Developmental stability is the tendency of morphological traits to resist the effects of developmental noise, and isWe found that 406 deficiencies significantly affected the mean of morphological traits, and 92 deficiencies increased FA. These results suggest that several genomic regions have the potential to affect developmental stability. They also suggest the possibility of the existence of trait-specific and trait-nonspecific mechanisms for stabilizing developmental processes. The new findings in this study could provide insight into the understanding of the genetic architecture underlying developmental stability.
Developmental processes of organisms are programmed to proceed in a finely regulated manner and finish within a certain period of time depending on the ambient environmental conditions. Therefore, variation in the developmental period under controlled genetic and environmental conditions indicates innate instability of the developmental process. In this study, we aimed to determine whether a molecular machinery exists that regulates the canalization of the developmental period and, if so, to test whether the same mechanism also stabilizes a morphological trait. To search for regions that influence the instability of the developmental period, we conducted genome-wide deficiency mapping with 441 isogenic deficiency strains covering 65.5% of the Drosophila melanogaster genome. We found that 11 independent deficiencies significantly increased the instability of the developmental period and 5 of these also significantly increased the fluctuating asymmetry of wing shape although there was no significant correlation between the instabilities of developmental period and wing shape in general. These results suggest that canalization processes of the developmental period and morphological traits are at least partially independent. Our findings emphasize the potential importance of temporal variation in development as an indicator of developmental stability and canalization and provide a novel perspective for understanding the regulation of phenotypic variability.
BackgroundTemperature adaptation is one of the most important determinants of distribution and population size of organisms in nature. Recently, quantitative trait loci (QTL) mapping and gene expression profiling approaches have been used for detecting candidate genes for heat resistance. However, the resolution of QTL mapping is not high enough to examine the individual effects of various genes in each QTL. Heat stress-responsive genes, characterized by gene expression profiling studies, are not necessarily responsible for heat resistance. Some of these genes may be regulated in association with the heat stress response of other genes.ResultsTo evaluate which heat-responsive genes are potential candidates for heat resistance with higher resolution than previous QTL mapping studies, we performed genome-wide deficiency screen for QTL for heat resistance. We screened 439 isogenic deficiency strains from the DrosDel project, covering 65.6% of the Drosophila melanogaster genome in order to map QTL for thermal resistance. As a result, we found 19 QTL for heat resistance, including 3 novel QTL outside the QTL found in previous studies.ConclusionThe QTL found in this study encompassed 19 heat-responsive genes found in the previous gene expression profiling studies, suggesting that they were strong candidates for heat resistance. This result provides new insights into the genetic architecture of heat resistance. It also emphasizes the advantages of genome-wide deficiency screen using isogenic deficiency libraries.
Environmental canalization is defined as a reduction in the effect of external environmental perturbations on a phenotype, while phenotypic plasticity is defined as the production of different phenotypes in alternative environments. These terms describe different aspects of the same phenomenon, that is, the sensitivity of the phenotype to the environment. Genetic regulation of the environmental sensitivity has been a central topic in the field of evolutionary biology. In this study, we performed deficiency screening to detect genomic regions with effects on the environmental sensitivity of Drosophila melanogaster sensory bristles.We used a collection of isogenic deficiency strains established by the DrosDel Project for screening. We screened 423 genomic deficiencies that encompassed approximately 63.6% of the entire D. melanogaster genome. We identified 29 genomic deficiencies showing significant effects on environmental sensitivity, suggesting that multiple genomic regions may influence phenotypic variation. We also found significant correlations among the effects of deficiencies on environmental sensitivity for different bristle traits, suggesting that the same genetic mechanism can regulate environmental sensitivity of multiple traits. Current highresolution mapping will facilitate the examination of individual candidate genes using mutations or RNAi approaches in future studies.
Biological clocks regulate various behavioural and physiological traits; slower circadian clocks are expected to slow down the development, suggesting a potential genetic correlation between the developmental period and circadian rhythm. However, a correlation between natural genetic variations in the developmental period and circadian rhythm has only been found in Bactrocera cucurbitae. The number of genetic factors that contribute to this genetic correlation is largely unclear. In this study, to examine whether natural genetic variations in the developmental period and circadian rhythm are correlated in Drosophila melanogaster, we performed an artificial disruptive selection on the developmental periods using wild-type strains and evaluated the circadian rhythms of the selected lines. To investigate whether multiple genetic factors mediate the genetic correlation, we reanalyzed previously published genome-wide deficiency screening data based on DrosDel isogenic deficiency strains and evaluated the effect of 438 genomic deficiencies on the developmental periods. We then randomly selected 32 genomic deficiencies with significant effects on the developmental periods and tested their effects on circadian rhythms. As a result, we found a significant response to selection for longer developmental periods and their correlated effects on circadian rhythms of the selected lines. We also found that 18 genomic regions had significant effects on the developmental periods and circadian rhythms, indicating their potential for mediating the genetic correlation between the developmental period and circadian rhythm. The novel findings of our study might lead to a better understanding of how this correlation is regulated genetically in broader taxonomic groups.
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