, the hindgut morphology in both males and hermaphrodites, and in some cases, the expression of a hindgut marker in hermaphrodite animals. Mutations in several of the genes also affect viability. On the basis of their mutant phenotypes, we propose that the genes fall into four distinct classes: (1) egl-5 is required for regional identity of the tail; (2) sem-4 is required for a variety of ectodermal and mesodermal cell types, including cells in the hindgut; (3) two genes, lin-49 and lin-59, affect development of many cells, including hindgut; and (4) three genes, mab-9, egl-38, and lin-48, are required for patterning fates within the hindgut, making certain hindgut cells different from others. We also describe a new allele of the Pax gene egl-38 that is temperature sensitive and affects the conserved β-hairpin of the EGL-38 paired domain. Our results suggest that a combination of different factors contribute to normal C. elegans hindgut development.

scholarly journals Metaphase to Anaphase (mat) Transition–Defective Mutants inCaenorhabditis elegans

2000 ◽  
Vol 151 (7) ◽  
pp. 1469-1482 ◽  
Author(s):  
Andy Golden ◽  
Penny L. Sadler ◽  
Matthew R. Wallenfang ◽  
Jill M. Schumacher ◽  
Danielle R. Hamill ◽  
...  
Keyword(s):  
Eukaryotic Cell ◽  
Temperature Sensitive ◽  
Anaphase Promoting Complex ◽  
C Elegans ◽  
Antibody Staining ◽  
Polar Bodies ◽  
Phosphohistone H3 ◽  
M Phase ◽  
Germline Proliferation ◽  
Meiosis I

The metaphase to anaphase transition is a critical stage of the eukaryotic cell cycle, and, thus, it is highly regulated. Errors during this transition can lead to chromosome segregation defects and death of the organism. In genetic screens for temperature-sensitive maternal effect embryonic lethal (Mel) mutants, we have identified 32 mutants in the nematode Caenorhabditis elegans in which fertilized embryos arrest as one-cell embryos. In these mutant embryos, the oocyte chromosomes arrest in metaphase of meiosis I without transitioning to anaphase or producing polar bodies. An additional block in M phase exit is evidenced by the failure to form pronuclei and the persistence of phosphohistone H3 and MPM-2 antibody staining. Spermatocyte meiosis is also perturbed; primary spermatocytes arrest in metaphase of meiosis I and fail to produce secondary spermatocytes. Analogous mitotic defects cause M phase delays in mitotic germline proliferation. We have named this class of mutants “mat” for metaphase to anaphase transition defective. These mutants, representing six different complementation groups, all map near genes that encode subunits of the anaphase promoting complex or cyclosome, and, here, we show that one of the genes, emb-27, encodes the C. elegans CDC16 ortholog.

A Cuticle Collagen Encoded by the lon-3 Gene May Be a Target of TGF-β Signaling in Determining Caenorhabditis elegans Body Shape

Genetics ◽  
2002 ◽  
Vol 162 (4) ◽  
pp. 1631-1639
Author(s):  
Yo Suzuki ◽  
Gail A Morris ◽  
Min Han ◽  
William B Wood
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Shape ◽  
Small Body ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Cellular Mechanisms ◽  
C Elegans ◽  
Gene Expression Analyses ◽  
Dose Dependent

Abstract The signaling pathway initiated by the TGF-β family member DBL-1 in Caenorhabditis elegans controls body shape in a dose-dependent manner. Loss-of-function (lf) mutations in the dbl-1 gene cause a short, small body (Sma phenotype), whereas overexpression of dbl-1 causes a long body (Lon phenotype). To understand the cellular mechanisms underlying these phenotypes, we have isolated suppressors of the Sma phenotype resulting from a dbl-1(lf) mutation. Two of these suppressors are mutations in the lon-3 gene, of which four additional alleles are known. We show that lon-3 encodes a collagen that is a component of the C. elegans cuticle. Genetic and reporter-gene expression analyses suggest that lon-3 is involved in determination of body shape and is post-transcriptionally regulated by the dbl-1 pathway. These results support the possibility that TGF-β signaling controls C. elegans body shape by regulating cuticle composition.

scholarly journals glp-3 Is Required for Mitosis and Meiosis in the Caenorhabditis elegans Germ Line

