Super-unstable mutations associated with P-M hybrid dysgenesis in Drosophila melanogaster

Super-unstable mutations occasionally appear either in natural populations of Drosophila melanogaster or in P-M hybrid dysgenesis. We found that they may be reproducibly obtained with a high frequency from crosses between males from the % MathType!MTEF!2!1!+-% feaafeart1ev1aaatCvAUfeBSjuyZL2yd9gzLbvyNv2CaerbuLwBLn% hiov2DGi1BTfMBaeXatLxBI9gBaerbd9wDYLwzYbItLDharqqtubsr% 4rNCHbGeaGqiVu0Je9sqqrpepC0xbbL8F4rqqrFfpeea0xe9Lq-Jc9% vqaqpepm0xbba9pwe9Q8fs0-yqaqpepae9pg0FirpepeKkFr0xfr-x% fr-xb9adbaqaaeGaciGaaiaabeqaamaabaabaaGcbaWaaubiaeqale% qabaWaaubiaeqameqaleaacaGGQaaaoeaacaWGHbGaam4raaaaa0qa% aiaadEhaaaaaaa!3A01!\[\mathop w\nolimits^{\mathop {aG}\nolimits^* } \] strain and females from the w ^aG* strain or its derivatives. Super-unstable mutations in the ocelliless, singed, white, yellow and other loci have been obtained. Each super-unstable mutation gives rise to a large family of new super-unstable mutations with a wide range of phenotypic expression. Mutations with the same phenotype often differ in the specificity of their potential for further mutation. As a rule, a super-unstable mutation is associated with a specific reversible mutation and paired alleles are formed in this way. Other mutations are usually irreversible, but new mutations of these may also form paired alleles. Active transposase encoded by transposable P elements is necessary to maintain super-instability. Finally, some preliminary molecular data are discussed which suggest that this type of super-instability is a result of interaction between P elements and a novel mobile element, designated as X.     

Structure and genomic organization of I elements involved in I-R hybrid dysgenesis in Drosophila melanogaster.

I-R hybrid dysgenesis in D. melanogaster is controlled by transposable elements known as I factors which terminate at their 3' ends by an A-rich sequence. Inducer strains contain active I factors. Both reactive and inducer stocks possess defective I elements. We have cloned various I elements from both categories of strains. The I elements having recently transposed in inducer strains have a structure closely related to that of active I factors. However we have isolated one such I element that is truncated at its 5' end. The I elements common to reactive and inducer strains are affected by various rearrangements and many point mutations. They do not appear to be simple derivatives of complete I factors.     

Visible mutations induced by P-M hybrid dysgenesis in Drosophila melanogaster result predominantly from P element insertions.

This study supplied no evidence that P-M hybrid dysgenesis is a general release mechanisms for transposon movement. Newly induced mutations (23 singed, three yellow, and one white) were generated by hybrid dysgenesis and were molecularly analyzed for the presence or absence of P element insertions. Only one dysgenically-induced insertion mutation out of 27 analyzed was the result of a non-P insert; this frequency is not statistically above the non-dysgenic control level. Thus, it appears that individual transposable elements families are independently regulated.     

Characteristic features of induced mutagenesis in hybrid dysgenesis systems of Drosophila melanogaster

The mutagenic effect of low-dose gamma-irradiation was studied in Drosophila melanogaster systems of hybrid dysgenesis by estimating polytene chromosome rearrangements, recombination frequency, and viability at the embryonic and postembryonic developmental stages. A dose of gamma-irradiation which had no effect detectable by routine line crossing proved to significantly reduce the number of recombinants in the H-E and P-M systems and mortality at postembryonic stages. However, this combined effect was obtained if irradiation followed transposition, i.e., it depended on the application sequence of the mutagenic factors. The reverse order of the mutagenic treatment led to summation of the effects: as compared to either control, the frequencies of the dominant allele mutations as well as the larval and pupal mortality in F2 increased significantly (at the level of 99.9%). This allowed us to estimate the contribution of extremely low-dose gamma-irradiation into the mutagenic effect, which was impossible under routine conditions.     

I-R hybrid dysgenesis in Drosophila melanogaster. Use of in situ hybridization to show the association of I factor DNA with induced sex-linked recessive lethals.

