The repressor effect of I-element\gag is maternally transmitted and increases with the transgene copy number. It is irrespective of either frame integrity or transcriptional orientation of the ORF, suggesting the involvement of a homology-dependent trans-silencing mechanism.
Regulation of I-element transposition in ovaries operates at different levels, including the positive and negative regulation of RNA levels, and negative regulation downstream of I-element RNA.
I-elements transpose with high frequency into pericentric regions of chromosome 2 and may play a role in the evolution of constitutive heterochromatin.
Changes introduced in the promoter regions of distinct LINEs allows transcriptional activators to stimulate cryptic Inr modules. The response of different promoter constructs to the same enhancer is significantly influenced by the number, position and type of core elements present.
Used in an investigation to address the relationship between retrotransposons and retroviruses and the coadaptation of these retroelements to their host genomes. Results indicate retrotransposons are heterogeneous in contrast to retroviruses, suggesting different modes of evolution by slippage-like mechanisms.
Study of TE distribution (P-element, hobo, I-element, copia, mdg1, mdg3, 412, 297 and roo) along chromosome arms shows no global tendency for the TE site occupancy frequency to negatively follow the recombination rate, except for the 3L arm. The tendency for TE insertion number to increase from base to tip of some chromosome arms is simply explicable by a positive relationship with DNA content along the chromosomes. So for all TEs, except hobo, there is no relationship between distribution of TE insertion numbers weighted by DNA content and recombination rate. hobo insertion site number is positively correlated with recombination rate.
An enhancer that stimulates gene expression in ovarian nurse cells lies between nucleotides 41 and 186. Nucleotides 138-157 are recognised by a sequence specific binding factors present in nuclear extracts of several tissues including ovaries. These bases are required for full promoter activity and for enhanced expression in ovaries.
Transposition frequency of I-elements is regulated by the reactivity of the mother, this reactivity is a cellular state maternally inherited but chromosomally determined. It is proposed that this reactivity level is one manifestation of an inducible repair-recombination system whose biological role might be analogous to the SOS response in bacteria. Inhibitors of DNA synthesis and γ rays enhance the reactivity level in a very similar way, this enhancement is heritable, cumulative and reversible.
Defective I elements introduced as single copy transgenes can act as regulators of reactivity. Some of the ancestral pericentromeric defective I elements found in all reactive strains may be the molecular determinants of reactivity.
Defective I-elements introduced as single copy transgenes can act as regulators of reactivity an suggest that some of the ancestral defective pericentromeric I-elements that can be found in all reactive strains could be the molecular determinants of reactivity.
Transposition frequency of I-elements is regulated by the reactivity of the mother, this reactivity is a cellular state maternally inherited but chromosomally determined. For identical genotypes the reactivity levels correlate with the sensitivity of oogenesis to γ rays. This strongly supports the proposal that the reactivity level is one manifestation of an inducible DNA repair system taking place in the female germ line.
The heterochromatic genes of chromosome 2 are highly mutable in I-R dysgenesis. I-element transpositions can generate heterochromatic deletions spanning 3-4 Mb of DNA.
The chromosomal distribution of a number of retrotransposons in an isolated population of D.melanogaster (from Ishigaki Island, Okinawa, Japan) has been determined.
Reactivity of females decreases upon ageing and subjection to heat treatment and the level of reactivity positively regulates I-element expression. Therefore I-element expression is influenced by ageing and heat treatment.
Polymorphism of transposable elements in inbred lines has been examined: P-element, gypsy, jockey, I-element, mdg1, 412, mdg3 and 297 sites are largely stable, whereas roo and copia sites are polymorphic.
The I-element belongs to class of transposable element that transpose via an RNA intermediate, and are responsible for the IR system of hybrid dysgenesis. An I-element may be defective or active. Many Drosophila species contain both active and defective elements. It is suggested that active ones were lost from D.melanogaster before the spread of I-element throughout the world, and that the recent invasion of active elements results from spread either from another species or from an isolated population of D.melanogaster.
Stability of 11 transposable element families compared by Southern blotting among individuals of lines that had been subjected to 30 generations of sister sib matings. 412, roo, blood, 297, 1731 and G-element all appear stable, whereas copia, hobo, I-element, gypsy and jockey elements show instability.
Transposition rates of mobile elements in lines AW and JH, in which spontaneous mutations have accumulated for about 400 generations, are studied. 412 and 17.6 elements rate of transposition is very low, I-element and hobo insertions occur much more frequently.
The rate of induced lethals in IR dysgenesis is not dependent on the inducer or reactive character of the chromosome but rather on interacting strains and the intensity of the I-R interaction.
Defective I-elements present in the pericentromeric heterochromatin contain many base pair substitutions as well as small and large insertions, deletions or duplications compared to active I-elements. These defective elements show an average of 94% sequence identity with each other and the transposable I-element. Both active and defective I-elements appear to have evolved from a common ancestor, and comparison with an active Dtei\I-element suggests that the defective heterochromatic I-elements may have become immobilised before the divergence of D.melanogaster and D.teissieri.
