Natural variation in reproductive timing and X-chromosome nondisjunction in Caenorhabditis elegans

Abstract Caenorhabditis elegans hermaphrodites first produce a limited number of sperm cells, before their germline switches to oogenesis. Production of progeny then ensues until sperm is depleted. Male production in the self-progeny of hermaphrodites occurs following X-chromosome nondisjunction during gametogenesis, and in the reference strain increases with age of the hermaphrodite parent. To enhance our understanding of the reproductive timecourse in C. elegans, we measured and compared progeny production and male proportion during the early and late reproductive periods of hermaphrodites for 96 wild C. elegans strains. We found that the two traits exhibited natural phenotypic variation with few outliers and a similar reproductive timing pattern as previous reports. Progeny number and male proportion were not correlated in the wild strains, implying that wild strains with a large brood size did not produce males at a higher rate. We also identified loci and candidate genetic variants significantly associated with male-production rate in the late and total reproductive periods. Our results provide an insight into life-history traits in wild C. elegans strains.

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Natural variations in reproductive aging phenotypes reveal the importance of early reproductive period in Caenorhabditis elegans

10.1101/2021.04.08.439028 ◽

2021 ◽

Author(s):

Jiseon Lim ◽

Jun Kim ◽

Junho Lee

Keyword(s):

Caenorhabditis Elegans ◽

X Chromosome ◽

Brood Size ◽

Current Knowledge ◽

Reproductive Capacity ◽

Initial Population ◽

Reproductive Aging ◽

C Elegans ◽

Wild Strains ◽

Chromosome Nondisjunction

Although reproductive capacity is a major factor in individual fitness, aging of the reproductive system precedes somatic aging and may reduce the total brood size. Genetic studies have led to the development of a body of evolutionary theory in the nematode Caenorhabditis elegans, but these studies did not take into account current knowledge about the natural history of C. elegans. To enhance our understanding of reproductive aging in C. elegans, we measured and compared two reproductive aging-related traitsthe number of progeny and the X-chromosome nondisjunction rateof 96 wild strains during early, late and total reproductive periods. We found that the two traits exhibited natural phenotypic variation, with few outliers, and that the brood size and the X-chromosome nondisjunction rate were not genetically correlated. Contrary to a previous hypothesis, that reproductive aging contributes to the generation of an optimal total number of offspring, we found that the total brood size did not converge to an optimal value, and early brood size was more constant than total brood size among wild strains. We speculate that reproductive aging is a by-product of a rapid increase in the initial population size, which might be related to the boom-and-bust lifestyle of C. elegans. We also identified loci and candidate genetic variants significantly associated with X-chromosome nondisjunction rate in the late and total reproductive periods. Our results provide an insight into reproductive aging in wild C. elegans strains.

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RADIATION-SENSITIVE MUTANTS OF CAENORHABDITIS ELEGANS

Genetics ◽

10.1093/genetics/102.2.159 ◽

1982 ◽

Vol 102 (2) ◽

pp. 159-178

Author(s):

Philip S Hartman ◽

Robert K Herman

Keyword(s):

Caenorhabditis Elegans ◽

X Chromosome ◽

Spontaneous Mutation ◽

Radiation Sensitivity ◽

Temperature Sensitive ◽

X Rays ◽

C Elegans ◽

Elevated Frequency ◽

Rad Mutants ◽

Chromosome Nondisjunction

ABSTRACT Nine rad (for abnormal radiation sensitivity) mutants hypersensitive to ultraviolet light were isolated in the small nematode Caenorhabditis elegans. The mutations are recessive to their wild-type alleles, map to four of the six linkage groups in C. elegans and define nine new games named rad-1 through rad-9. Two of the mutants—rad-1 and rad-2—are very hypersensitive to X rays, and three—rad-2, rad-3 and rad-4—are hypersensitive to methyl methanesulfonate under particular conditions of exposure. The hypersensitivity of these mutants to more than one DNA-damaging agent suggests that they may be abnormal in DNA repair. One mutant—rad-5, a temperature-sensitive sterile mutant—shows an elevated frequency of spontaneous mutation at more than one locus; rad-4, which shows a cold-sensitive embryogenesis, reduces meiotic X-chromosome nondisjunction tenfold and partially suppresses some but not all mutations that increase meiotic X-chromosome nondisjunction; the viability of rad-6 hermaphrodites is half that of rad-6 males at 25°; and newly mature (but not older) rad-8 hermaphrodites produce many inviable embryo progeny. Meiotic recombination frequencies were measured for seven rad mutants and found to be close to normal.

