scholarly journals Temperature, stress and spontaneous mutation in Caenorhabditis briggsae and Caenorhabditis elegans

2013 ◽  
Vol 9 (1) ◽  
pp. 20120334 ◽  
Author(s):  
Chikako Matsuba ◽  
Dejerianne G. Ostrow ◽  
Matthew P. Salomon ◽  
Amit Tolani ◽  
Charles F. Baer
Keyword(s):  
Caenorhabditis Elegans ◽  
Mutation Rate ◽  
Physiological Stress ◽  
Spontaneous Mutation ◽  
Caenorhabditis Briggsae ◽  
C Elegans ◽  
Microsatellite Mutation Rate ◽  
The Difference ◽  
Microsatellite Mutation ◽  
Stress Dependent

Mutation rate often increases with environmental temperature, but establishing causality is complicated. Asymmetry between physiological stress and deviation from the optimal temperature means that temperature and stress are often confounded. We allowed mutations to accumulate in two species of Caenorhabditis for approximately 100 generations at 18°C and for approximately 165 generations at 26°C; 26°C is stressful for Caenorhabditis elegans but not for Caenorhabditis briggsae . We report mutation rates at a set of microsatellite loci and estimates of the per-generation decay of fitness (Δ M w ), the genomic mutation rate for fitness ( U ) and the average effect of a new mutation ( E [ a ]), assayed at both temperatures. In C. elegans , the microsatellite mutation rate is significantly greater at 26°C than at 18°C whereas in C. briggsae there is only a slight, non-significant increase in mutation rate at 26°C, consistent with stress-dependent mutation in C. elegans . The fitness data from both species qualitatively reinforce the microsatellite results. The fitness results of C. elegans are potentially complicated by selection but also suggest temperature-dependent mutation; the difference between the two species suggests that physiological stress plays a significant role in the mutational process.

scholarly journals The Rate of Spontaneous Mutation for Life-History Traits in Caenorhabditis elegans

Genetics ◽  
1999 ◽  
Vol 151 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Larissa L Vassilieva ◽  
Michael Lynch
Keyword(s):  
Life History ◽  
Caenorhabditis Elegans ◽  
Mutation Rate ◽  
Life History Traits ◽  
Deleterious Mutation ◽  
Spontaneous Mutation ◽  
Spontaneous Mutations ◽  
Homozygous State ◽  
Mutational Effect ◽  
Biological Differences

Abstract Spontaneous mutations were accumulated in 100 replicate lines of Caenorhabditis elegans over a period of ∼50 generations. Periodic assays of these lines and comparison to a frozen control suggest that the deleterious mutation rate for typical life-history characters in this species is at least 0.05 per diploid genome per generation, with the average mutational effect on the order of 14% or less in the homozygous state and the average mutational heritability ∼0.0034. While the average mutation rate per character and the average mutational heritability for this species are somewhat lower than previous estimates for Drosophila, these differences can be reconciled to a large extent when the biological differences between these species are taken into consideration.

scholarly journals Heterozygosity increases microsatellite mutation rate

2016 ◽  
Vol 12 (1) ◽  
pp. 20150929 ◽  
Author(s):  
William Amos
Keyword(s):  
Mutation Rate ◽  
Feedback Loop ◽  
Strong Support ◽  
Heterozygous Site ◽  
Direct Support ◽  
Rare Alleles ◽  
Microsatellite Mutation Rate ◽  
Surrogate Measure ◽  
Microsatellite Mutation ◽  
The Impact

Whole genome sequencing of families of Arabidopsis has recently lent strong support to the heterozygote instability (HI) hypothesis that heterozygosity locally increases mutation rate. However, there is an important theoretical difference between the impact on base substitutions, where mutation rate increases in regions surrounding a heterozygous site, and the impact of HI on sequences such as microsatellites, where mutations are likely to occur at the heterozygous site itself. At microsatellite loci, HI should create a positive feedback loop, with heterozygosity and mutation rate mutually increasing each other. Direct support for HI acting on microsatellites is limited and contradictory. I therefore analysed AC microsatellites in 1163 genome sequences from the 1000 genomes project. I used the presence of rare alleles, which are likely to be very recent in origin, as a surrogate measure of mutation rate. I show that rare alleles are more likely to occur at locus-population combinations with higher heterozygosity even when all populations carry exactly the same number of alleles.

