scholarly journals Pattern formation in the nematode epidermis: determination of the arrangement of peripheral sense organs in the C. elegans male tail

Development ◽  
1991 ◽  
Vol 113 (2) ◽  
pp. 515-526 ◽  
Author(s):  
S.E. Baird ◽  
D.H. Fitch ◽  
I.A. Kassem ◽  
S.W. Emmons
Keyword(s):  
Developmental Process ◽  
Wild Type ◽  
Sense Organs ◽  
Male Tail ◽  
C Elegans ◽  
Active Mechanism ◽  
Ray Cells ◽  
Indirect Immunofluorescence Staining ◽  
A Cell

The developmental process that determines the arrangement of ray sensilla in the Caenorhabditis elegans male tail has been studied. It is shown that the adult arrangement of rays is determined by the placement of ray cells at specific sites in the epidermis of the last larval (L4) stage. Placement of ray cells at specific epidermal sites results from the generation of neurons and support cells in the epidermis near to their final positions, and the subsequent refinement of these positions by an active mechanism involving specific cellular associations. Positions of ray cells and adjacent epidermal cells have been studied during ray development by means of indirect immunofluorescence staining with an antibody to a cell junctional antigen. Mutations are described in six genes that alter the adult arrangement of the rays, frequently resulting in fusion of rays. Changes in the adult pattern of rays in mutants appear to result from prior changes in the epidermal positions of ray cells, and for two mutants it is suggested that this may be due to the inappropriate clustering of processes from neurons and support cells of adjacent rays. Development of the wild-type arrangement of rays appears to require the specification of molecular differences between the rays that affect the specificity of their cellular associations.

A novel disintegrin domain protein affects early cell type specification and pattern formation inDictyostelium

Development ◽  
2002 ◽  
Vol 129 (10) ◽  
pp. 2381-2389
Author(s):  
Timothy R. Varney ◽  
Hoa Ho ◽  
Chere’ Petty ◽  
Daphne D. Blumberg
Keyword(s):  
Cell Fate ◽  
Cellular Slime Mold ◽  
Wild Type ◽  
Cell Type ◽  
C Elegans ◽  
Disintegrin Domain ◽  
A Cell ◽  
Cellular Slime ◽  
And Migration ◽  
Type Specification

The cellular slime mold, Dictyostelium discoideum is a non-metazoan organism, yet we now demonstrate that a disintegrin domain-containing protein, the product of the ampA gene, plays a role in cell type specification. Disintegrin domain-containing proteins are involved in Notch signaling in Drosophila and C. elegans via an ectodomain shedding mechanism that depends on a metalloprotease domain. The Dictyostelium protein lacks a metalloprotease domain. Nonetheless, analysis of cell type specific reporter gene expression during development of the ampA null strain identifies patterning defects that define two distinct roles for the AmpA protein in specifying cell fate. In the absence of a functional ampA gene, cells prematurely specify as prespore cells. Prestalk cell differentiation and migration are delayed. Both of these defects can be rescued by the inclusion of 10% wild-type cells in the developing null mutant aggregates, indicating that the defect is non-cell autonomous. The ampA gene is also demonstrated to be necessary in a cell-autonomous manner for the correct localization of anterior-like cells to the upper cup of the fruiting body. When derived from ampA null cells, the anterior-like cells are unable to localize to positions in the interior of the developing mounds. Wild-type cells can rescue defects in morphogenesis by substituting for null cells when they differentiate as anterior-like cells, but they cannot rescue the ability of ampA null cells to fill this role. Thus, in spite of its simpler structure, the Dictyostelium ampA protein carries out the same diversity of functions that have been observed for the ADAM and ADAMTS families in metazoans.

Transformation of the germ line into muscle in mes-1 mutant embryos of C. elegans

Development ◽  
1995 ◽  
Vol 121 (9) ◽  
pp. 2961-2972 ◽  
Author(s):  
S. Strome ◽  
P. Martin ◽  
E. Schierenberg ◽  
J. Paulsen
Keyword(s):  
Cell Fate ◽  
Germ Cells ◽  
Germ Line ◽  
Primordial Germ Cells ◽  
Primordial Germ Cell ◽  
Wild Type ◽  
C Elegans ◽  
Stem Cell Divisions ◽  
Asymmetric Partitioning