Genetics ◽  
1997 ◽  
Vol 145 (1) ◽  
pp. 111-121 ◽  
Author(s):  
Lisa C Kadyk ◽  
Eric J Lambie ◽  
Judith Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Germ Cells ◽  
Germ Line ◽  
Stem Cell Population ◽  
Phenotypic Characterization ◽  
Loss Of Function ◽  
Dapi Staining ◽  
Cell Cycles ◽  
C Elegans ◽  
Mitosis And Meiosis

The germ line is the only tissue in Caenorhabditis elegans in which a stem cell population continues to divide mitotically throughout life; hence the cell cycles of the germ line and the soma are regulated differently. Here we report the genetic and phenotypic characterization of the glp-3 gene. In animals homozygous for each of five recessive loss-of-function alleles, germ cells in both hermaphrodites and males fail to progress through mitosis and meiosis, but somatic cells appear to divide normally. Germ cells in animals grown at 15° appear by DAPI staining to be uniformly arrested at the G2/M transition with <20 germ cells per gonad on average, suggesting a checkpoint-mediated arrest. In contrast, germ cells in mutant animals grown at 25° frequently proliferate slowly during adulthood, eventually forming small germ lines with several hundred germ cells. Nevertheless, cells in these small germ lines never undergo meiosis. Double mutant analysis with mutations in other genes affecting germ cell proliferation supports the idea that glp-3 may encode a gene product that is required for the mitotic and meiotic cell cycles in the C. elegans germ line.

scholarly journals MATERNAL-ZYGOTIC GENE INTERACTIONS DURING FORMATION OF THE DORSOVENTRAL PATTERN IN DROSOPHILA EMBRYOS

Genetics ◽  
1983 ◽  
Vol 105 (3) ◽  
pp. 615-632 ◽  
Author(s):  
Pat Simpson
Keyword(s):  
Early Embryo ◽  
Drosophila Embryo ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Mutant Genotype ◽  
Dominant Phenotype ◽  
Zygotic Gene ◽  
Definition Of ◽  
Mutant Phenotypes ◽  
Dominant Lethality

ABSTRACT Maternal-zygotic interactions involving the three genes dorsal (dl), twist (twi) and snail (sna) are described. The results suggest that all three are involved in the process by which the dorsoventral pattern of the Drosophila embryo is established. First, the lethal embryonic mutant phenotypes are rather similar. In homozygous twi or sna embryos invagination of the ventral presumptive mesodermal cells fails to occur, and the resulting embryos are devoid of internal organs. This is very similar to the dominant phenotype described for dl; in the case of dl, however, the effect is a maternal one dependent on the mutant genotype of the female. Second, a synergistic interaction has been found whereby dominant lethality of twi  - or sna-bearing zygotes is observed in embryos derived from heterozygous dl females at high temperature. The temperature sensitivity of this interaction permitted definition of a temperature-sensitive period which is probably that of dl. This was found to extend from approximately 12 hr prior to oviposition to 2— 3 hr of embryogenesis. A zygotic action for the dl gene in addition to the maternal effect was revealed by the finding that extra doses of dl  + in the zygotes can partially rescue the dominant lethality of heterozygous twi embryos derived from heterozygous dl females. Two possible interpretations of the synergism are considered: (1) twi and sna are activated in the embryos as a result of positional signals placed in the egg as a consequence of the functioning of the dl gene during oogenesis and, thus, play a role in embryonic determination. (2) The gene products of dl  + and twi  + (or sna  +) combine to produce a functional molecule that is involved in the specification of dorsoventral pattern in the early embryo.

scholarly journals Polymodal Functionality of C. elegans OLL Neurons in Mechanosensation and Thermosensation

2021 ◽  
Author(s):  
Yuedan Fan ◽  
Wenjuan Zou ◽  
Jia Liu ◽  
Umar Al-Sheikh ◽  
Hankui Cheng ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Sensory Neurons ◽  
Molecular Mechanisms ◽  
Temperature Sensitive ◽  
Cold Sensation ◽  
Cold Response ◽  
C Elegans ◽  
Sensory Modalities ◽  
A Cell ◽  
Bona Fide

