Naturally occurring genetic variation affects Drosophila photoreceptor determination

Polaczyk, Patricia J.; Gasperini, Robert; Gibson, Greg

doi:10.1007/s004270050137

Cited by 67 publications

(51 citation statements)

References 28 publications

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“…Sex are neutral in low density but have detectable effects in high larval density. Similarly Vieira et al (2000) found specificity was also noted in the study of eye development by Polacysk et al (1998), discussed above. The that life span QTL tested in various stress and temperature regimes show a high degree of conditional neutralauthors remark that, since visual function is presumably equally necessary in both sexes, sex dependence would ity: Of the 17 QTL detected all were environment specific, i.e., were detectable only in a specific treatment.…”

Section: Mackay 2002) Consequently It Has Previously Beensupporting

confidence: 52%

“…Another striking example for conditional neutrality due to epistasis is of interactions. In the variable interaction scenario (the "moving rug"), neither state before or after the change provided by Polacysk et al (1998). Although eye development in Drosophila is a highly stereotypic process, is particularly robust, but there is extensive line crossing of mutational effects (cf.…”

Section: Mackay 2002) Consequently It Has Previously Beenmentioning

confidence: 99%

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The Population Genetic Theory of Hidden Variation and Genetic Robustness

2004

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One of the most solid generalizations of transmission genetics is that the phenotypic variance of populations carrying a major mutation is increased relative to the wild type. At least some part of this higher variance is genetic and due to release of previously hidden variation. Similarly, stressful environments also lead to the expression of hidden variation. These two observations have been considered as evidence that the wild type has evolved robustness against genetic variation, i.e., genetic canalization. In this article we present a general model for the interaction of a major mutation or a novel environment with the additive genetic basis of a quantitative character under stabilizing selection. We introduce an approximation to the genetic variance in mutation-selection-drift balance that includes the previously used stochastic Gaussian and house-of-cards approximations as limiting cases. We then show that the release of hidden genetic variation is a generic property of models with epistasis or genotype-environment interaction, regardless of whether the wild-type genotype is canalized or not. As a consequence, the additive genetic variance increases upon a change in the environment or the genetic background even if the mutant character state is as robust as the wild-type character. Estimates show that this predicted increase can be considerable, in particular in large populations and if there are conditionally neutral alleles at the loci underlying the trait. A brief review of the relevant literature suggests that the assumptions of this model are likely to be generic for polygenic traits. We conclude that the release of hidden genetic variance due to a major mutation or environmental stress does not demonstrate canalization of the wild-type genotype.

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Section: Mackay 2002) Consequently It Has Previously Beensupporting

confidence: 52%

Section: Mackay 2002) Consequently It Has Previously Beenmentioning

confidence: 99%

The Population Genetic Theory of Hidden Variation and Genetic Robustness

2004

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“…The ability to suppress environmental or genetic noise is the hallmark of genetic canalization, as illustrated by the classical experiments of Waddington (16,(20)(21)(22)(23), Waddington and Robertson (24), Rendel (25,26), and others (27)(28)(29)(30). One possible explanation of our results, therefore, is that the expression of within-species variation is suppressed or is too small to be detected by our experiments.…”

Section: Discussionmentioning

confidence: 52%

Canalization of segmentation and its evolution in Drosophila

Lott

Kreitman

Pálsson

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

161

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Segmentation in Drosophila embryogenesis occurs through a hierarchical cascade of regulatory gene expression driven by the establishment of a diffusion-mediated morphogen gradient. Here, we investigate the response of this pattern formation process to genetic variation and evolution in egg size. Specifically, we ask whether spatial localization of gap genes Kruppel (Kr) and giant (gt) and the pair-rule gene even-skipped (eve) during cellularization is robust to genetic variation in embryo length in three Drosophila melanogaster isolines and two closely related species. We identified two wild-derived strains of D. melanogaster whose eggs differ by Ϸ25% in length when reared under identical conditions. These two lines, a D. melanogaster laboratory stock (w1118), and offspring from crosses between the lines all exhibit precise scaling in the placement of gap and pair-rule gene expression along the anterior-posterior axis in relation to embryo length. Genetic analysis indicates that this scaling is maternally controlled. Maternal regulation of scaling must be required for consistent localization of segmentation gene expression because embryo size, a genetically variable and adaptive trait, is maternally inherited. We also investigated spatial scaling between these D. melanogaster lines and single lines of Drosophila sechellia and Drosophila simulans, the latter two differing by Ϸ25% in egg length. In contrast to the robust scaling we observed within species, localization of gene expression relative to embryo length differs significantly between the three species. Thus, the developmental mechanism that assures robust scaling within a species does not prevent rapid evolution between species.buffering ͉ development ͉ embryo size ͉ genetic variation ͉ scaling

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“…that the wild type of an organism, that is to say, the form which occurs in Nature under the influence of natural selection, is much less variable in appearance than the majority of the mutant races'' (1). Corroborating Waddington's observation are a number of experiments demonstrating increased phenotypic variance under extreme genetic or environmental perturbation (2)(3)(4)(5)(6). A key insight of Waddington was that the constancy of wild-type phenotypes in the face of genetic and environmental perturbations is best viewed as a buffering of the developmental process.…”

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confidence: 96%

Waddington's canalization revisited: Developmental stability and evolution

Siegal

Bergman

2002

Proc. Natl. Acad. Sci. U.S.A.

568

653

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Most species maintain abundant genetic variation and experience a range of environmental conditions, yet phenotypic variation is low. That is, development is robust to changes in genotype and environment. It has been claimed that this robustness, termed canalization, evolves because of long-term natural selection for optimal phenotypes. We show that the developmental process, here modeled as a network of interacting transcriptional regulators, constrains the genetic system to produce canalization, even without selection toward an optimum. The extent of canalization, measured as the insensitivity to mutation of a network's equilibrium state, depends on the complexity of the network, such that more highly connected networks evolve to be more canalized. We argue that canalization may be an inevitable consequence of complex developmental-genetic processes and thus requires no explanation in terms of evolution to suppress phenotypic variation.

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Naturally occurring genetic variation affects Drosophila photoreceptor determination

Cited by 67 publications

References 28 publications

The Population Genetic Theory of Hidden Variation and Genetic Robustness

The Population Genetic Theory of Hidden Variation and Genetic Robustness

Canalization of segmentation and its evolution in Drosophila

Waddington's canalization revisited: Developmental stability and evolution

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