The purpose of this paper is the genetic visualization by in situ hybridization of 130 sex-linked recessive lethals plus a non-lethal induced by I-R dysgenesis. This collection of lethals involves inducer strains which differ in the position of the I elements on the X chromosomes. The I-R interaction was strong. Our previous results have shown that about 30% of the induced recessive lethals are associated with cytologically visible chromosomal rearrangements. (1) The rearrangements induced by I-R-type hybrid dysgenesis often exhibit homology with the I factor at the level of one or both junction points, depending on the types of chromosome rearrangements. These results suggest that the chromosome rearrangements arise directly from the transposition of I elements. However, the breakpoints of some types of cytologically non-visible deficiencies and of 2 small cytologically visible deficiencies do not present detectable homology with the I factor. (2) The majority of rearrangements do not involve the I elements already present on the paternal X chromosome. (3) The hybridization signal distributions on the X chromosome are not uniform. They present peaks of various heights which may correspond to specific anchoring areas of copies of I in the course of integration. (4) The data presented here agree with the literature with respect to the mean number of copies of I per X chromosome and to the excess of copies of I at locus 1A. Two rearrangement formation mechanisms are envisaged: crossing-over and 'target' exchanges.     

The molecular basis of I-R hybrid dysgenesis in Drosophila melanogaster: identification, cloning, and properties of the I factor

We have analyzed two mutations of the white-eye gene, which arose in flies subject to I-R hybrid dysgenesis. These mutations are associated with insertions of apparently identical 5.4 kb sequences, which we have cloned. We believe that these insertions are copies of the I factor controlling I-R hybrid dysgenesis. The I factor is not a member of the copia-like or fold-back classes of transposable elements and has no sequence homology with the P factor that controls P-M dysgenesis. All strains of D. melanogaster contain I-factor sequences. Those present in reactive strains must represent inactive I elements. I elements have a remarkably similar sequence organization in all reactive strains and are located in peri-centromeric regions. Inducer strains appear to contain both I elements, located in peri-centromeric regions, and 10-15 copies of the complete I factor at sites on the chromosome arms.     

KP elements repress P-induced hybrid dysgenesis in Drosophila melanogaster.

Molecular and genetic analysis has revealed a specific P factor deletion derivative (the KP element) which is able to repress P-induced hybrid dysgenesis. All naturally occurring strains lacking the P cytotype (M') that were examined, throughout the world contain up to 30 copies of KP per haploid genome together with complete P factors. The KP element is derived from the P factor by an internal deletion of 1753 bp removing nucleotides 808-2560 and is transcribed to yield an abundant 0.8-kb poly(A)+ RNA with the coding capacity for an in-frame 207 amino acid polypeptide. Genetic crosses show that KP elements preferentially accumulate in the presence of P factors and suppress hybrid dysgenesis. Suppression is transmitted through both sexes and is thus distinct from the maternally transmitted P cytotype mode of suppression. The spread of KP elements is probably due to the continual selection of individuals with the highest numbers of KP elements in which P-induced hybrid dysgenesis is suppressed.     

The I-R system of hybrid dysgenesis in Drosophila melanogaster: influence on SF females sterility of their inducer and reactive paternal chromosomes.

A specific kind of sterile F1 female, denoted SF, arises when females from strains known as reactive are crossed with males from the complementary class of strains (inducer). It has been shown that this sterility results from the interaction between the maternal reactive cytoplasm and any one of the paternal inducer chromosomes. This interaction yields other dysgenic traits including non-disjunction and mutations. In this note, the abilities of paternal gametes containing various combinations of inducer and reactive chromosomes to give more or less sterile SF females when fertilising standard reactive oocytes were compared. Although they did not cause SF sterility, reactive chromosomes, when present in sperm containing at least one inducer chromosome, were found to influence the intensity of sterility: variations of SF sterility were observed between SF females which differed only by one paternally inherited reactive chromosome. Reactive chromosomes are known to control the cytoplasmic state of reactive females. The present results suggest that this chromosomal control also takes place in SF females.     

P-M hybrid dysgenesis affects juvenile hormone metabolism in Drosophila melanogaster females

This paper studies the metabolism of the juvenile hormone, which affects gonads functioning in Drosophila melanogaster females under P-M hybrid dysgenesis. It is shown that dysgenic females grown at 29°C have increased levels of the juvenile hormone (its degradation and stress reactivity are reduced), which apparently is a compensatory response to ovarian hypoplasia.     

Alteration of chromosome structure in ovarian nurse cells of Drosophila melanogaster by hybrid dysgenesis

The impact of hybrid dysgenesis on the chromosome structure of Drosophila melanogaster ovarian nurse cells was studied. In the examined lines and interlinear hybrids (including those yielded by dysgenic crosses in the P-M and I-R systems of hybrid dysgenesis), disturbed chromosome synapsis was revealed. The disturbance was somewhat similar to that observed in interspecific hybrids. Quantitative analysis showed that the mean frequency of nuclei with defective chromosome pairing ranged from 60.4 to 76%. FISH analysis of ovarian nurse chromosomes of Canton S x Berlin hybrids showed differences in the label localization in asynaptic homologs of arm 2L, which probably results in disrupted homolog pairing and reveal interlinear differences in localization of mobile genetic elements. Our results conform to Sved's model stating that hybrid dysgenesis is based on disorganization of the germline nuclear space.