Mutations in the maternal-effect sterile gene mes-1 cause the offspring of homozygous mutant mothers to develop into sterile adults. Lineage analysis revealed that mutant offspring are sterile because they fail to form primordial germ cells during embryogenesis. In wild-type embryos, the primordial germ cell P4 is generated via a series of four unequal stem-cell divisions of the zygote. mes-1 embryos display a premature and progressive loss of polarity in these divisions: P0 and P1 undergo apparently normal unequal divisions and cytoplasmic partitioning, but P2 (in some embryos) and P3 (in most embryos) display defects in cleavage asymmetry and fail to partition lineage-specific components to only one daughter cell. As an apparent consequence of these defects, P4 is transformed into a muscle precursor, like its somatic sister cell D, and generates up to 20 body muscle cells instead of germ cells. Our results show that the wild-type mes-1 gene participates in promoting unequal germ-line divisions and asymmetric partitioning events and thus the determination of cell fate in early C. elegans embryos.

scholarly journals Regulation of body length and male tail ray pattern formation of Caenorhabditis elegans by a member of TGF-beta family

Development ◽  
1999 ◽  
Vol 126 (6) ◽  
pp. 1337-1347 ◽  
Author(s):  
K. Morita ◽  
K.L. Chow ◽  
N. Ueno
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Length ◽  
Target Genes ◽  
Dependent Manner ◽  
Tgf Beta ◽  
Wild Type ◽  
Male Tail ◽  
C Elegans ◽  
Sensory Ray ◽  
Epistasis Analysis

We have identified a new member of the TGF-beta superfamily, CET-1, from Caenorhabditis elegans, which is expressed in the ventral nerve cord and other neurons. cet-1 null mutants have shortened bodies and male tail abnormal phenotype resembling sma mutants, suggesting cet-1, sma-2, sma-3 and sma-4 share a common pathway. Overexpression experiments demonstrated that cet-1 function requires wild-type sma genes. Interestingly, CET-1 appears to affect body length in a dose-dependent manner. Heterozygotes for cet-1 displayed body lengths ranging between null mutant and wild type, and overexpression of CET-1 in wild-type worms elongated body length close to lon mutants. In male sensory ray patterning, lack of cet-1 function results in ray fusions. Epistasis analysis revealed that mab-21 lies downstream and is negatively regulated by the cet-1/sma pathway in the male tail. Our results show that cet-1 controls diverse biological processes during C. elegans development probably through different target genes.

scholarly journals A cell that dies during wild-type C. elegans development can function as a neuron in a ced-3 mutant

Cell ◽  
1987 ◽  
Vol 51 (6) ◽  
pp. 1071-1078 ◽  
Author(s):  
Leon Avery ◽  
H.Robert Horvitz
Keyword(s):  
Wild Type ◽  
C Elegans ◽  
A Cell ◽  
Type C

scholarly journals Extrinsic repair of injured dendrites as a paradigm for regeneration by fusion

2016 ◽  
Author(s):  
Meital Oren-Suissa ◽  
Tamar Gattegno ◽  
Veronika Kravtsov ◽  
Benjamin Podbilewicz
Keyword(s):  
Axonal Regeneration ◽  
Wild Type ◽  
C Elegans ◽  
Enveloped Virus ◽  
Neuronal Dendrites ◽  
A Cell ◽  
The Central Nervous System ◽  
Regenerative Ability ◽  
Genetically Determined ◽  
Neuronal Arborization

AbstractInjury triggers regeneration of axons and dendrites. Research identified factors required for axonal regeneration outside the CNS, but little is known about regeneration triggered by dendrotomy. Here we study neuronal plasticity triggered by dendrotomy and determine the fate of complex PVD arbors following laser surgery of dendrites. We find that severed primary dendrites grow towards each other and reconnect via branch fusion. Simultaneously, terminal branches lose self-avoidance and grow towards each other, meeting and fusing at the tips via an AFF-1-mediated process. Ectopic branch growth is identified as a step in the regeneration process required for bypassing the lesion site. Failure of reconnection to the severed dendrites results in degeneration of the distal end of the neuron. We discover pruning of excess branches via EFF-1 that acts to recover the original wild-type arborization pattern in a cell-autonomous process. In contrast, AFF-1 activity during dendritic auto-fusion is derived from the lateral seam cells and not autonomously from the PVD neuron. We propose a model in which AFF-1-vesicles derived from the epidermal seam cells fuse neuronal dendrites from without. Thus, EFF-1 and AFF-1 fusion proteins emerge as new players in neuronal arborization and maintenance of arbor connectivity following injury inC. elegans. Our results demonstrate that there is a genetically determined multi-step pathway to repair broken dendrites in which EFF-1 and AFF-1 act on different steps of the pathway. Intrinsic EFF-1 is essential for dendritic pruning after injury and extrinsic AFF-1 mediates dendrite fusion to bypass injuries.Author summaryNeurons in the central nervous system have very limited regenerative ability, they fail to remodel following amputation and only in some invertebrates, axons can repair themselves by fusion. Some genetic pathways have been identified for axonal regeneration but few studies exist on dendrite regeneration following injury. To determine how neurons regenerate dendrites following injury we study theC. elegansPVD polymodal neurons that display an arborized pattern of repetitive menorah-like structures. We injure dendrites by laser microsurgery, follow their fate and show that broken primary dendrites often regenerate via fusion. We describe how PVD dendrites regenerate and present roles for EFF-1 and AFF-1 proteins in fusion and remodeling of menorahs. Menorahs lose self-avoidance and AFF-1 fuses them, bypassing the injury site. Branch sprouting, EFF-1-mediated pruning, and arbor simplification completes regeneration. When auto-fusion fails the distal arbor degenerates. Surprisingly, AFF-1 acts non-cell autonomously to mediate dendrite fusion. We propose that extracellular vesicles derived from the lateral epidermis fuse severed dendrites in a process reminiscent of enveloped virus-mediated cell fusion without infection.

