At the beginning of the 1970s Picard and L’Heritier reported that crosses between particular strains of Drosophila melanogaster produce progeny exhibiting genetic abnormalities. In 1976 Picard reported that the factor responsible for IR hybrid dysgenesis is a transposable element, the first discovered in Drosophila, and named it the I factor. The determination of its sequence showed that it belongs to the class of non-long terminal repeat retrotransposons (NLRs) also known as long interspersed nucleotidic elements (LINEs). The I factor is one of the models used to study the mechanism of transposition of NLRs because it can be mobilized at high frequency by dysgenic crosses, giving the opportunity to study the molecular mechanism of transposition in vivo. The D. melanogaster species can be divided into two classes of strains according to the IR system of hybrid dysgenesis, inducer (or I) and reactive (or R). I strains contain several complete and functional I factors, R strains do not. The mechanism of transposition of the I factor is thought to be related to target-primed reverse transcription (TPRT) requiring a full-length RNA intermediate. The study of deletion derivatives indicates that the sequences comprised between nucleotides 41 and 100 might be involved in the inhibition of somatic expression. The study of deletion derivatives showed that more than one region of the protein is involved in DNA binding and that the cysteine-rich motifs are not essential for this, but are required for the formation of the high molecular weight structures.

I Elements in Drosophila melanogaster

The genetic determination of resistance to the sterility-producing genetic elements called P factors was studied in a strain characterized as neutral ( Q ) in the P-M system of hybrid dysgenesis. Sixteen lines were synthesized, representing all possible homozygous combinations of the three major chromosomes and differing maternal cytoplasms of an original resistant ( Q ) and susceptible ( M ) strain.—The results provide a detailed genetic analysis of the determination of cytotype (which mediates resistance or susceptibility to P factors) in the absence of the P-M dysgenic interaction. They extend the findings of Engels (1979) by providing specific information on both the location and relative magnitude of effect of cytotype-determining chromosomal factors and their interaction over time with maternally transmitted cytoplasm.—Cytotype was found to be primarily controlled by the genotype, but the maternal cytoplasm, under some circumstances, has an important short-term effect. Major cytotype-determining chromosomal factors are localized to the distal half of the X chromosome. However, there was also evidence for minor factors located on the major autosomes, particularly chromosome 3. Under certain circumstances, cytotypic switches in either direction can be produced in a single generation by the substitution of an X chromosome carrying a major cytotype determinant. This may provide an explanation of why reciprocal differences have sometimes been interpreted as direct effects of X -chromosome suppressors. However, slow but systematic changes of M to P cytotype were observed in five synthesized lines of mixed origin over twenty generations with no chromosomal substitution. Alternative explanations of these changes in terms of delayed effects of minor autosomal factors or of the transposability of cytotype determinants are discussed.

https://www.genetics.org/content/genetics/98/2/275.full.pdf

Hybrid dysgenesis in Drosophila melanogaster: the genetics of cytotype determination in a neutral strain.

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.

The I-R system of hybrid dysgenesis in Drosophila Melanogaster: Are I factor insertions responsible for the mutator effect of the I-R interaction?

The polymorphism of the mobile elements Mdg-1 (a copia-like element) and I (an element involved in I-R hybrid dysgenesis) was analysed in a mass-mated population of Drosophila melanogaster by in situ hybridization, using biotinylated DNA probes, on polytene chromosomes. The Mdg-1 and I elements were inserted independently but were within the same bulk of DNA insertion points of the Drosophila genome, which contained on average about 30 insertion sites for each element. The X chromosome contained the lowest copy number of elements while 2R and 3R had the highest number: 3R had the highest variability. There was no correlation between the copy numbers of elements among the chromosome arms. The average expected per locus heterozygosity was equal to 0.17 for both the Mdg-1 and the I elements. Although these two elements differ in sequence, they appeared to behave similarly in the Drosophila melanogaster genome. This suggests that they may compete for target insertion sites and may be under the same control mechanisms.

Polymorphism of the Mdg-1 and I mobile elements in Drosophila melanogaster

1 1 Several experiments were carried out to study, in the I-R hybrid dysgenesis system, the induction of recessive sex-linked lethal mutations in the progeny of SF females (obtained from crosses of ♀ R by ♂ I) or of RSF females (obtained from crosses of ♀ I by ♂ R) 2 2 Induced lethals were found in the progenies of SF females but not in those of RSF females 3 3 The frequency of induced lethals decreased as SF females grew older 4 4 A difference in the frequency of the induced lethals according to the reactive or inducer chromosome origin seemed apparent Such frequency systematically appeared to be higher for the chromosomes of reactive origin 5 5 The correlation between the rate of induced lethals and the intensity of the I-R interaction, as well as the characteristics of the lethals obtained and their non-random distribution, are in agreement with the hypothesis that the mutations are the consequence of the transposition of the I factor

Hybrid dysgenesis in Drosophila melanogaster: I. Further evidence for and characterization of the mutator effect of the inducer-reactive interaction

M1 Drosophila melanogaster laboratory strains fall into two main classes (inducer and reactive) on the basis of a quite specific kind of partial intersterility. All strains from the wild are inducer. The genetic element responsible for the inducer condition (I factor) is found on most of the inducer strains chromosomes: a chromosome carrying the / fac tor (i + chromosome) is characterized by its ability to give rise, when introduced by a paternal gamete into a reactive oocyte, to a female showing reduced fertility; chromosomes of inducer strains which do not carry I are denoted i °. Another result of the nucleocytoplasmic interaction between the I factor and the reactive cytoplasm, is the ability of i ° and reactive originating chromosomes to irreversibly acquire I, independently of any classical genetic recombination. However, this so-called chromosomal contamination does not occur in inducer i+/i ° heterozygous females. Using such females, mapping experiments showed that I can be located at a single locus on the w ct .f X chromosome and a single locus on the b bw second chromosome (approximate locations: 1-33 and 2-61) and at probably two independent loci on the see third chromosomes. Abnormal second chromosome transmission frequencies were observed; they do not seem to be related to previously reported segregation distortion phenomena.

Non mendelian female sterility in Drosophila melanogaster: I-factor mapping on inducer chromosomes

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Non mendelian female sterility in Drosophila melanogaster: I-factor mapping on inducer chromosomes