FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
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Citation
Pelisson, A. (1981). The I-R system of hybrid dysgenesis in Drosophila melanogaster: Are I factor insertions responsible for the mutator effect of the I-R interaction?  Mol. Gen. Genet. 183(): 123--129.
FlyBase ID
FBrf0037054
Publication Type
Research paper
Abstract
When Drosophila melanogaster males coming from a class of strains known as inducer are crossed with females from the complementary class (reactive), a quite specific kind of sterile female (SF) is obtained that exhibits other dysgenic traits such as non-disjunctions and non-randomly distributed mutations. This syndrome is caused by the interaction of the 'I factor' linked to inducer chromosomes with the maternally inherited reactive state 'R'. This I--R interaction is also responsible for 'chromosomal contamination' that is likely to result from very frequent I factor insertions into reactive chromosomes. Such insertions might be responsible for the I--R induced mutations and some data concerning this hypothesis are reported here. Out of nine I--R-generated mutants one, the whiteIR1 (wIRI) allele, is closely linked to an I factor, which maps either at the site of the mutation or within less than 0.02 map units. In addition, wIR1 is somewhat unstable when transmitted through SF females. In contrast, the typical I factor does not seem to be associated with any of the eight other mutants as judged by their inability to induce the female sterility characteristic of the I--R syndrome. The possibility is discussed that most of I--R-induced mutations are nevertheless caused by insertions of either undetectable I factors of other transposable elements, not related to I, whose transposition is dependent on the I--R interaction.
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Mol. Gen. Genet.
    Title
    Molecular and General Genetics
    Publication Year
    1967-2001
    ISBN/ISSN
    0026-8925
    Data From Reference
    Aberrations (2)
    Alleles (4)
    Genes (8)
    Natural transposons (1)
    Insertions (1)