The occurrence of I-type reactions in lines previously known to be R-type is examined and also if such transitions to I-type are restricted to weak R-type lines. In a few cases where R-type lines have branched into sublines, transitions occurred from R-type to I-type.
F-elements encode an open reading frame (ORF) that encodes a protein exhibiting extensive homology to the reverse transcriptase-like domain of the potential product of the I-element. This observation suggests F-elements and I-elements are closely related and presumably are mobilised within the genome by a similar mechanism.
First described by Bucheton et al. as insertions associated with w gene mutations induced by I-R hybrid dysgenesis. The base sequence of a complete I element has been determined by Fawcett et al. (1986) and the restriction map shown in Lindsley, Zimm, 1992 p. 1103 is based on this sequence. There are no sites for the enzymes BamHI, EcoRI, SacI, SalI, SmaI, or XhoI. Incomplete I elements that have recently inserted in the genome have deleted varying amounts from the 5' end of the sequence of a complete element (Busseau et al., 1989a). Incomplete elements that have been in the genome for a long time are located in pericentromeric regions and differ from complete elements by many base substitutions and internal or terminal deletions or both (Crozatier et al., 1988). Mutations induced by I-R hybrid dysgenesis include apparent point mutations due to insertion of I elements and chromosome rearrangements due to recombination between I elements (Sang et al., 1984; Busseau et al., 1989b).
Other Information
Etymology
External Crossreferences and Linkouts ( 13 )
Crossreferences
GenBank Nucleotide
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A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
The repressor effect of I-element\gag is maternally transmitted and increases with the transgene copy number. It is irrespective of either frame integrity or transcriptional orientation of the ORF, suggesting the involvement of a homology-dependent trans-silencing mechanism.
Regulation of I-element transposition in ovaries operates at different levels, including the positive and negative regulation of RNA levels, and negative regulation downstream of I-element RNA.
No transposition was detected in progeny after heat shock of parents.
I-elements transpose with high frequency into pericentric regions of chromosome 2 and may play a role in the evolution of constitutive heterochromatin.
Changes introduced in the promoter regions of distinct LINEs allows transcriptional activators to stimulate cryptic Inr modules. The response of different promoter constructs to the same enhancer is significantly influenced by the number, position and type of core elements present.
F-element, I-element and Doc basal promoters share the same architecture and functional organisation.
Used in an investigation to address the relationship between retrotransposons and retroviruses and the coadaptation of these retroelements to their host genomes. Results indicate retrotransposons are heterogeneous in contrast to retroviruses, suggesting different modes of evolution by slippage-like mechanisms.
One of a class of genes with TATA-less promoters that have the conserved DPE sequence.
Study of TE distribution (P-element, hobo, I-element, copia, mdg1, mdg3, 412, 297 and roo) along chromosome arms shows no global tendency for the TE site occupancy frequency to negatively follow the recombination rate, except for the 3L arm. The tendency for TE insertion number to increase from base to tip of some chromosome arms is simply explicable by a positive relationship with DNA content along the chromosomes. So for all TEs, except hobo, there is no relationship between distribution of TE insertion numbers weighted by DNA content and recombination rate. hobo insertion site number is positively correlated with recombination rate.
An enhancer that stimulates gene expression in ovarian nurse cells lies between nucleotides 41 and 186. Nucleotides 138-157 are recognised by a sequence specific binding factors present in nuclear extracts of several tissues including ovaries. These bases are required for full promoter activity and for enhanced expression in ovaries.
Transposition frequency of I-elements is regulated by the reactivity of the mother, this reactivity is a cellular state maternally inherited but chromosomally determined. It is proposed that this reactivity level is one manifestation of an inducible repair-recombination system whose biological role might be analogous to the SOS response in bacteria. Inhibitors of DNA synthesis and γ rays enhance the reactivity level in a very similar way, this enhancement is heritable, cumulative and reversible.
The distribution of I-elements in heterochromatin has been studied by in situ hybridisation to mitotic chromosomes.
Defective I elements introduced as single copy transgenes can act as regulators of reactivity. Some of the ancestral pericentromeric defective I elements found in all reactive strains may be the molecular determinants of reactivity.
Defective I-elements introduced as single copy transgenes can act as regulators of reactivity an suggest that some of the ancestral defective pericentromeric I-elements that can be found in all reactive strains could be the molecular determinants of reactivity.
Transposition frequency of I-elements is regulated by the reactivity of the mother, this reactivity is a cellular state maternally inherited but chromosomally determined. For identical genotypes the reactivity levels correlate with the sensitivity of oogenesis to γ rays. This strongly supports the proposal that the reactivity level is one manifestation of an inducible DNA repair system taking place in the female germ line.
