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[
International Worm Meeting,
2013]
An obvious feature of living organisms is that their development is robust to variation in the environmental circumstances in which the organism finds itself - within limits. That is, the phenotype is more or less "canalized" (canalized "robust"). The "more or less" is of considerable interest to evolutionary biologists, for a variety of reasons, i.e., under what environmental or genetic circumstances does development become more or less canalized? Environmental canalization can be quantified as the phenotypic variation among genetically identical individuals raised in a uniform environment - the "(micro)environmental variance" in the lingo of quantitative genetics, V(E). Here we provide quantitative estimates of the effects of spontaneous mutations on V(E) for a variety of phenotypic traits subject to different selective regimes. Three general quantitative trends emerge. First, in almost all cases, mutation accumulation tends to de-canalize the phenotype (i.e., V(E) increases), typically at a rate similar to the rate of change of the trait itself. Second, there is a strong positive association between the rate of increase of V(E) for a trait and the mutational variance, V(M) for the trait itself. Third, and most intriguingly, mutations affecting V(E) for a trait appear to be usually under stronger selection than mutations affecting the trait itself.
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[
International Worm Meeting,
2009]
The development of many phenotypic traits is canalized (robust) with respect to environmental variation, i.e., the same phenotype develops irrespective of the environmental circumstances in which the developing individual finds itself. Canalization is adaptive when natural selection favors the same phenotype in different environmental contexts. We have previously documented that spontaneous mutations de-canalize several phenotypic traits - fecundity, body volume, and vulval development - in a predictable way. Canalization of a phenotypic trait necessarily requires variability in some underlying mechanism, but the nature of the controls is rarely known. Here we present evidence that the accumulation of spontaneous mutations actually REDUCES environmental variance in gene expression. We compared transcript abundance of > 7000 genes in four lines of C. elegans that had accumulated mutations for ~280 generations ("MA lines") to that of the common (presumably unmutated) ancestor of those lines, using standard dye-swap microarray methodology. Contrary to our a priori expectation, MA lines exhibited significantly LESS environmental variance for transcript abundance than did their common ancestor. This unexpected result is consistent with what would be predicted if variability in gene expression provides the controlling mechanism underlying phenotypic canalization. These results must be considered highly preliminary for several reasons, which we discuss, but a plausible mechanism underlying phenotypic canalization is obvious.
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[
Development & Evolution Meeting,
2008]
The evolution of canalization - the robustness of the phenotype to environmental or genetic perturbation - has attracted considerable recent interest. A key step toward understanding the evolution of any phenotype is to characterize the rate at which mutation introduces genetic variation for the trait (the mutational variance, VM) and the average directional effects of mutations on the trait mean (deltaM). In this study, the mutational parameters for canalization of productivity and body volume are quantified in two sets of mutation accumulation lines of nematodes in the genus Caenorhabditis and compared to the mutational parameters for the traits themselves. Four results emerge: (1) spontaneous mutations consistently de-canalize the phenotype; (2) the mutational parameters for de-canalization - VM (quantified as mutational heritability) and deltaM - are of the same order of magnitude as the same parameters for the traits themselves; (3) the mutational parameters for canalization are roughly correlated with the parameters for the traits themselves across taxa; and (4) there is no evidence that residual segregating overdominant loci contribute to the decay of canalization. These results suggest that canalization is readily evolvable, and that any evolutionary factor that causes mutations to accumulate will, on average, de-canalize the phenotype.
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[
International Worm Meeting,
2003]
The rate and effects of spontaneous mutations are of tremendous theoretical and practical importance in many areas of biology, but there are reliable data for only three multicellular taxa: C. elegans, Drosophila melanogaster, and Arabidopsis thaliana, and the interpretation of the data is highly controversial. Classical experiments in Drosophila suggest a mutational degradation of fitness of about 1% per generation, which implies a mutation rate on the order of one new deleterious mutation per diploid genome per generation. Conversely, data from the N2 strain of C. elegans and Arabidopsis and some new data from Drosophila melanogaster suggest that the genomic mutation rate may be an order of magnitude less than previously thought. The large phylogenetic distance between these taxa and the lack of systematically replicated studies precludes generalization, even within species. Here I report results from an experiment in which spontaneous mutations were allowed to accumulate for 100 generations in two strains of three species of androdioecious Rhabditid nematodes (C. elegans, C. briggsae, Oscheius myriophila), with the goal of partitioning the variance in mutational properties (decline in fitness, genomic mutation rate, and average effect of new mutations) within and among taxa. The results are quite clear: relative to the classical Drosophila experiments, in Rhabditid nematodes the decline in fitness and the genomic mutation rate are uniformly low, and there is relatively little variation within or among species. Two important conclusions follow: (1) the mutational properties of taxa may be conserved over long periods of evolutionary time, suggestive of strong stabilizing selection on the mutation rate. (2) Alternatively, the mutational properties of some taxa (e.g., D. melanogaster) may be much more variable than others (e.g., Rhabditid nematodes), in which case generalization from studies in a few model organisms may not be justified.
