Combinatorial control of touch receptor neuron expression in Caenorhabditis elegans

Six touch receptor neurons with distinctive morphological features sense gentle touch in Caenorhabditis elegans. Previous studies have identified three genes (lin-32, unc-86 and mec-3) that regulate touch cell development. However, since other cell types also require these genes, we suspected that other genes help restrict the expression of touch cell characteristics to the six neurons seen in the wild type. To identify such genes, we have examined mutants defective in genes required for the development of other C. elegans cells for changes in the pattern of touch cell-specific features. Mutations in seven genes either reduce (lin-14) or increase (lin-4, egl-44, egl-46, sem-4, ced-3 and ced-4) the number of touch receptor-like cells. The combinatorial action of these genes, all of which are required for the production of many cell types, restrict the number of cells expressing touch receptor characteristics in wild-type animals by acting as positive and negative regulators and by removing cells by programmed cell death.

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Caenorhabditis elegans triple null mutant lacking UDP-N-acetyl-D-glucosamine:α-3-D-mannoside β1,2-N-acetylglucosaminyltransferase I

Biochemical Journal ◽

10.1042/bj20040793 ◽

2004 ◽

Vol 382 (3) ◽

pp. 995-1001 ◽

Cited By ~ 46

Author(s):

Shaoxian ZHU ◽

Andrew HANNEMAN ◽

Vernon N. REINHOLD ◽

Andrew M. SPENCE ◽

Harry SCHACHTER

Keyword(s):

Caenorhabditis Elegans ◽

Chromosome Number ◽

Null Mutant ◽

Wild Type ◽

Knock Out ◽

C Elegans ◽

In The Wild ◽

Wild Type Worm ◽

Type C ◽

Nematode Worm

We have previously reported, from the nematode worm Caenor-habditis elegans, three genes (gly-12, gly-13 and gly-14) encoding enzymically active UDP-N-acetyl-D-glucosamine:α-3-D-mannoside β1,2-N-acetylglucosaminyltransferase I (GnT I), an enzyme essential for hybrid, paucimannose and complex N-glycan synthesis. We now describe a worm with null mutations in all three GnT I genes, gly-14 (III);gly-12 gly-13 (X) (III and X refer to the chromosome number). The triple-knock-out (TKO) worms have a normal phenotype, although they do not express GnT I activity and do not synthesize 31 paucimannose, complex and fucosylated oligomannose N-glycans present in the wild-type worm. The TKO worm has increased amounts of non-fucosylated oligomannose N-glycan structures, a finding consistent with the site of GnT I action. Five fucosylated oligomannose N-glycan structures were observed in TKO, but not wild-type, worms, indicating the presence of unusual GnT I-independent fucosyltransferases. It is concluded that wild-type C. elegans makes a large number of GnT I-dependent N-glycans that are not essential for normal worm development under laboratory conditions. The TKO worm may be more susceptible to mutations in other genes, thereby providing an approach for the identification of genes that interact with GnT I.

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Comparing Caenorhabditis elegans gentle and harsh touch response behavior using a multiplexed hydraulic microfluidic device

10.1101/162990 ◽

2017 ◽

Author(s):

Patrick D. McClanahan ◽

Joyce H. Xu ◽

Christopher Fang-Yen

Keyword(s):

Caenorhabditis Elegans ◽

Microfluidic Device ◽

Receptive Fields ◽

The Body ◽

Mechanical Stimuli ◽

C Elegans ◽

Response Characteristics ◽

Touch Receptor Neurons ◽

Touch Response ◽

Receptor Neurons

AbstractThe roundworm Caenorhabditis elegans is an important model system for understanding the genetics and physiology of touch. Classical assays for C. elegans touch, which involve manually touching the animal with a probe and observing its response, are limited by their low throughput and qualitative nature. We developed a microfluidic device in which several dozen animals are subject to spatially localized mechanical stimuli with variable amplitude. The device contains 64 sinusoidal channels through which worms crawl, and hydraulic valves that deliver touch stimuli to the worms. We used this assay to characterize the behavioral responses to gentle touch stimuli and the less well studied harsh (nociceptive) touch stimuli. First, we measured the relative response thresholds of gentle and harsh touch. Next, we quantified differences in the receptive fields between wild type worms and a mutant with non-functioning posterior touch receptor neurons. We showed that under gentle touch the receptive field of the anterior touch receptor neurons extends into the posterior half of the body. Finally, we found that the behavioral response to gentle touch does not depend on the locomotion of the animal immediately prior to the stimulus, but does depend on the location of the previous touch. Responses to harsh touch, on the other hand, did not depend on either previous velocity or stimulus location. Differences in gentle and harsh touch response characteristics may reflect the different innervation of the respective mechanosensory cells. Our assay will facilitate studies of mechanosensation, sensory adaptation, and nociception.