scholarly journals The Caenorhabditis elegans Homologue of Deleted in Azoospermia Is Involved in the Sperm/Oocyte Switch

2006 ◽  
Vol 17 (7) ◽  
pp. 3147-3155 ◽  
Author(s):  
Muneyoshi Otori ◽  
Takeshi Karashima ◽  
Masayuki Yamamoto
Keyword(s):  
Caenorhabditis Elegans ◽  
Caenorhabditis Briggsae ◽  
Essential Factor ◽  
Female Meiosis ◽  
Stem Cell Proliferation ◽  
C Elegans ◽  
Essential Step ◽  
Deleted In Azoospermia ◽  
Translational Regulators ◽  
Daz Gene

The Deleted in Azoospermia (DAZ) gene family encodes putative translational activators that are required for meiosis and other aspects of gametogenesis in animals. The single Caenorhabditis elegans homologue of DAZ, daz-1, is an essential factor for female meiosis. Here, we show that daz-1 is important for the switch from spermatogenesis to oogenesis (the sperm/oocyte switch), which is an essential step for the hermaphrodite germline to produce oocytes. RNA interference of the daz-1 orthologue in a related nematode, Caenorhabditis briggsae, resulted in a complete loss of the sperm/oocyte switch. The C. elegans hermaphrodite deficient in daz-1 also revealed a failure in the sperm/oocyte switch if the genetic background was conditional masculinization of germline. DAZ-1 could bind specifically to mRNAs encoding the FBF proteins, which are translational regulators for the sperm/oocyte switch and germ stem cell proliferation. Expression of the FBF proteins seemed to be lowered in the daz-1 mutant at the stage for the sperm/oocyte switch. Conversely, a mutation in gld-3, a gene that functionally counteracts FBF, could partially restore oogenesis in the daz-1 mutant. Together, we propose that daz-1 plays a role upstream of the pathway for germ cell sex determination.

Analysis of the VPE sequences in the Caenorhabditis elegans vit-2 promoter with extrachromosomal tandem array-containing transgenic strains

1994 ◽  
Vol 14 (1) ◽  
pp. 484-491
Author(s):  
M MacMorris ◽  
J Spieth ◽  
C Madej ◽  
K Lea ◽  
T Blumenthal
Keyword(s):  
Caenorhabditis Elegans ◽  
Fusion Gene ◽  
Caenorhabditis Briggsae ◽  
Unique Role ◽  
Promoter Function ◽  
C Elegans ◽  
Low Copy Number ◽  
Genes Encoding ◽  
Transgenic Lines ◽  
Adult Hermaphrodite

The Caenorhabditis elegans vit genes, encoding vitellogenins, are abundantly expressed in the adult hermaphrodite intestine. Two repeated elements, vit promoter element 1 (VPE1 [TGTCAAT]) and VPE2 (CTGATAA), have been identified in the 5' flanking DNA of each of the vit genes of C. elegans and Caenorhabditis briggsae. These elements have previously been shown to be needed for correctly regulated expression of a vit-2/vit-6 fusion gene in low-copy-number, integrated transgenes. Here we extend the analysis of the function of VPE1 and VPE2 by using transgenic lines carrying large, extrachromosomal arrays of the test genes. The results validate the use of such arrays for transgenic analysis of gene regulation in C. elegans, by confirming previous findings showing that the VPE1 at -45 and both VPE2s are sites of activation. Additional experiments now indicate that when the -45 VPE1 is inverted or replaced by a VPE2, nearly total loss of promoter function results, suggesting that the highly conserved -45 VPE1 plays a unique role in vit-2 promoter function. In contrast, single mutations eliminating the three upstream VPE1s are without effect. However, in combination in double and triple mutants, these upstream VPE1 mutations cause drastic reductions in expression levels. The -150 VPE2 can be replaced by a XhoI site (CTCGAG), and the -90 VPE2 can be eliminated, as long as the overlapping VPE1 is left intact, but when these two replacements are combined, activity is lost. Thus, the promoter must have at least one VPE2 and it must have at least two VPE1s, one at -45 and one additional upstream element.

scholarly journals Microsatellite Mutation Rate during Allohexaploidization of Newly Resynthesized Wheat

