scholarly journals Factors contributing to the hybrid dysgenesis syndrome in Drosophila virilis

1998 ◽  
Vol 71 (2) ◽  
pp. 109-117 ◽  
Author(s):  
JORGE VIEIRA ◽  
CRISTINA P. VIEIRA ◽  
DANIEL L. HARTL ◽  
ELENA R. LOZOVSKAYA

A hybrid dysgenesis syndrome in Drosophila virilis is associated with the mobilization of at least four unrelated transposable elements designated Helena, Paris, Penelope and Ulysses. We carried out 42 crosses between eight strains differing in transposable element copy number in order to assess their contributions to hybrid dysgenesis. Linear regression and stepwise regression analysis was performed to estimate the correlation between the difference in euchromatic transposable element number between the parental flies of different strains involved in the crosses and the percentage, in the progeny of these crosses, of males with atrophic gonads. Male gonadal atrophy is a typical manifestation of the D. virilis hybrid dysgenesis syndrome. About half the variability in the level of male gonadal atrophy can be attributed to Penelope and Paris/Helena. Other factors also seem to play a significant role in hybrid dysgenesis in D. virilis, including maternally transmitted host factors and/or uncontrolled environmental variation. In the course of this work a novel transposable element named Telemac was found. Telemac is also mobilized in hybrid dysgenesis but does not appear to play a major causative role.

2018 ◽  
Author(s):  
Lucas W. Hemmer ◽  
Guilherme Dias ◽  
Brittny Smith ◽  
Kelley Van Vaerenberghe ◽  
Ashley Howard ◽  
...  

ABSTRACTGermline DNA damage is a double-edged sword. Programmed double-strand breaks establish the foundation for meiotic recombination and chromosome segregation. However, double-strand breaks also pose a significant challenge for genome stability. Because of this, meiotic double-strand break formation is tightly regulated. However, natural selection can favor selfish behavior in the germline and transposable elements can cause double-strand breaks independent of the carefully regulated meiotic process. To understand how the regulatory mechanisms of meiotic recombination accommodate unregulated transposition, we have characterized the female recombination landscape in a syndrome of hybrid dysgenesis inDrosophila virilis. In this system, a cross between two strains ofD. viriliswith divergent transposable element and piRNA profiles results in germline transposition of diverse transposable elements, reduced fertility, and male recombination. We sought to determine how increased transposition during hybrid dysgenesis might perturb the meiotic recombination landscape. Our results show that the overall frequency and distribution of meiotic recombination is extremely robust to germline transposable element activation. However, we also find that hybrid dysgenesis can result in mitotic recombination within the female germline. Overall, these results show that landscape of meiotic recombination may be insensitive to the DNA damage caused by transposition during early development.


1996 ◽  
Vol 67 (3) ◽  
pp. 219-226 ◽  
Author(s):  
C. Bazin ◽  
D. Higuet

SummaryCurrently in the hobo system of hybrid dysgenesis, strain classification is based on the presence/absence of the 2·6 kb Xho I restriction fragment. Using this criterion, strains are classified as: (1) H strains when full-size elements are detected by presence of a 2·6 kb Xho I restriction fragment; they can also contain internally deleted elements; (2) DH strains when only deleted elements are detected (Xho I restriction fragment less than 2·6 kb); (3) E strains, devoid of any restriction fragment equal to or less than 2·6 kb in length. In addition, the strains can be classified on their ability to generate gonadal atrophy (GD sterility) when males of a studied strain are crossed with females from an E strain (dysgenic cross). Here we try to define the nature of the dysgenic cross, which leads us to analyse the different components of the dysgenic syndrome and to look for eventual correlations between them. Molecular analysis, GD sterility tests, hobo mobilization with the haw strain and the vgal strain, and hereditary transmission of the instability at the vg locus have been assayed in different strains. We show that the occurrence of GD sterility depends on the tested H strains as expected, but also on the E strains used. On the other hand we do not find any correlation between the different dysgenic parameters. Our data reveal that molecular and GD sterility tests are not sufficient to classify strains in the hobo system, and that all the components of the dysgenic syndrome must be taken into account. Our results are discussed with regard to active and full-size elements in relation to the structure of the S region where an amino acid sequence (TPE) presents a repetition polymorphism


Genetics ◽  
1990 ◽  
Vol 126 (3) ◽  
pp. 619-623 ◽  
Author(s):  
E R Lozovskaya ◽  
V S Scheinker ◽  
M B Evgen'ev