AbstractSensory modalities are important for survival but the molecular mechanisms remain challenging due to the polymodal functionality of sensory neurons. Here, we report the C. elegans outer labial lateral (OLL) sensilla sensory neurons respond to touch and cold. Mechanosensation of OLL neurons resulted in cell-autonomous mechanically-evoked Ca2+ transients and rapidly-adapting mechanoreceptor currents with a very short latency. Mechanotransduction of OLL neurons might be carried by a novel Na+ conductance channel, which is insensitive to amiloride. The bona fide mechano-gated Na+-selective degenerin/epithelial Na+ channels, TRP-4, TMC, and Piezo proteins are not involved in this mechanosensation. Interestingly, OLL neurons also mediated cold but not warm responses in a cell-autonomous manner. We further showed that the cold response of OLL neurons is not mediated by the cold receptor TRPA-1 or the temperature-sensitive glutamate receptor GLR-3. Thus, we propose the polymodal functionality of OLL neurons in mechanosensation and cold sensation.

scholarly journals Goα Regulates Volatile Anesthetic Action in Caenorhabditis elegans

Genetics ◽  
2001 ◽  
Vol 158 (2) ◽  
pp. 643-655 ◽  
Author(s):  
Bruno van Swinderen ◽  
Laura B Metz ◽  
Laynie D Shebester ◽  
Jane E Mendel ◽  
Paul W Sternberg ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Novel Mutation ◽  
Volatile Anesthetic ◽  
Loss Of Function ◽  
Wild Type ◽  
Α Subunit ◽  
C Elegans ◽  
Missense Mutant ◽  
Anesthetic Action ◽  
Mutant Phenotypes

Abstract To identify genes controlling volatile anesthetic (VA) action, we have screened through existing Caenorhabditis elegans mutants and found that strains with a reduction in Go signaling are VA resistant. Loss-of-function mutants of the gene goa-1, which codes for the α-subunit of Go, have EC50s for the VA isoflurane of 1.7- to 2.4-fold that of wild type. Strains overexpressing egl-10, which codes for an RGS protein negatively regulating goa-1, are also isoflurane resistant. However, sensitivity to halothane, a structurally distinct VA, is differentially affected by Go pathway mutants. The RGS overexpressing strains, a goa-1 missense mutant found to carry a novel mutation near the GTP-binding domain, and eat-16(rf) mutants, which suppress goa-1(gf) mutations, are all halothane resistant; goa-1(null) mutants have wild-type sensitivities. Double mutant strains carrying mutations in both goa-1 and unc-64, which codes for a neuronal syntaxin previously found to regulate VA sensitivity, show that the syntaxin mutant phenotypes depend in part on goa-1 expression. Pharmacological assays using the cholinesterase inhibitor aldicarb suggest that VAs and GOA-1 similarly downregulate cholinergic neurotransmitter release in C. elegans. Thus, the mechanism of action of VAs in C. elegans is regulated by Goα, and presynaptic Goα-effectors are candidate VA molecular targets.

scholarly journals Mutations that Affect Channel Opening of Innexin Hemichannels in the C. elegans Gonad

2020 ◽  
Author(s):  
Todd Starich ◽  
David Greenstein
Keyword(s):  
Cell Proliferation ◽  
Gap Junctions ◽  
Germ Cell ◽  
Structural Model ◽  
Loss Of Function ◽  
C Elegans ◽  
Somatic Gonad ◽  
Channel Opening ◽  
Germline Proliferation ◽  
Germ Cell Proliferation

In C. elegans, gap junctions couple cells of the somatic gonad with the germline to support germ cell proliferation and gametogenesis. We previously characterized a strong loss-of-function mutation (T239I) affecting the second extracellular loop (EL2) of the somatic INX-8 hemichannel subunit. These mutant hemichannels form non-functional gap junctions with germline-expressed innexins. Here we describe the characterization of mutations that restore germ cell proliferation in the T239I EL2 mutant background. We recovered seven intragenic mutations located in diverse domains of INX-8 but not the EL domains. These second-site mutations compensate for the original channel defect to varying degrees, from nearly complete wild-type rescue, to partial rescue of germline proliferation. One suppressor mutation (E350K) supports the innexin cryo-EM structural model that the channel pore opening is surrounded by a cytoplasmic dome. Two suppressor mutations (S9L and I36N) may form leaky hemichannels that support germline proliferation but cause the demise of somatic sheath cells. Phenotypic analyses of three other suppressors reveal an equivalency in the rescue of germline proliferation and comparable delays in gametogenesis but a graded rescue of fertility. These latter mutations may be useful to probe interactions with the biochemical pathways that produce the molecules transiting through soma-germline gap junctions.