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Structural and functional diversity in the neuronal microtubules of Caenorhabditis elegans.

The Journal of Cell Biology ◽

10.1083/jcb.93.1.15 ◽

1982 ◽

Vol 93 (1) ◽

pp. 15-23 ◽

Cited By ~ 147

Author(s):

M Chalfie ◽

J N Thomson

Keyword(s):

Caenorhabditis Elegans ◽

Colchicine Treatment ◽

Variable Number ◽

Sensory Transduction ◽

Partial Replacement ◽

C Elegans ◽

Touch Receptor Neurons ◽

Touch Sensitivity ◽

Receptor Neurons

Tannic acid fixation reveals differences in the number of protofilaments between microtubules (MTs) in the nematode Caenorhabditis elegans. Most cells have MTs with 11 protofilaments but the six touch receptor neurons (the microtubule cells) have MTs with 15 protofilaments. No 13-protofilament (13-p) MT has been seen. The modified cilia of sensory neurons also possess unusual structures. The cilia contain nine outer doublets with A subfibers of 13 protofilaments and B subfibers of 11 protofilaments and a variable number of inner singlet MTs containing 11 protofilaments. The 15-p MTs but not the 11-p MTs are eliminated by colchicine-treatment or by mutation of the gene mec-7. Concomitantly, touch sensitivity is also lost. However, whereas colchicine treatment leads to the loss of all MTs from the microtubule cells, mutations in mec-7 result in the partial replacement of the 15-p MTs with 11-p MTs. Benzimidazoles (benomyl and nocodazole) have more general effects on C. elegans (slow growth, severe uncoordination, and loss of processes from the ventral cord) but do not affect the 15-p MTs. Benomyl will, however, disrupt the replacement 11-p MTs found in the microtubule cells of mec-7 mutants. The 11-p and 15-p MTs also respond differently to temperature and fixation conditions. It is likely that either type of MT will suffice for the proper outgrowth of the microtubule cell process, but only the 15-p MT can function in the specialized role of sensory transduction of the microtubule cells.

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Regulated distribution of mitochondria in touch receptor neurons of C. elegans influences touch response

10.1101/2020.07.26.221523 ◽

2020 ◽

Author(s):

Anjali Awasthi ◽

Souvik Modi ◽

Sneha Hegde ◽

Anusheela Chatterjee ◽

Sudip Mondal ◽

...

Keyword(s):

Molecular Motors ◽

Neuronal Function ◽

Mitochondrial Density ◽

Neuronal Process ◽

C Elegans ◽

Touch Receptor Neurons ◽

Touch Response ◽

Receptor Neurons ◽

Touch Receptor Neuron

AbstractDensity of mitochondria and their localization at specific sub-cellular regions of the neurons is regulated by molecular motors, their adaptors and the cytoskeleton. However, the regulation of the mitochondrial density, the positioning of mitochondria along the neuronal process and the role of axonal mitochondria in neuronal function remain poorly understood. This study shows that the density of mitochondria in C. elegans touch receptor neuron processes remains constant through development. Simulations show that mitochondrial positioning along parts of the neuronal process that are devoid of synapses is regulated. Additionally, we also demonstrate that axonal mitochondria are necessary for maintaining touch responsiveness.

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Inhibition of cell fate repressors secures the differentiation of the touch receptor neurons of Caenorhabditis elegans

10.1101/320978 ◽

2018 ◽

Author(s):

Chaogu Zheng ◽

Felix Qiaochu Jin ◽

Brian Loeber Trippe ◽

Ji Wu ◽

Martin Chalfie

Keyword(s):

Caenorhabditis Elegans ◽

Cell Fate ◽

Reciprocal Inhibition ◽

Transcriptional Repressors ◽

Downstream Effector ◽

Effector Genes ◽

Touch Receptor Neurons ◽

Summary Statement ◽

Receptor Neurons ◽

Touch Receptor Neuron

AbstractTerminal differentiation generates the specialized features and functions that allow postmitotic cells to acquire their distinguishing characteristics. This process is thought to be controlled by transcription factors called “terminal selectors” that directly activate a set of downstream effector genes. In Caenorhabditis elegans the differentiation of both the mechanosensory touch receptor neurons (TRNs) and the multidendritic nociceptor FLP neurons utilize the terminal selectors UNC-86 and MEC-3. The FLP neurons fail to activate TRN genes, however, because a complex of two transcriptional repressors (EGL-44/EGL-46) prevents their expression. Here we show that the ZEB family transcriptional factor ZAG-1 promotes TRN differentiation not by activating TRN genes but by preventing the expression of EGL-44/EGL-46. Since EGL-44/EGL-46 also inhibits the production of ZAG-1, these proteins form a bistable, negative feedback loop that regulates the choice between the two neuronal fates.Summary statement:Transcriptional repressors regulate binary fate choices through reciprocal inhibition during terminal neuronal differentiation. Specifically, ZEB family transcription factor safeguards fate specification of touch receptor neuron by inhibiting TEA domain-containing repressor.