The Effect of Mianserin on Lifespan of Caenorhabditis elegans is Abolished by Glucose

2021 ◽  
Vol 13 ◽  
Author(s):  
Abdullah Almotayri ◽  
Jency Thomas ◽  
Mihiri Munasinghe ◽  
Markandeya Jois
Keyword(s):  
Caenorhabditis Elegans ◽  
Scaffolding Protein ◽  
Lifespan Extension ◽  
Wild Type ◽  
E Coli ◽  
C Elegans ◽  
Risk Of Death ◽  
Increased Risk ◽  
Antidepressant Use ◽  
Extension Effect

Background: The antidepressant mianserin has been shown to extend the lifespan of Caenorhabditis elegans (C. elegans), a well-established model organism used in aging research. The extension of lifespan in C. elegans was shown to be dependent on increased expression of the scaffolding protein (ANK3/unc-44). In contrast, antidepressant use in humans is associated with an increased risk of death. The C. elegans in the laboratory are fed Escherichia coli (E. coli), a diet high in protein and low in carbohydrate, whereas a typical human diet is high in carbohydrates. We hypothesized that dietary carbohydrates might mitigate the lifespan-extension effect of mianserin. Objective: To investigate the effect of glucose added to the diet of C. elegans on the lifespan-extension effect of mianserin. Methods: Wild-type Bristol N2 and ANK3/unc-44 inactivating mutants were cultured on agar plates containing nematode growth medium and fed E. coli. Treatment groups included (C) control, (M50) 50 μM mianserin, (G) 73 mM glucose, and (M50G) 50 μM mianserin and 73 mM glucose. Lifespan was determined by monitoring the worms until they died. Statistical analysis was performed using the Kaplan-Meier version of the log-rank test. Results: Mianserin treatment resulted in a 12% increase in lifespan (P<0.05) of wild-type Bristol N2 worms but reduced lifespan by 6% in ANK3/unc-44 mutants, consistent with previous research. The addition of glucose to the diet reduced the lifespan of both strains of worms and abolished the lifespan-extension by mianserin. Conclusion: The addition of glucose to the diet of C. elegans abolishes the lifespan-extension effects of mianserin.

scholarly journals The NALCN Channel Regulator UNC-80 Functions in a Subset of Interneurons To Regulate Caenorhabditis elegans Reversal Behavior

2019 ◽  
Vol 10 (1) ◽  
pp. 199-210 ◽  
Author(s):  
Chuanman Zhou ◽  
Jintao Luo ◽  
Xiaohui He ◽  
Qian Zhou ◽  
Yunxia He ◽  
...  
Keyword(s):  
Plant Hormone ◽  
Neuronal Excitability ◽  
Resting Membrane Potential ◽  
Loss Of Function ◽  
Wild Type ◽  
C Elegans ◽  
Link Type ◽  
Complex Functions ◽  
And Function ◽  
Multiple Loss