Abstract A new example of "hybrid dysgenesis" has been demonstrated in the F1 progeny of crosses between two different strains of Drosophila virilis. The dysgenic traits were observed only in hybrids obtained when wild-type females (of the Batumi strain 9 from Georgia, USSR) were crossed to males from a marker strain (the long-established laboratory strain, strain 160, carrying recessive markers on all its autosomes). The phenomena observed include high frequencies of male and female sterility, male recombination, chromosomal nondisjunction, transmission ratio distortion and the appearance of numerous visible mutations at different loci in the progeny of dysgenic crosses. The sterility demonstrated in the present study is similar to that of P-M dysgenesis in Drosophila melanogaster and apparently results from underdevelopment of the gonads in both sexes, this phenomenon being sensitive to developmental temperature. However, in contrast to the P-M and I-R dysgenic systems in D. melanogaster, in D. virilis the highest level of sterility (95-98%) occurs at 23-25 degrees. Several of the mutations isolated from the progeny of dysgenic crosses (e.g., singed) proved to be unstable and reverted to wild type. We hypothesize that a mobile element ("Ulysses") which we have recently isolated from a dysgenically induced white eye mutation may be responsible for the phenomena observed.


Genetics ◽  
1996 ◽  
Vol 143 (1) ◽  
pp. 365-374 ◽  
Author(s):  
Allan R Lohe ◽  
Daniel L Hartl

Abstract An important goal in molecular genetics has been to identify a transposable element that might serve as an efficient transformation vector in diverse species of insects. The transposable element mariner occurs naturally in a wide variety of insects. Although virtually all mariner elements are nonfunctional, the Mosl element isolated from Drosophila mauritiana is functional. Mosl was injected into the pole-cell region of embryos of D. virilis, which last shared a common ancestor with D. mauritiana 40 million years ago. Mosl PCR fragments were detected in several pools of DNA from progeny of injected animals, and backcross lines were established. Because Go lines were pooled, possibly only one transformation event was actually obtained, yielding a minimum frequency of 4%. Mosl segregated in a Mendelian fashion, demonstrating chromosomal integration. The copy number increased by spontaneous mobilization. In situ hybridization confirmed multiple polymorphic locations of Mosl. Integration results in a characteristic 2-bp TA duplication. One Mosl element integrated into a tandem array of 370-bp repeats. Some copies may have integrated into heterochromatin, as evidenced by their ability to support PCR amplification despite absence of a signal in Southern and in situ hybridizations.


2015 ◽  
Vol 815 ◽  
pp. 227-232 ◽  
Author(s):  
Ying Yu ◽  
Shu Hong Xie ◽  
Qing Feng Zhan

A practical way to manipulate the magnetic anisotropy of magnetostrictive FeGa thin films grown on flexible polyethylene terephthalate (PET) substrates is introduced in this study. The effect of film thickness on magnetic properties and magnetostriction constant of polycrystalline FeGa thin films was investigated. The anisotropy field Hk of flexible FeGa films, i.e., the saturation field determined by fitting the hysteresis curves measured along the hard axis, was enhanced with increasing the tensile strain applied along the easy axis of the thin films, but this enhancement via strain became unconspicuous with increasing the thickness of FeGa films. In order to study the magnetic sensitivity of thin films responding to the external stress, we applied different strains on these films and measure the corresponding anisotropy field. Moreover, the effective magnetostriction constant of FeGa films was calculated from the changes of both anisotropy field and external strain based on the Villari effect. A Neel’s phenomenological model was developed to illustrate that the effective anisotropy field of FeGa thin films was contributed from both the constant volume term and the inverse thickness dependent surface term. Therefore, the magnetic properties for the volume and surface of FeGa thin films were different, which has been verified in this work by using vibrating sample magnetometer (VSM) and magneto-optic Kerr effect (MOKE) system. The anisotropy field contributed by the surface of FeGa film and obtained by MOKE is smaller than that contributed by the film volume and measured by VSM. We ascribed the difference in Hk to the relaxation of the effective strain applied on the films with increasing the thickness of films.


