scholarly journals A test for the role of natural selection in the stabilization of transposable element copy number in a population of Drosophila melanogaster

1987 ◽  
Vol 49 (1) ◽  
pp. 31-41 ◽  
Author(s):  
Elizabeth Montgomery ◽  
Brian Charlesworth ◽  
Charles H. Langley
Keyword(s):  
Drosophila Melanogaster ◽  
Natural Selection ◽  
Copy Number ◽  
Chromosomal Location ◽  
Theoretical Predictions ◽  
Mutant Phenotypes ◽  
Genomic Regions ◽  
Simple Selection ◽  
Transposable Element Copy

SummaryThe numbers of members of three families of copia-like elements were counted on twenty X, 2nd and 3rd chromosomes collected from a natural population of Drosophila melanogaster. Theoretical predictions were computed for two models of copy number stabilization: (1) element frequencies are regulated by a simple genetic process such as copy number dependent transposition or excision, independent of chromosomal location; (2) elements are eliminated by natural selection against mutational effects of their insertion into the chromosome. Since insertions into the X can be expected to suffer more selection than autosomal insertions, due to expression of mutant phenotypes in the hemizygous state, hypothesis 2, called the disproportional model, predicts that the proportion of elements on the X will be smaller than the proportion of the genome contributed by the X, while hypothesis 1, called the equiproportional model, predicts that this proportionality will be unaffected. Two of the elements, 297 and roo, showed no evidence for deficiency of X-linked elements, but the data for a third element, 412, were consistent with the prediction based on the selective model.These results indicate that simple selection against mutational effects of insertions of transposable elements is not generally adequate to account for their distribution within populations. We argue that a mechanism such as recombination between elements at different chromosomal sites, leading to rearrangements with highly deleterious, dominant effects could play a role in stabilizing copy number. This process would lead to a higher abundance of elements in genomic regions with restricted crossing over. We present some data indicating such an effect, and discuss possible interpretations.

scholarly journals The Genomic Distribution of L1 Elements: The Role of Insertion Bias and Natural Selection

2006 ◽  
Vol 2006 ◽  
pp. 1-5 ◽  
Author(s):  
Todd Graham ◽  
Stephane Boissinot
Keyword(s):  
Natural Selection ◽  
Gene Function ◽  
Negative Selection ◽  
Genomic Distribution ◽  
Alu Elements ◽  
Ectopic Recombination ◽  
Genomic Regions ◽  
Positive Effect ◽  
Biased Distribution

LINE-1 (L1) retrotransposons constitute the most successful family of retroelements in mammals and account for as much as 20% of mammalian DNA. L1 elements can be found in all genomic regions but they are far more abundant in AT-rich, gene-poor, and low-recombining regions of the genome. In addition, the sex chromosomes and some genes seem disproportionately enriched in L1 elements. Insertion bias and selective processes can both account for this biased distribution of L1 elements. L1 elements do not appear to insert randomly in the genome and this insertion bias can at least partially explain the genomic distribution of L1. The contrasted distribution of L1 and Alu elements suggests that postinsertional processes play a major role in shaping L1 distribution. The most likely mechanism is the loss of recently integrated L1 elements that are deleterious (negative selection) either because of disruption of gene function or their ability to mediate ectopic recombination. By comparison, the retention of L1 elements because of some positive effect is limited to a small fraction of the genome. Understanding the respective importance of insertion bias and selection will require a better knowledge of insertion mechanisms and the dynamics of L1 inserts in populations.

scholarly journals A Test of Neutrality Based on Interlocus Associations

Genetics ◽  
1997 ◽  
Vol 146 (3) ◽  
pp. 1197-1206 ◽  
Author(s):  
John K Kelly
Keyword(s):  
Drosophila Melanogaster ◽  
Natural Selection ◽  
Neutral Theory ◽  
Upper Bounds ◽  
Statistical Properties ◽  
Neutral Model ◽  
Genetic Associations ◽  
Evolutionary Processes ◽  
Expected Values ◽  
Genomic Regions

The evolutionary processes governing variability within genomic regions of low recombination have been the focus of many studies. Here, I investigate the statistical properties of a measure of intrlocus genetic associations under the assumption that mutations are selectively neutral and sites are completely linked. This measure, denoted ZnS, is based on the squared correlation of allelic identity at pairs of polymorphic sites. Upper bounds for ZnS are determined by simulations. Various deviations from the neutral model, including several different forms of natural selection, will inflate the value of ZnS relative to its neutral theory expectations. Larger than expected values of ZnS are observed in genetic samples from the yellow-ac-scute and Adh regions of Drosophila melanogaster.

scholarly journals Localization of P elements, copy number regulation, and cytotype determination in Drosophila melanogaster

1990 ◽  
Vol 56 (1) ◽  
pp. 3-14 ◽  
Author(s):  
C. Biémont ◽  
S. Ronsseray ◽  
D. Anxolabéhère ◽  
H. Izaabel ◽  
C. Gautier
Keyword(s):  
Drosophila Melanogaster ◽  
Copy Number ◽  
Chromosomal Location ◽  
Inbred Lines ◽  
P Element ◽  
P Elements ◽  
Left And Right ◽  
Element Activity ◽  
Copy Number Regulation