The heterochromatic genes of chromosome 2 are highly mutable in I-R dysgenesis. I-element transpositions can generate heterochromatic deletions spanning 3-4 Mb of DNA.
The distribution of a number of transposable elements has been studied in 10 Harwich mutation accumulation lines.
The distribution of transposable elements within heterochromatin indicates that they are major structural components of the heterochromatin.
Dsec\I-element and Dmau\I-element are more closely related to the chromosomal I-elements of D.melanogaster than to those in any species. No sequence difference is observed between 2 chromosomal I-elements from D.melanogaster and one from D.simulans. This supports the idea that defective chromocentral I-elements of D.melanogaster originated before the species diverged and the chromosomal I-elements were eliminated. Chromosomal I-elements recently reinvaded natural populations of D.melanogaster, possibly by horizontal transfer from D.simulans.
The chromosomal distribution of a number of retrotransposons in an isolated population of D.melanogaster (from Ishigaki Island, Okinawa, Japan) has been determined.
The I-element can induce target duplication as well as target deletion upon transposition.
I-element mediated rearrangements occur during I-element insertion or through ectopic recombination after the insertion.
I-element transposition occurs as a meiotic event between stage 2 and 10 of oogenesis and is regulated at the transcriptional level.
Reactivity of females decreases upon ageing and subjection to heat treatment and the level of reactivity positively regulates I-element expression. Therefore I-element expression is influenced by ageing and heat treatment.
The feasibility of using the I-element as the tag in site-selected mutagenesis has been demonstrated.
Polymorphism of transposable elements in inbred lines has been examined: P-element, gypsy, jockey, I-element, mdg1, 412, mdg3 and 297 sites are largely stable, whereas roo and copia sites are polymorphic.
The I-element belongs to class of transposable element that transpose via an RNA intermediate, and are responsible for the IR system of hybrid dysgenesis. An I-element may be defective or active. Many Drosophila species contain both active and defective elements. It is suggested that active ones were lost from D.melanogaster before the spread of I-element throughout the world, and that the recent invasion of active elements results from spread either from another species or from an isolated population of D.melanogaster.
I-element transposition occurs as a meiotic event between stage 2 and 10 of oogenesis and is regulated at the transcriptional level.
Stability of 11 transposable element families compared by Southern blotting among individuals of lines that had been subjected to 30 generations of sister sib matings. 412, roo, blood, 297, 1731 and G-element all appear stable, whereas copia, hobo, I-element, gypsy and jockey elements show instability.
A marked I-element has been used to show that the I-element transposes through an RNA intermediate.
I-element transcription during I-R hybrid dysgenesis has been studied.
Transposition rates of mobile elements in lines AW and JH, in which spontaneous mutations have accumulated for about 400 generations, are studied. 412 and 17.6 elements rate of transposition is very low, I-element and hobo insertions occur much more frequently.
The rate of induced lethals in IR dysgenesis is not dependent on the inducer or reactive character of the chromosome but rather on interacting strains and the intensity of the I-R interaction.
Defective I-elements present in the pericentromeric heterochromatin contain many base pair substitutions as well as small and large insertions, deletions or duplications compared to active I-elements. These defective elements show an average of 94% sequence identity with each other and the transposable I-element. Both active and defective I-elements appear to have evolved from a common ancestor, and comparison with an active Dtei\I-element suggests that the defective heterochromatic I-elements may have become immobilised before the divergence of D.melanogaster and D.teissieri.
The occurrence of I-type reactions in lines previously known to be R-type is examined and also if such transitions to I-type are restricted to weak R-type lines. In a few cases where R-type lines have branched into sublines, transitions occurred from R-type to I-type.
I-elements are involved in chromosome rearrangements at the y locus.
F-elements encode an open reading frame (ORF) that encodes a protein exhibiting extensive homology to the reverse transcriptase-like domain of the potential product of the I-element. This observation suggests F-elements and I-elements are closely related and presumably are mobilised within the genome by a similar mechanism.
A number of IR hybrid dysgenesis induced mutations have been studied to investigate the mechanism of IR hybrid dysgenesis.
First described by Bucheton et al. as insertions associated with w gene mutations induced by I-R hybrid dysgenesis. The base sequence of a complete I element has been determined by Fawcett et al. (1986) and the restriction map shown in Lindsley, Zimm, 1992 p. 1103 is based on this sequence. There are no sites for the enzymes BamHI, EcoRI, SacI, SalI, SmaI, or XhoI. Incomplete I elements that have recently inserted in the genome have deleted varying amounts from the 5' end of the sequence of a complete element (Busseau et al., 1989a). Incomplete elements that have been in the genome for a long time are located in pericentromeric regions and differ from complete elements by many base substitutions and internal or terminal deletions or both (Crozatier et al., 1988). Mutations induced by I-R hybrid dysgenesis include apparent point mutations due to insertion of I elements and chromosome rearrangements due to recombination between I elements (Sang et al., 1984; Busseau et al., 1989b).