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

Current Aging Science ◽

10.2174/1874609813999210104203614 ◽

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.

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Sperm Competition in the Absence of Fertilization in Caenorhabditis elegans

Genetics ◽

10.1093/genetics/152.1.201 ◽

1999 ◽

Vol 152 (1) ◽

pp. 201-208 ◽

Cited By ~ 2

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.

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A Deficiency Screen for Zygotic Loci Required for Establishment and Patterning of the Epidermis in Caenorhabditis elegans

Genetics ◽

10.1093/genetics/146.1.185 ◽

1997 ◽

Vol 146 (1) ◽

pp. 185-206 ◽

Cited By ~ 1

Author(s):

Rebecca M Terns ◽

Peggy Kroll-Conner ◽

Jiangwen Zhu ◽

Sooyoun Chung ◽

Joel H Rothman

Keyword(s):

Caenorhabditis Elegans ◽

Cell Types ◽

Epidermal Cells ◽

Epidermal Differentiation ◽

Apparent Effect ◽

Internal Organs ◽

C Elegans ◽

Seam Cell ◽

Genomic Regions ◽

Caenorhabditis Elegans Genome

To identify genomic regions required for establishment and patterning of the epidermis, we screened 58 deficiencies that collectively delete at least ∼67% of the Caenorhabditis elegans genome. The epidermal pattern of deficiency homozygous embryos was analyzed by examining expression of a marker specific for one of the three major epidermal cell types, the seam cells. The organization of the epidermis and internal organs was also analyzed using a monoclonal antibody specific for epithelial adherens junctions. While seven deficiencies had no apparent effect on seam cell production, 21 were found to result in subnormal, and five in excess numbers of these cells. An additional 23 deficiencies blocked expression of the seam cell marker, in some cases without preventing cell proliferation. Two deficiencies result in multinucleate seam cells. Deficiencies were also identified that result in subnormal numbers of epidermal cells, hyperfusion of epidermal cells into a large syncytium, or aberrant epidermal differentiation. Finally, analysis of internal epithelia revealed deficiencies that cause defects in formation of internal organs, including circularization of the intestine and bifurcation of the pharynx lumen. This study reveals that many regions of the C. elegans genome are required zygotically for patterning of the epidermis and other epithelia.

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

Nutrition and Healthy Aging ◽

10.3233/nha-210121 ◽

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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Genetic, Behavioral and Environmental Determinants of Male Longevity in Caenorhabditis elegans

Genetics ◽

10.1093/genetics/154.4.1597 ◽

2000 ◽

Vol 154 (4) ◽

pp. 1597-1610 ◽

Cited By ~ 1

Author(s):

David Gems ◽

Donald L Riddle

Keyword(s):

Caenorhabditis Elegans ◽

Life Span ◽

Wild Type ◽

Neuronal Function ◽

Nematode Caenorhabditis Elegans ◽

Wild Isolate ◽

Young Males ◽

C Elegans ◽

Single Sex ◽

Solitary Males

Abstract Males of the nematode Caenorhabditis elegans are shorter lived than hermaphrodites when maintained in single-sex groups. We observed that groups of young males form clumps and that solitary males live longer, indicating that male-male interactions reduce life span. By contrast, grouped or isolated hermaphrodites exhibited the same longevity. In one wild isolate of C. elegans, AB2, there was evidence of copulation between males. Nine uncoordinated (unc) mutations were used to block clumping behavior. These mutations had little effect on hermaphrodite life span in most cases, yet many increased male longevity even beyond that of solitary wild-type males. In one case, the neuronal function mutant unc-64(e246), hermaphrodite life span was also increased by up to 60%. The longevity of unc-4(e120), unc-13(e51), and unc-32(e189) males exceeded that of hermaphrodites by 70–120%. This difference appears to reflect a difference in sex-specific life span potential revealed in the absence of male behavior that is detrimental to survival. The greater longevity of males appears not to be affected by daf-2, but is influenced by daf-16. In the absence of male-male interactions, median (but not maximum) male life span was variable. This variability was reduced when dead bacteria were used as food. Maintenance on dead bacteria extended both male and hermaphrodite longevity.

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