SummarySeventeen highly-inbred lines of Drosophila melanogaster extracted from an M′ strain (in the P/M system of hybrid dysgenesis) were studied for their cytotype and the number and chromosomal location of complete and defective P elements. While most lines were of M cytotype, three presented a P cytotype (the condition that represses P-element activity) and one was intermediate between M and P. All lines were found to possess K.P elements and only eight to bear full-sized P elements. Only the lines with full-sized P elements showed detectable changes in their P-insertion pattern over generations; their rates of gain and of loss of P-element sites were equal to 0·12 and 0·09 per genome, per generation, respectively. There was no correlation between these two rates within lines, suggesting independent transpositions and excisions in the inbred genomes. The results of both Southern blot analysis and in situ hybridization of probes made from left and right sides of the P element strongly suggested the presence of a putative complete P element in region 1A of the X chromosome in the three lines with a P cytotype; the absence of P copy in this 1A region in lines with an M cytotype, favours the hypothesis that the P element inserted in 1A could play a major role in the P-cytotype determination. Insertion of a defective 2 kb P element was also observed in region 93F in 9 of the 13 M lines. The regulation of the P-element copy number in our lines appeared not to be associated with the ratio of full-length and defective P elements.

scholarly journals On the role of unequal exchange in the containment of transposable element copy number

1988 ◽  
Vol 52 (3) ◽  
pp. 223-235 ◽  
Author(s):  
Charles H. Langley ◽  
Elizabeth Montgomery ◽  
Richard Hudson ◽  
Norman Kaplan ◽  
Brian Charlesworth
Keyword(s):  
Transposable Element ◽  
Copy Number ◽  
Natural Populations ◽  
Crossing Over ◽  
Relevant Parameter ◽  
Normal Crossing ◽  
Unequal Exchange ◽  
Parameter Ranges ◽  
Transposable Element Copy

SummaryA population genetics model of the role of asymmetric pairing and unequal exchange in the stabilization of transposable element copy number in natural populations is proposed and analysed. Monte Carlo simulations indicate that the approximations incorporated into the analysis are robust in the relevant parameter ranges. Given several simple assumptions concerning transposition and excision, equal and unequal exchange, and chromosome structure, predictions of the relative numbers of transposable elements in various regions of the Drosophila melanogaster genome are compared to the observed distribution of roo/B104 elements across chromosomal regions with differing rates of exchange, and between X chromosomes and autosomes. There is no indication of an accumulation of elements in the distal regions of chromosomes, which is expected if unequal exchange is reduced concomitantly with normal crossing over in the distal regions. There is, however, an indication of an excess of elements relative to physical length in the proximal regions of the chromosomes, which also have restricted crossing over. This observation is qualitatively consistent with the model's predictions. The observed distribution of elements between the mid-sections of the X chromosomes and autosomes is consistent with the predictions of one of two models of unequal exchange.

scholarly journals Natural selection and parallel clinal and seasonal changes in Drosophila melanogaster

2020 ◽  
Author(s):  
Murillo F. Rodrigues ◽  
Maria D. Vibranovski ◽  
Rodrigo Cogni
Keyword(s):  
Drosophila Melanogaster ◽  
Seasonal Variation ◽  
Natural Selection ◽  
Allele Frequency ◽  
Allele Frequencies ◽  
Clinal Variation ◽  
Spatial And Seasonal Variation ◽  
Genome Wide ◽  
A Genome

AbstractSpatial and seasonal variation in the environment are ubiquitous. Environmental heterogeneity can affect natural populations and lead to covariation between environment and allele frequencies. Drosophila melanogaster is known to harbor polymorphisms that change both with latitude and seasons. Identifying the role of selection in driving these changes is not trivial, because non-adaptive processes can cause similar patterns. Given the environment changes in similar ways across seasons and along the latitudinal gradient, one promising approach may be to look for parallelism between clinal and seasonal change. Here, we test whether there is a genome-wide relationship between clinal and seasonal variation, and whether the pattern is consistent with selection. We investigate the role of natural selection in driving these allele frequency changes. Allele frequency estimates were obtained from pooled samples from seven different locations along the east coast of the US, and across seasons within Pennsylvania. We show that there is a genome-wide pattern of clinal variation mirroring seasonal variation, which cannot be explained by linked selection alone. This pattern is stronger for coding than intergenic regions, consistent with natural selection. We find that the genome-wide relationship between clinal and seasonal variation could be explained by about 4% of the common autosomal variants being under selection. Our results highlight the contribution of natural selection in driving fluctuations in allele frequencies in D. melanogaster.

scholarly journals Transformation of Drosophila melanogaster with the wild-type myosin heavy-chain gene: rescue of mutant phenotypes and analysis of defects caused by overexpression.

1994 ◽  
Vol 126 (3) ◽  
pp. 689-699 ◽  
Author(s):  
R M Cripps ◽  
K D Becker ◽  
M Mardahl ◽  
W A Kronert ◽  
D Hodges ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Copy Number ◽  
Chain Gene ◽  
Wild Type ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene ◽  
Flight Muscles ◽  
Mutant Phenotypes

We have transformed Drosophila melanogaster with a genomic construct containing the entire wild-type myosin heavy-chain gene, Mhc, together with approximately 9 kb of flanking DNA on each side. Three independent lines stably express myosin heavy-chain protein (MHC) at approximately wild-type levels. The MHC produced is functional since it rescues the mutant phenotypes of a number of different Mhc alleles: the amorphic allele Mhc1, the indirect flight muscle and jump muscle-specific amorphic allele Mhc10, and the hypomorphic allele Mhc2. We show that the Mhc2 mutation is due to the insertion of a transposable element in an intron of Mhc. Since a reduction in MHC in the indirect flight muscles alters the myosin/actin protein ratio and results in myofibrillar defects, we determined the effects of an increase in the effective copy number of Mhc. The presence of four copies of Mhc results in overabundance of the protein and a flightless phenotype. Electron microscopy reveals concomitant defects in the indirect flight muscles, with excess thick filaments at the periphery of the myofibrils. Further increases in copy number are lethal. These results demonstrate the usefulness and potential of the transgenic system to study myosin function in Drosophila. They also show that overexpression of wild-type protein in muscle may disrupt the function of not only the indirect flight but also other muscles of the organism.

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