NALCN (Na+leak channel, non-selective) is a conserved, voltage-insensitive cation channel that regulates resting membrane potential and neuronal excitability. UNC79 and UNC80 are key regulators of the channel function. However, the behavioral effects of the channel complex are not entirely clear and the neurons in which the channel functions remain to be identified. In a forward genetic screen for C. elegans mutants with defective avoidance response to the plant hormone methyl salicylate (MeSa), we isolated multiple loss-of-function mutations in unc-80 and unc-79. C. elegans NALCN mutants exhibited similarly defective MeSa avoidance. Interestingly, NALCN, unc-80 and unc-79 mutants all showed wild type-like responses to other attractive or repelling odorants, suggesting that NALCN does not broadly affect odor detection or related forward and reversal behaviors. To understand in which neurons the channel functions, we determined the identities of a subset of unc-80-expressing neurons. We found that unc-79 and unc-80 are expressed and function in overlapping neurons, which verified previous assumptions. Neuron-specific transgene rescue and knockdown experiments suggest that the command interneurons AVA and AVE and the anterior guidepost neuron AVG can play a sufficient role in mediating unc-80 regulation of the MeSa avoidance. Though primarily based on genetic analyses, our results further imply that MeSa might activate NALCN by direct or indirect actions. Altogether, we provide an initial look into the key neurons in which the NALCN channel complex functions and identify a novel function of the channel in regulating C. elegans reversal behavior through command interneurons.

scholarly journals Sperm Competition in the Absence of Fertilization in Caenorhabditis elegans

Genetics ◽  
1999 ◽  
Vol 152 (1) ◽  
pp. 201-208 ◽  
Author(s):  
Andrew Singson ◽  
Katherine L Hill ◽  
Steven W L’Hernault
Keyword(s):  
Caenorhabditis Elegans ◽  
Sperm Competition ◽  
Sperm Function ◽  
Sperm Precedence ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Normal Sperm ◽  
Self Fertilization ◽  
Competition Assays

Abstract Hermaphrodite self-fertilization is the primary mode of reproduction in the nematode Caenorhabditis elegans. However, when a hermaphrodite is crossed with a male, nearly all of the oocytes are fertilized by male-derived sperm. This sperm precedence during reproduction is due to the competitive superiority of male-derived sperm and results in a functional suppression of hermaphrodite self-fertility. In this study, mutant males that inseminate fertilization-defective sperm were used to reveal that sperm competition within a hermaphrodite does not require successful fertilization. However, sperm competition does require normal sperm motility. Additionally, sperm competition is not an absolute process because oocytes not fertilized by male-derived sperm can sometimes be fertilized by hermaphrodite-derived sperm. These results indicate that outcrossed progeny result from a wild-type cross because male-derived sperm are competitively superior and hermaphrodite-derived sperm become unavailable to oocytes. The sperm competition assays described in this study will be useful in further classifying the large number of currently identified mutations that alter sperm function and development in C. elegans.

Streblus asper Lour. exerts MAPK and SKN-1 mediated anti-aging, anti-photoaging activities and imparts neuroprotection by ameliorating Aβ in Caenorhabditis elegans

2021 ◽  
pp. 1-17
Author(s):  
Mani Iyer Prasanth ◽  
James Michael Brimson ◽  
Dicson Sheeja Malar ◽  
Anchalee Prasansuklab ◽  
Tewin Tencomnao
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Stress Resistance ◽  
Vital Role ◽  
Transgenic Strain ◽  
Wild Type ◽  
Neuroprotective Effects ◽  
C Elegans ◽  
Streblus Asper

BACKGROUND: Streblus asper Lour., has been reported to have anti-aging and neuroprotective efficacies in vitro. OBJECTIVE: To analyze the anti-aging, anti-photoaging and neuroprotective efficacies of S. asper in Caenorhabditis elegans. METHODS: C. elegans (wild type and gene specific mutants) were treated with S. asper extract and analyzed for lifespan and other health benefits through physiological assays, fluorescence microscopy, qPCR and Western blot. RESULTS: The plant extract was found to increase the lifespan, reduce the accumulation of lipofuscin and modulate the expression of candidate genes. It could extend the lifespan of both daf-16 and daf-2 mutants whereas the pmk-1 mutant showed no effect. The activation of skn-1 was observed in skn-1::GFP transgenic strain and in qPCR expression. Further, the extract can extend the lifespan of UV-A exposed nematodes along with reducing ROS levels. Additionally, the extract also extends lifespan and reduces paralysis in Aβ transgenic strain, apart from reducing Aβ expression. CONCLUSIONS: S. asper was able to extend the lifespan and healthspan of C. elegans which was independent of DAF-16 pathway but dependent on SKN-1 and MAPK which could play a vital role in eliciting the anti-aging, anti-photoaging and neuroprotective effects, as the extract could impart oxidative stress resistance and neuroprotection.

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