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The Caenorhabditis elegans DEG-3/DES-2 Channel Is a Betaine-Gated Receptor Insensitive to Monepantel

Molecules ◽

10.3390/molecules27010312 ◽

2022 ◽

Vol 27 (1) ◽

pp. 312

Author(s):

Tina V. A. Hansen ◽

Heinz Sager ◽

Céline E. Toutain ◽

Elise Courtot ◽

Cédric Neveu ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Nicotinic Acetylcholine Receptors ◽

Acetylcholine Receptors ◽

Parasitic Nematode ◽

Nematode Species ◽

Xenopus Laevis Oocytes ◽

Allosteric Modulators ◽

C Elegans ◽

Electrode Voltage ◽

Insight Into

Natural plant compounds, such as betaine, are described to have nematocidal properties. Betaine also acts as a neurotransmitter in the free-living model nematode Caenorhabditis elegans, where it is required for normal motility. Worm motility is mediated by nicotinic acetylcholine receptors (nAChRs), including subunits from the nematode-specific DEG-3 group. Not all types of nAChRs in this group are associated with motility, and one of these is the DEG-3/DES-2 channel from C. elegans, which is involved in nociception and possibly chemotaxis. Interestingly, the activity of DEG-3/DES-2 channel from the parasitic nematode of ruminants, Haemonchus contortus, is modulated by monepantel and its sulfone metabolite, which belong to the amino-acetonitrile derivative anthelmintic drug class. Here, our aim was to advance the pharmacological knowledge of the DEG-3/DES-2 channel from C. elegans by functionally expressing the DEG-3/DES-2 channel in Xenopus laevis oocytes and using two-electrode voltage-clamp electrophysiology. We found that the DEG-3/DES-2 channel was more sensitive to betaine than ACh and choline, but insensitive to monepantel and monepantel sulfone when used as direct agonists and as allosteric modulators in co-application with betaine. These findings provide important insight into the pharmacology of DEG-3/DES-2 from C. elegans and highlight the pharmacological differences between non-parasitic and parasitic nematode species.

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Inter-generational consequences for growing Caenorhabditis elegans in liquid

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2018.0125 ◽

2019 ◽

Vol 374 (1770) ◽

pp. 20180125 ◽

Cited By ~ 6

Author(s):

Itamar Lev ◽

Roberta Bril ◽

Yunan Liu ◽

Lucila Inés Ceré ◽

Oded Rechavi

Keyword(s):

Caenorhabditis Elegans ◽

Early Life ◽

Epigenetic Inheritance ◽

Evolutionary Medicine ◽

C Elegans ◽

Generational Effects ◽

Large Populations ◽

Two Generations ◽

Generational Changes ◽

In The Wild

In recent years, studies in Caenorhabditis elegans nematodes have shown that different stresses can generate multigenerational changes. Here, we show that worms that grow in liquid media, and also their plate-grown progeny, are different from worms whose ancestors were grown on plates. It has been suggested that C. elegans might encounter liquid environments in nature, although actual observations in the wild are few and far between. By contrast, in the laboratory, growing worms in liquid is commonplace, and often used as an alternative to growing worms on agar plates, to control the composition of the worms' diet, to starve (and synchronize) worms or to grow large populations for biochemical assays. We found that plate-grown descendants of M9 liquid medium-grown worms were longer than control worms, and the heritable effects were already apparent very early in development. We tested for the involvement of different known epigenetic inheritance mechanisms, but could not find a single mutant in which these inter-generational effects are cancelled. While we found that growing in liquid always leads to inter-generational changes in the worms’ size, trans-generational effects were found to be variable, and in some cases, the effects were gone after one to two generations. These results demonstrate that standard cultivation conditions in early life can dramatically change the worms' physiology in adulthood, and can also affect the next generations. This article is part of the theme issue ‘Developing differences: early-life effects and evolutionary medicine’.

