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  • DNA Repair in Drosophila: Mutagens, Models, and Missing Genes
    Jeff Sekelsky
    Genetics February 2017 205: 471-490; https://doi.org/10.1534/genetics.116.186759
    ...in different progeny, and conduct molecular assays that may give insight into mechanism (e.g., Lafave et al. 2014). A number of assays for DSB repair have been developed. In these assays, breaks are induced by excision of transposable elements, expression of a site-specic endonuclease such as I ~~~
  • Molecular Population Genetics
    Sònia Casillas, Antonio Barbadilla
    Genetics March 2017 205: 1003-1035; https://doi.org/10.1534/genetics.116.196493
    ...relations and conveys no information about the underlying evolutionary forces. Also, they show that the discriminatory power of electrophoresis to detect protein variation is a decreasing function of the number of segregating sites. In summary, and given the limitations of protein electrophoresis to measure ~~~
  • The Centrioles, Centrosomes, Basal Bodies, and Cilia of Drosophila melanogaster
    Ramona Lattao, Levente Kovács, David M. Glover
    Genetics May 2017 206: 33-53; https://doi.org/10.1534/genetics.116.198168
    ....0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 1Corresponding author: Department of Genetics, University of Cambridge, Downing Site, Downing Street Cambridge CB2 3EH ~~~
  • Dosage Compensation in Drosophila—a Model for the Coordinate Regulation of Transcription
    Mitzi I. Kuroda, Andres Hilfiker, John C. Lucchesi
    Genetics October 2016 204: 435-450; https://doi.org/10.1534/genetics.115.185108
    ...X Chromosome 438 MOF Catalyzes Site-Specic Histone H4 Acetylation on the Male X 439 Discovery of the roX RNAs leads to the spreading model for X-chromosome targeting of dosage compensation 441 Sex-Specic Biogenesis of the MSL Complex 441 Identication of the MSL complex 441 How the complex ~~~
  • You have access
    Dosage Compensation in Drosophila—a Model for the Coordinate Regulation of Transcription
    Mitzi I. Kuroda, Andres Hilfiker, John C. Lucchesi
    Genetics Oct 2016, 204 (2) 435-450; DOI: 10.1534/genetics.115.185108
    Figure 6
    Figure 6
    By Mitzi I. Kuroda, Andres Hilfiker and John C. Lucchesi
    Model for MSL targeting of the X chromosome. Initial assembly occurs on the sites of roX RNA synthesis and may nucleate at CESs before spreading in cis to produce the wild-type MSL pattern on the X chromosome. Assembly is limited to CES in the absence of MSL3 protein (adapted from Kelley et al. 1999).
  • You have access
    Dosage Compensation in Drosophila—a Model for the Coordinate Regulation of Transcription
    Mitzi I. Kuroda, Andres Hilfiker, John C. Lucchesi
    Genetics Oct 2016, 204 (2) 435-450; DOI: 10.1534/genetics.115.185108
    Figure 9
    Figure 9
    By Mitzi I. Kuroda, Andres Hilfiker and John C. Lucchesi
    Recovery of the CESs and their consensus sequence. Crossing scheme that results in recovery of msl3 mutant male embryos, along with their msl3+ sisters. Since only males express MSL2, ChIP of the total population results in selective recovery of MSL2 sites remaining in the absence of MSL3, also known as the CESs. The Multiple EM for Motif Elicitation algorithm revealed a consensus MRE logo based on the 150 sites recovered (adapted from Alekseyenko et al. 2008).
  • Open Access
    Molecular Population Genetics
    Sònia Casillas, Antonio Barbadilla
    Genetics Mar 2017, 205 (3) 1003-1035; DOI: 10.1534/genetics.116.196493
    Figure 3
    Figure 3
    By Sònia Casillas and Antonio Barbadilla
    Molecular evolutionary rate (K) as a function of (A) the DFE, (B) the probability of fixation of new mutations entering the population, and (C) the rate at which new mutations enter the population per site per generation (see text for details). Different selection coefficients of mutations are colored in a gradient from maroon (strongly deleterious), red (slightly deleterious), gray (neutral), light green (slightly advantageous), and dark green (advantageous).
  • Open Access
    Molecular Population Genetics
    Sònia Casillas, Antonio Barbadilla
    Genetics Mar 2017, 205 (3) 1003-1035; DOI: 10.1534/genetics.116.196493
    Figure 5
    Figure 5
    By Sònia Casillas and Antonio Barbadilla
    Representation of the cost of linkage on selected sites, or HRi. Arrows indicate adaptive (green) and deleterious (red) mutations, while their length indicates the intensity of selection. (A) When two or more adaptive mutations occur in separate haplotypes without recombination (left), only one of them can be fixed in the population and thus mutations compete for their fixation. However, when recombination is sufficiently high (right), the two haplotypes can exchange alleles and generate a new haplotype that carries both adaptive mutations and can be fixed. (B) In the presence of both adaptive and deleterious mutations without recombination (left), all alleles compete; as a result, deleterious alleles may be dragged to fixation if the intensity of selection favoring a nearby adaptive mutation is high, or adaptive alleles may be lost if the joint strength of negative selection is higher. With recombination (right), deleterious alleles can be removed and adaptive alleles can be fixed without interfering with each other. Adapted from Barrón (2015).
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