Genetics ◽  
1994 ◽  
Vol 138 (4) ◽  
pp. 1163-1170 ◽  
Author(s):  
E Wojcik ◽  
A M Murphy ◽  
H Fares ◽  
K Dang-Vu ◽  
S I Tsubota

Abstract A hybrid dysgenesis-induced mutation, enhancer of rudimentaryp1 (e(r)p1), is a recessive enhancer of a weak rudimentary mutant phenotype in Drosophila melanogaster. The e(r) gene was cloned using P element tagging and localized to region 8B on the X chromosome. It encodes a 1.0-kb and a 1.2-kb transcript. The 1.0-kb transcript is present in both adult males and females, while the 1.2-kb transcript is predominantly found in females. The difference in the lengths of the two e(r) transcripts is caused by two different polyadenylation sites spaced 228 bp apart. The amounts of both of these transcripts are drastically reduced in the e(r)p1 mutant. The P element in e(r)p1 is inserted in the 5'-untranslated leader region near the start of transcription. It may be producing its effect by suppressing transcription and/or by providing transcription termination and polyadenylation signals. The putative e(r) protein is 104 amino acids in length and bears no striking resemblance to protein sequences in GenBank or PIR. While its biochemical function is unknown at this time, sequence analysis indicates that the e(r) protein is highly conserved and, presumably, functionally very important. The amino acid sequences of the D. melanogaster and the Drosophila virilis proteins are 95% identical.


Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Paola Caielli ◽  
Viola Sanga ◽  
Raffaella Motta ◽  
Michele Battistel ◽  
Lorenzo Calò ◽  
...  

Background: blockade of the RAAS lowered the incidence of Diabetes Mellitus in randomized clinical trials, but whether the de-activation of the RAAS can elicit the same beneficial effect in patients with renovascular hypertension (RVH) is unknown. Aim: to verify if endovascular treatment (EVT) could improve glycemic control in patients with atherosclerotic RVH. Methods: in the METRAS study (http://clinicaltrials.gov/show/NCT01208714, a randomized clinical trial comparing the effect of EVT on top of optimal medical therapy versus medical therapy alone (OMT) on GFR of the ischemic and contralateral kidney in patients with atherosclerotic RVH), glycemic control, as assessed by HbA1c at baseline and repeatedly during follow-up, was a pre-specified secondary endpoint of the study. Results: between June 2010 and March 2014, 16 patients were randomly assigned to EVT plus optimal medical therapy (n = 9) or OMT alone (n = 7). At baseline the 2 groups showed no significant difference of age, clinical and demographical features. All the patients, except two in the EVT group, were on a RAAS blocker. At 2 years follow-up HbA1c increased in patients on OMT (59±12 mmol/mol) from baseline values (45±16 mmol/mol, p<0.001). By contrast, in the patients assigned to EVT HbA1c remained stable (42±7 mmol/mol at baseline vs 41±5 mmol/mol at follow-up; p = NS; p<0.001 vs OMT at follow-up). When analyzed after multivariate adjustment for age, HbA1c at enrollment, and presence/absence of DM, the difference between the arms remained highly significant (p<0.001). Conclusions: in patients with atherosclerotic RVH and chronic activation of the RAAS, deactivation of the RAAS by means of EVT was associated with no increase in plasma levels of HbA1c over long term follow-up. At variance, similar patients assigned to optimized medical therapy alone showed worsened glycemic control over time. These findings support the contention of a causative role of RAAS activation in the incidence/progression of DM.


Much has been learned about transposable genetic elements in Drosophila , but questions still remain, especially concerning their evolutionary significance. Three such questions are considered here, (i) Has the behaviour of transposable elements been most influenced by natural selection at the level of the organism, the population, or the elements themselves? (ii) How did the elements originate in the genome of the species? (iii) Why are laboratory stocks different from natural populations with respect to their transposable element composition? No final answers to these questions are yet available, but by focusing on the two families of hybrid dysgenesis-causing elements, the P and I factors, we can draw some tentative conclusions.


1992 ◽  
Vol 60 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Dominique Higuet ◽  
Dominique Anxolabéhére ◽  
Danielle Nouaud

SummaryTransposable P elements in Drosophila melanogaster cause hybrid dysgenesis if their mobility is not repressed. The ability to regulate the dysgenic activity of the P elements depends on several mechanisms, one of which hypothesized that a particular deleted P element (the KP element) results in a non-susceptibility which is biparentally transmitted. In this study totally nonsusceptible lines, and susceptible lines containing exclusively KP elements (IINS2 line and IIS2 line) were isolated from a M' strain. We show that non-susceptibility is correlated with a particular insertion of one KP element located at the cytological site 47D1. The repression ability of the GD sterility is determined by a recessive chromosomal factor, and cannot be due to the KP-element number. Here the repression of the P mobility is associated with reduction of the P transcripts and the inhibition of P promoter activity.


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