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New strains for tissue-specific RNAi studies in Caenorhabditis elegans

10.1101/283325 ◽

2018 ◽

Author(s):

Jason S. Watts ◽

Henry F. Harrison ◽

Shizue Omi ◽

Quentin Guenthers ◽

James Dalelio ◽

...

Keyword(s):

Fatty Acid ◽

Caenorhabditis Elegans ◽

Gene Function ◽

Target Genes ◽

Resistant Mutant ◽

Knockout Mutant ◽

Tissue Specific ◽

Double Stranded Rna ◽

C Elegans ◽

Insight Into

AbstractRNA interference is a powerful tool for dissecting gene function. In Caenorhabditis elegans, ingestion of double stranded RNA causes strong, systemic knockdown of target genes. Further insight into gene function can be revealed by tissue-specific RNAi techniques. Currently available tissue-specific C. elegans strains rely on rescue of RNAi function in a desired tissue or cell in an otherwise RNAi deficient genetic background. We attempted to assess the contribution of specific tissues to polyunsaturated fatty acid (PUFA) synthesis using currently available tissue-specific RNAi strains. We discovered that rde-1 (ne219), a commonly used RNAi-resistant mutant strain, retains considerable RNAi capacity against RNAi directed at PUFA synthesis genes. By measuring changes in the fatty acid products of the desaturase enzymes that synthesize PUFAs, we found that the before mentioned strain, rde-1 (ne219) and the reported germline only RNAi strain, rrf-1 (pk1417) are not appropriate genetic backgrounds for tissue-specific RNAi experiments. However, the knockout mutant rde-1 (ne300) was strongly resistant to dsRNA induced RNAi, and thus is more appropriate for construction of a robust tissue-specific RNAi strains. Using newly constructed strains in the rde-1(null) background, we found considerable desaturase activity in intestinal, epidermal, and germline tissues, but not in muscle. The RNAi-specific strains reported in this study will be useful tools for C. elegans researchers studying a variety of biological processes.

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Feeding recombinant Royalactin: Measures of improved lifespan and mitochondrial function in Caenorhabditis elegans

10.1101/2020.09.14.296053 ◽

2020 ◽

Author(s):

Xia Li ◽

Thomas L. Ingram ◽

Ying Wang ◽

Kamila Derecka ◽

Nathan Courtier ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Mitochondrial Function ◽

Royal Jelly ◽

Biological Functions ◽

C Elegans ◽

Beneficial Effects ◽

Physiological Processes ◽

Royal Jelly Protein ◽

Insight Into ◽

Over Time

AbstractAgeing, the decline of biological functions over time, is inherent to eukaryotes. Female honeybees attain a long-lived queen phenotype upon continuous consumption of royal jelly, whereas restricted supply of this nutritional substance promotes the development of worker bees, which are short-lived. An abundant protein found within royal jelly is major royal jelly protein 1 (MRJP1), also known as ‘Royalactin’. Health- and lifespan promoting effects have been attributed to Royalactin in species from diverse animal taxa, suggesting it acts on phylogenetically conserved physiological processes. Here, we explore the effects of feeding the nematode Caenorhabditis elegans with Escherichia coli that express a recombinant form of Royalactin (RArec). We confirm that consumption of RArec increases body size, improves locomotion and extends lifespan. We discover a link between Royalactin and mitochondria, organelles which play a key part in the ageing process: both spare respiratory capacity and morphology indicate improved mitochondrial function in RArec fed C. elegans. These results demonstrate the feasibility of using recombinant Royalactin to gain further insight into processes of healthy ageing in many species.RArec production allows insight into potential beneficial effects across species.

