Genes That Can Alter Bristle Number by Directly Affecting SOP Equivalence Groups or Inhibitory Fields

A semi-lethal, sterile allele of the smooth locus (2-91.5), sm3, was discovered in an artificial selection line for low abdominal bristle number that had been started from a P-M dysgenic cross. The fitness effects and extremely low bristle number phenotype of the allele could not be separated by recombination from a P-element insertion at cytological location 56E, and precise excision of the P element at this site was associated with reversion to wild type. The smooth gene was cloned using the P-element insertion as a tag. The gene encodes a 2.6-kb transcript derived from 10 exons and covers a genomic region of at least 80 kb. The Drosophila smooth gene shares substantial sequence identity with a group of RNA binding proteins, with the closest relationship being to the human heterogeneous nuclear ribonucleoprotein L gene. The smooth gene is by definition an abdominal bristle number quantitative trait locus, but further work is required to discern whether naturally occurring allelic variation at this locus is a source of genetic variation for abdominal bristle number in natural populations.

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The expression of additive and nonadditive genetic variation under stress.

Genetics ◽

10.1093/genetics/140.3.1149 ◽

1995 ◽

Vol 140 (3) ◽

pp. 1149-1159

Author(s):

M W Blows ◽

M B Sokolowski

Keyword(s):

Genetic Variation ◽

Development Time ◽

Genetic Effects ◽

Hybrid Breakdown ◽

Bristle Number ◽

Gene Complexes ◽

General Expectation ◽

Faster Development ◽

Seven Generations ◽

Additive Genetic Effects

Abstract Experimental lines of Drosophila melanogaster derived from a natural population, which had been isolated in the laboratory for approximately 70 generations, were crossed to determine if the expression of additive, dominance and epistatic genetic variation in development time and viability was associated with the environment. No association was found between the level of additive genetic effects and environmental value for either trait, but nonadditive genetic effects increased at both extremes of the environmental range for development time. The expression of high levels of dominance and epistatic genetic variation at environmental extremes may be a general expectation for some traits. The disruption of the epistatic gene complexes in the parental lines resulted in hybrid breakdown toward faster development and there was some indication of hybrid breakdown toward higher viability. A combination of genetic drift and natural selection had therefore resulted in different epistatic gene complexes being selected after approximately 70 generations from a common genetic base. After crossing, the hybrid populations were observed for 10 generations. Epistasis contributed on average 12 hr in development time. Fluctuating asymmetry in sternopleural bristle number also evolved in the hybrid populations, decreasing by > 18% in the first seven generations after hybridization.

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Hybrid dysgenesis-induced quantitative variation on the X chromosome of Drosophila melanogaster.

Genetics ◽

10.1093/genetics/124.3.627 ◽

1990 ◽

Vol 124 (3) ◽

pp. 627-636

Author(s):

C Q Lai ◽

T F Mackay

Keyword(s):

Drosophila Melanogaster ◽

X Chromosome ◽

Quantitative Traits ◽

Natural Populations ◽

Quantitative Variation ◽

Hybrid Dysgenesis ◽

X Chromosomes ◽

Bristle Number ◽

Seven Generations ◽

Polygenic Variation

Abstract To determine the ability of the P-M hybrid dysgenesis system of Drosophila melanogaster to generate mutations affecting quantitative traits, X chromosome lines were constructed in which replicates of isogenic M and P strain X chromosomes were exposed to a dysgenic cross, a nondysgenic cross, or a control cross, and recovered in common autosomal backgrounds. Mutational heritabilities of abdominal and sternopleural bristle score were in general exceptionally high-of the same magnitude as heritabilities of these traits in natural populations. P strain chromosomes were eight times more mutable than M strain chromosomes, and dysgenic crosses three times more effective than nondysgenic crosses in inducing polygenic variation. However, mutational heritabilities of the bristle traits were appreciable for P strain chromosomes passed through one nondysgenic cross, and for M strain chromosomes backcrossed for seven generations to inbred P strain females, a result consistent with previous observations on mutations affecting quantitative traits arising from nondysgenic crosses. The new variation resulting from one generation of mutagenesis was caused by a few lines with large effects on bristle score, and all mutations reduced bristle number.

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VARIATION IN BRISTLE NUMBER OF DROSOPHILA MELANOGASTER

Acta Zoologica ◽

10.1111/j.1463-6395.1952.tb00366.x ◽

1952 ◽

Vol 33 (3) ◽

pp. 277-307 ◽

Cited By ~ 26

Author(s):

MARIANNE RASMUSON

Keyword(s):

Drosophila Melanogaster ◽

Bristle Number

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REGULATION OF ANTERIOR AND POSTERIOR SCUTELLAR BRISTLE NUMBER IN DROSOPHILA

Genetics ◽

10.1093/genetics/66.4.685 ◽

1970 ◽

Vol 66 (4) ◽

pp. 685-694

Author(s):

B D H Latter ◽

W R Scowcroft

Keyword(s):

Bristle Number

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EFFECTS OF POPULATION SIZE AND SELECTION INTENSITY ON RESPONSES TO DISRUPTIVE SELECTION IN DROSOPHILA MELANOGASTER

Genetics ◽

10.1093/genetics/78.2.715 ◽

1974 ◽

Vol 78 (2) ◽

pp. 715-735

Author(s):

J S F Barker ◽

L J E Karlsson

Keyword(s):

Assortative Mating ◽

Random Mating ◽

Female Parent ◽

Disruptive Selection ◽

Lethal Gene ◽

Selection Intensity ◽

Bristle Number ◽

Isolation Index ◽

Selection Intensities ◽

High Selection

ABSTRACT Disruptive selection for sternopleural bristle number with opportunity for random mating was done in the four treatment combinations of two population sizes (40 pairs and 8 pairs of selected parents) and two selection intensities (1 in 40 and 1 in 2). In each generation, matings among selected parents were observed in a mating chamber, and progeny collected separately from each female parent. In the high number, high selection intensity treatment, divergence between the high and low parts ceased about generation 11. The isolation index increased rapidly to generation 3, but then fluctuated to termination of the population at generation 17. The overall isolation index was significant, indicating a real tendency to assortative mating. The failure of the isolation index to increase after generation 3 was attributed to lower average mating fitness of high males (due to inbreeding) and reduced receptivity of low females (due to a homozygous lethal gene with a large effect on sternopleural bristle number in heterozygotes). In the two low number treatments, isolation indices fluctuated from generation to generation with no obvious trends, and none of the overall isolation indices were significantly different from zero. The high number, low selection intensity treatment showed very little divergence, and one of the replicates showed, in contrast with expectation and the high number, high selection intensity treatment, a significant tendency to disassortative mating. Intense disruptive selection may lead to assortative mating.

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