scholarly journals An intracellular pathogen response pathway promotes proteostasis in C. elegans

2017 ◽  
Author(s):  
Kirthi C. Reddy ◽  
Tal Dror ◽  
Jessica N. Sowa ◽  
Johan Panek ◽  
Kevin Chen ◽  
...  
Keyword(s):  
Ubiquitin Ligase ◽  
Intracellular Pathogen ◽  
Forward Genetic Screen ◽  
C Elegans ◽  
Transcriptional Signature ◽  
Proteotoxic Stress ◽  
Ubiquitin Ligase Complex ◽  
Pathogen Response ◽  
Mutant Phenotypes ◽  
Increased Activity

SummaryMaintenance of proteostasis is critical for organismal health. Here we describe a novel pathway that promotes proteostasis, identified through the analysis of C. elegans genes upregulated by intracellular infection. We named this distinct transcriptional signature the Intracellular Pathogen Response (IPR), and it includes upregulation of several predicted ubiquitin ligase complex components such as the cullin cul-6. Through a forward genetic screen we found pals-22, a gene of previously unknown function, to be a repressor of the cul-6/Cullin gene and other IPR gene expression. Interestingly, pals-22 mutants have increased thermotolerance and reduced levels of stress-induced polyglutamine aggregates, likely due to upregulated IPR expression. We found the enhanced stress resistance of pals-22 mutants to be dependent on cul-6, suggesting that pals-22 mutants have increased activity of a CUL-6/Cullin-containing ubiquitin ligase complex. pals-22 mutant phenotypes are distinct from the well-studied heat shock and insulin signaling pathways, indicating that the IPR is a novel pathway that protects animals from proteotoxic stress.

Host-mediated RNAi of a Notch-like receptor gene inMeloidogyne incognitainduces nematode resistance

Parasitology ◽  
2018 ◽  
Vol 145 (14) ◽  
pp. 1896-1906
Author(s):  
Deshika Kohli ◽  
Parameswaran Chidambaranathan ◽  
J. Prasanth Tej Kumar ◽  
Ashish Kumar Singh ◽  
Anil Kumar ◽  
...  
Keyword(s):  
Transmembrane Domain ◽  
Receptor Gene ◽  
Nematode Resistance ◽  
Receptor Protein ◽  
Binding Motifs ◽  
C Elegans ◽  
Transgenic Lines ◽  
Germline Proliferation ◽  
Epidermal Growth ◽  
Almost All

AbstractGLP-1 (abnormal germline proliferation) is a Notch-like receptor protein that plays an essential role in pharyngeal development. In this study, an orthologue ofCaenorhabditis elegans glp-1was identified inMeloidogyne incognita. A computational analysis revealed that the orthologue contained almost all the domains present in theC. elegansgene: specifically, the LIN-12/Notch repeat, the ankyrin repeat, a transmembrane domain and different ligand-binding motifs were present in orthologue, but the epidermal growth factor-like motif was not observed. An expression analysis showed differential expression ofglp-1throughout the life cycle ofM. incognita, with relatively higher expression in the egg stage. To evaluate the silencing efficacy ofMi-glp-1, transgenicArabidopsisplants carrying double-stranded RNA constructs ofglp-1were generated, and infection of these plants withM. incognitaresulted in a 47–50% reduction in the numbers of galls, females and egg masses. Females obtained from the transgenic RNAi lines exhibited 40–60% reductions in the transcript levels of the targetedglp-1gene compared with females isolated from the control plants. Second-generation juveniles (J2s), which were descendants of the infected females from the transgenic lines, showed aberrant phenotypes. These J2s exhibited a significant decrease in the overall distance from the stylet to the metacorpus region, and this effect was accompanied by disruption around the metacorporeal bulb of the pharynx. The present study suggests a role for this gene in organ (pharynx) development during embryogenesis inM. incognitaand its potential use as a target in the management of nematode infestations in plants.

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