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Punctuated loci on chromosome IV determine natural variation in Orsay virus susceptibility of Caenorhabditis elegans strains Bristol N2 and Hawaiian CB4856

Journal of Virology ◽

10.1128/jvi.02430-20 ◽

2021 ◽

Author(s):

Mark G. Sterken ◽

Lisa van Sluijs ◽

Yiru A. Wang ◽

Wannisa Ritmahan ◽

Mitra L. Gultom ◽

...

Keyword(s):

Genetic Variation ◽

Caenorhabditis Elegans ◽

Virus Infection ◽

Genetic Architecture ◽

Recombinant Inbred Lines ◽

Model Organism ◽

C Elegans ◽

Viral Susceptibility ◽

Orsay Virus ◽

Insight Into

Host-pathogen interactions play a major role in evolutionary selection and shape natural genetic variation. The genetically distinct Caenorhabditis elegans strains, Bristol N2 and Hawaiian CB4856, are differentially susceptible to the Orsay virus (OrV). Here we report the dissection of the genetic architecture of susceptibility to OrV infection. We compare OrV infection in the relatively resistant wild-type CB4856 strain to the more susceptible canonical N2 strain. To gain insight into the genetic architecture of viral susceptibility, 52 fully sequenced recombinant inbred lines (CB4856 x N2 RILs) were exposed to OrV. This led to the identification of two loci on chromosome IV associated with OrV resistance. To verify the two loci and gain additional insight into the genetic architecture controlling virus infection, introgression lines (ILs) that together cover chromosome IV, were exposed to OrV. Of the 27 ILs used, 17 had an CB4856 introgression in an N2 background and 10 had an N2 introgression in a CB4856 background. Infection of the ILs confirmed and fine-mapped the locus underlying variation in OrV susceptibility and we found that a single nucleotide polymorphism in cul-6 may contribute to the difference in OrV susceptibility between N2 and CB4856. An allele swap experiment showed the strain CB4856 became as susceptible as the N2 strain by having an N2 cul-6 allele, although having the CB4856 cul-6 allele did not increase resistance in N2. Additionally, we found that multiple strains with non-overlapping introgressions showed a distinct infection phenotype from the parental strain, indicating that there are punctuated locations on chromosome IV determining OrV susceptibility. Thus, our findings reveal the genetic complexity of OrV susceptibility in C. elegans and suggest that viral susceptibility is governed by multiple genes. Importance Genetic variation determines the viral susceptibility of hosts. Yet, pinpointing which genetic variants determine viral susceptibility remains challenging. Here, we have exploited the genetic tractability of the model organism C. elegans to dissect the genetic architecture of Orsay virus infection. Our results provide novel insight into natural determinants of Orsay virus infection.

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Meiotic mutants that cause a polar decrease in recombination on the X chromosome in Caenorhabditis elegans.

Genetics ◽

10.1093/genetics/136.1.119 ◽

1994 ◽

Vol 136 (1) ◽

pp. 119-127

Author(s):

S A Broverman ◽

P M Meneely

Keyword(s):

Caenorhabditis Elegans ◽

Genetic Map ◽

X Chromosome ◽

Recessive Mutations ◽

Feature Characteristic ◽

Comparable Effect ◽

Chromosome Recombination ◽

The Right ◽

Chromosome Nondisjunction ◽

Pairing Region

Abstract Recessive mutations in three autosomal genes, him-1, him-5 and him-8, cause high levels of X chromosome nondisjunction in hermaphrodites of Caenorhabditis elegans, with no comparable effect on autosomal disjunction. Each of the mutants has reduced levels of X chromosome recombination, correlating with the increase in nondisjunction. However, normal or elevated levels of recombination occur at the end of the X chromosome hypothesized to contain the pairing region (the left end), with recombination levels decreasing in regions approaching the right end. Thus, both the number and the distribution of X chromosome exchange events are altered in these mutants. As a result, the genetic map of the X chromosome in the him mutants exhibits a clustering of genes due to reduced recombination, a feature characteristic of the genetic map of the autosomes in non-mutant animals. We hypothesize that these him genes are needed for some processive event that initiates near the left end of the X chromosome.

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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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