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[
Evolutionary Biology of Caenorhabditis and Other Nematodes,
2010]
Evolutionary theory predicts that, all else equal, the mutation rate should evolve to zero because deleterious mutations are so much more prevalent than beneficial mutations. All else is not equal: the mutation rate is never zero. Further, mutation rate demonstrably varies between and within species. In principle, the strength of natural selection to reduce the mutation rate should be stronger in self-fertilizing organisms than in related outcrossing organisms, perhaps much stronger. However, the relative efficacy of selection on mutation rate relative to the many other factors influencing the evolution of any species is poorly understood - that is, what is the empirical relevance of the theory? To address this question we allowed mutations to accumulate in the relative absence of natural selection for ~100 generations in several sets of "mutation accumulation" (MA) lines in several species of gonochoristic Caenorhabditis (C. remanei, C. brenneri, C.
sp5); we have previously conducted similar experiments in self-compatible rhabditids. The results are very clear: in every case the rate of mutational decay is substantially greater in the gonochoristic taxa than in the self-compatible C. elegans (~4X greater) and C. briggsae (~2X greater). Residual heterozygosity in the ancestral controls of these MA lines introduces some complications in interpreting the results, but there is reason to believe the results are not primarily due to inbreeding depression resulting from ancestral variation. The results suggest that natural selection operates to optimize the mutation rate in Caenorhabditis and that the strength (or efficiency) of selection differs consistently on the basis of mating system, as predicted by theory.
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[
International Worm Meeting,
2005]
Deleterious mutations are of fundamental importance to all aspects of organismal biology. Evolutionary geneticists have expended tremendous effort to estimate the genome-wide rate of mutation and the effects of new mutations on fitness, but the degree to which genomic mutational properties vary within and between taxa is largely unknown, particularly in multicellular organisms. Beginning with two highly inbred strains from each of three species in the nematode family Rhabditidae (Caenorhabditis briggsae, Caenorhabditis elegans, and Oscheius myriophila) we allowed mutations to accumulate in the relative absence of natural selection for over 200 generations. We document significant variation in the rate of decay of fitness due to new mutations between strains and between species: C. briggsae declines in fitness approximately twice as fast as C. elegans or O. myriophila. Estimates of the per-generation mutational decay of fitness were very consistent within strains between assays 100 generations apart. The results were very similar when fitness was assayed at 20C and 25C, although the relative fitness of the unmutated controls differed among species at the two temperatures. We report the mutational correlation between fitness in the different thermal environments. Rate of mutational decay in fitness was positively associated with genomic mutation rate and negatively associated with average mutational effect. These results provide unambiguous experimental evidence for substantial variation in genome-wide properties of mutation both within and between species and reinforce conclusions from previous experiments that the cumulative effects on fitness of new mutations can differ markedly among related taxa.
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[
Worm Breeder's Gazette,
1992]
unc-4 LacZ expression in A-type motor neurons David M. Miller and Charles J. Niemeyer, Dept. of Cell Biology, Duke Univ. Medical Ctr, Durham, NC 27710
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[
International Worm Meeting,
2011]
It has been known for a long time that environmental stress and mutations of large effect increase sensitivity to random environmental noise ("microenvironmental variance", VE). We recently quantified the effects of spontaneous mutation on VE in two species of nematodes in the genus Caenorhabditis, C. briggsae and C. elegans and found that the increase in VE for lifetime productivity is on the same order as that of the change in the trait mean, which is consistently greater in C. briggsae than in C. elegans. Here we report results from a new experiment in which mutations were allowed to accumulate at high (26 deg C) and low (18 deg C) temperatures in the same two species and fitness subsequently assayed at high and low temperatures. In C. briggsae, VE increased more with MA at 26 than at 18; there was little effect of MA temperature in C. elegans. Similarly, in C. briggsae the increase in VE was greater when assayed at high temperature; there was little effect of assay temperature in C. elegans. These results suggest that there is an important class of temperature-sensitive mutations in C. briggsae which in turn affect sensitivity to microenvironmental variation that is not present in C. elegans.
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[
Parasitol Today,
1992]
Nematode movement is reliant upon the somatic musculature that runs longitudinally along the body wall. Neuromuscular synapses occur in the ventral and dorsal cords and employ the excitatory neurotransmitter, acetylcholine (ACh), for modulation of muscle activity. Acetylcholine activity is terminated by hydrolysis by acetylcholinesterase (AChE). Here, Charles Opperman and Stella Chang discuss the molecular forms and potential role of this enzyme.
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[
International Worm Meeting,
2017]
A functional metabolic network is key for an organism's survival, and thus for its fitness. Spontaneous mutations reduce fitness, so it stands to reason they affect metabolism in some way. However, not all metabolites are equally important in maintaining organismal function, and the relationship between mutation and an organism's metabolic network has rarely been investigated. By investigating a set of mutation accumulation(MA) lines of Caenorhabditis elegans, we aim to better understand the effect mutations have on the metabolic network. Using a set of 43 MA lines and their ancestor, a pool of 29 metabolites was measured for changes in mean metabolite concentration (?M) and mutational variance (VM). We constructed a metabolic network map of these metabolites for C. elegans from the KEGG database, with the aim of characterizing the relationship between VM, ?M, and heritability found for these 29 metabolites and features of the metabolic network. Initial analysis shows a positive association between the largest k-core grouping of a metabolite and ?M and VM.