2012 ◽  
Vol 13 (12) ◽  
pp. 12533-12543 ◽  
Author(s):  
Jiangtao Luo ◽  
Ming Hao ◽  
Li Zhang ◽  
Jixiang Chen ◽  
Lianquan Zhang ◽  
...  
Keyword(s):  
Mutation Rate ◽  
Microsatellite Mutation Rate ◽  
Microsatellite Mutation

RADIATION-SENSITIVE MUTANTS OF CAENORHABDITIS ELEGANS

Genetics ◽  
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.

scholarly journals Mutation rate and spectrum in Caenorhabditis elegans mutation accumulation lines subjected to RNAi-induced knockdown of the mismatch repair gene msh-2

2021 ◽  
Author(s):  
Vaishali Katju ◽  
Anke Konrad ◽  
Thaddeus C. Deiss ◽  
Ulfar Bergthorsson
Keyword(s):  
Caenorhabditis Elegans ◽  
Mismatch Repair ◽  
Mutation Rate ◽  
Copy Number ◽  
Mutation Accumulation ◽  
Mutation Rates ◽  
Mutational Bias ◽  
C Elegans ◽  
Small Indels ◽  
Local Sequence

DNA mismatch repair (MMR), an evolutionarily conserved repair pathway shared by prokaryotic and eukaryotic species alike, influences molecular evolution by detecting and correcting mismatches that escape DNA polymerase proofreading, thereby protecting genetic fidelity, reducing the mutational load, and preventing lethality. Herein we conduct the first genome-wide evaluation of the alterations to the mutation rate and spectrum under impaired activity of the MutS homolog, msh-2, in Caenorhabditis elegans. We performed mutation accumulation (MA) under RNAi-induced knockdown of msh-2 for 50 generations in obligately outcrossing fog-2(lf) lines, followed by next-generation sequencing of 19 MA lines and the ancestral control. msh-2 impairment substantially increased the frequency of nuclear base substitutions (~23x) and small indels (~328x) relative to wildtype. However, we observed no increase in the mutation rates of mtDNA, and copy-number changes of single-copy genes. There was a marked increase in copy-number variation of rDNA genes under MMR impairment. In C. elegans, msh-2 repairs transitions more efficiently than transversions as well as increases the AT mutational bias relative to wildtype. The local sequence context, including sequence complexity, G+C-content, and flanking bases influenced the mutation rate. The X chromosome had a lower substitution and higher indel rate than autosomes, which can either result from sex-specific mutation rates or a nonrandom distribution of mutable sites in the genome. Comparison of MMR impairment in C. elegans to that in other species shows that the specificity of the MMR varies between taxa, and is more efficient in detecting and repairing small indels in eukaryotes relative to prokaryotes.

TOXIC ACTION OF COPPER, CADMIUM AND LEAD ON FREE-LIVING SOIL NEMATODES CAENORHABDITIS ELEGANS AND CAENORHABDITIS BRIGGSAE

2021 ◽  
Vol 1 (1) ◽  
pp. 43-46
Author(s):  
A. V. Egorova ◽  
Т. В. Kalinnikova ◽  
R. R. Shagidullin
Keyword(s):  
Heavy Metals ◽  
Caenorhabditis Elegans ◽  
Nicotinic Acetylcholine Receptors ◽  
Toxic Action ◽  
Model Organisms ◽  
Soil Nematodes ◽  
Caenorhabditis Briggsae ◽  
Free Living ◽  
C Elegans ◽  
Cadmium And Lead

Heavy metals are one of the most common pollutants in environment. The aim of this work was to test the hypothesis assuming that one of mechanisms of toxic action of copper, cadmium and lead on invertebrates’ organisms is adaptive activation of cholinergic synaptic transmission. In experiments with two free-living soil nematodes, namely Caenorhabditis elegans and Caenorhabditis briggsae, it has been shown that Cu2+, Cd2+ and Pb2+ ions at concentrations of 60 and 120 µM enhanced the negative effects of the nicotinic acetylcholine receptors agonist levamisole on the nematodes’ organisms. Under combined action of levamisole and heavy metals on organisms of C. elegans and C. briggsae the mean time of nematodes paralysis (complete loss of the ability to swim) was reduced. The results of this work show that nematodes C. elegans and C. briggsae can be used as model organisms to study mechanisms of toxic action of heavy metals.

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