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  • Drosophila melanogaster  (2)
  • Sxl expression  (1)
  • rDNA genes  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Clonal analysis in hybrids between Drosophila melanogaster and Drosophila simulans (1994)
    Springer
    Development genes and evolution 204 (1994), S. 112-117 
    Details
    ISSN: 1432-041X
    Keywords: Drosophila melanogaster ; Drosophila simulans ; Hybrids ; Clonal analysis ; Lhr
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract We have analysed the viability of cellular clones induced by mitotic recombination in Drosophila melanogaster/D. simulans hybrid females during larval growth. These clones contain a portion of either melanogaster or simulans genomes in homozygosity. Analysis has been carried out for the X and the second chromosomes, as well as for the 3L chromosome arm. Clones were not found in certain structures, and in others they appeared in a very low frequency. Only in abdominal tergites was a significant number of clones observed, although their frequency was lower than in melanogaster abdomens. The bigger the portion of the genome that is homozygous, the less viable is the recombinant melano-gaster/simulans hybrid clone. The few clones that appeared may represent cases in which mitotic recombination took place in distal chromosome intervals, so that the clones contained a small portion of either melanogaster or simulans chromosomes in homozygosity. Moreover, Lhr, a gene of D. simulans that suppresses the lethality of male and female melanogaster/simulans hybrids, does not suppress the lethality of the recombinant melanogaster/simulans clones. Thus, it appears that there is not just a single gene, but at least one per tested chromosome arm (and maybe more) that cause hybrid lethality. Therefore, the two species, D. melanogaster and D. simulans, have diverged to such a degree that the absence of part of the genome of one species cannot be substituted by the corresponding part of the genome of the other, probably due to the formation of co-adapted gene complexes in both species following their divergent evolution after speciation. The disruption of those coadapted gene complexes would cause the lethality of the recombinant hybrid clones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00361105
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The gene fl(2)d is required for various Sxl-controlled processes in Drosophila females (1991)
    Springer
    Development genes and evolution 200 (1991), S. 172-176 
    Details
    ISSN: 1432-041X
    Keywords: Drosophila ; Sxl expression ; fl(2)d ; Adult life
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary In Drosophila melanogaster, the gene Sex-lethal (Sxl) controls the processes of sex determination, dosage compensation, oogenesis and sexual behaviour. The control of Sxl is by alternative splicing of its primary RNA. We have identified a gene, female-lethal-2-d (fl(2)d), which is needed for the female-specific splicing of Sxl RNA and which also has a vital function independent of Sxl. Here we analyse other aspects of the gene fl(2)d. Specifically, we have analysed the effect of the temperature-sensitive mutation fl(2)d 1 on the viability of adult flies homozygous for this mutation. We have found that the viability of the mutant females is reduced, while that of the mutant males is not affected. In addition, the capacity of the mutant females to be inseminated is considerably reduced, whilst all the mutant males are able to inseminate females. These effects on females are suppressed by Sxl M1. However, the fat body cells of fl(2)d 1 homozygous females are able to synthesize yolk proteins at the restrictive temperature. We have also carried out, in males, a clonal analysis of fl(2)d 2, a mutation lethal in both sexes. We have found that the clones are fully viable. We conclude that the gene fl(2)d seems to be necessary during the adult life of females for the processes that require Sxl + activity. Moreover, the Sxl-independent vital function of fl(2)d seems to be required in both sexes only during larval development.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00190237
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  • 3
    Electronic Resource
    Electronic Resource
    Indirect evidence of alteration in the expression of the rDNA genes in interspecific hybrids betweenDrosophila melanogaster andDrosophila simulans (1996)
    Springer
    Molecular genetics and genomics 250 (1996), S. 89-96 
    Details
    ISSN: 1617-4623
    Keywords: rDNA genes ; Hybrids ; Drosophila melanogaster ; Drosophila simulans
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Crosses betweenDrosophila melanogaster females andD. simulans males produce viable hybrid females, while males are lethal. These males are rescued if they carry theD. simulans Lhr gene. This paper reports that females of the wild-typeD. melanogaster population Staket do not produce viable hybrid males when crossed withD. simulans Lhr males, a phenomenon which we designate as the Staket phenotype. The agent responsible for this phenomenon was found to be the StaketX chromosome (X mel ,Stk). Analysis of the Staket phenotype showed that it is suppressed by extra copies ofD. melanogaster rDNA genes and that theX mel ,Stk chromosome manifests a weak bobbed phenotype inD. melanogaster X mel ,Stk/0 males. The numbers of functional rDNA genes inX mel ,Stk andX mel ,y w (control) chromosomes were found not to differ significantly. Thus a reduction in rDNA gene number cannot account for the weak bobbedX mel ,Stk phenotype let alone the Staket phenotype. The rRNA precursor molecules transcribed from theX mel ,Stk rDNA genes seem to be correctly processed in both intraspecific (melanogaster) and interspecific (melanogaster-simulans) conditions. It is therefore suggested that theX mel ,Stk rDNA genes are inefficiently transcribed in themelanogaster-simulans hybrids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02191828
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    Paper (German National Licenses)
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