scholarly journals Cellular aspects of gonadal atrophy in Drosophila P-M hybrid dysgenesis

2017 ◽  
Vol 424 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Natalia V. Dorogova ◽  
Elena Us. Bolobolova ◽  
Lyudmila P. Zakharenko
2016 ◽  
Author(s):  
Natalia Dorogova ◽  
Elena Bolobolova ◽  
Lyudmila Zakharenko

Gonadal atrophy is the most typical and dramatic manifestation of intraspecific hybrid dysgenesis syndrome leading to sterility of Drosophila melanogaster dysgenic progeny. The P-M system of hybrid dysgenesis is primarily associated with germ cell degeneration during the early stages of Drosophila development at elevated temperatures. In the present study, we have defined the phase of germ cell death as beginning at the end of embryogenesis immediately following gonad formation. The early stages of germ cell formation in dysgenic flies showed sensitivity to developmental temperature increases at any stage of the Drosophila life cycle including the imago. Analysis of germ cell reactions to hybrid dysgenesis induction revealed significant changes in subcellular structure, especially mitochondria, prior to germ cell breakdown. The mitochondrial pathology can be the reason for the activation of cell death pathways in dysgenic germ cells and lead to gonadal atrophy.


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.


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


Author(s):  
R. A. Turner ◽  
A. E. Rodin ◽  
D. K. Roberts

There have been many reports which establish a relationship between the pineal and sexual structures, including gonadal hypertrophy after pinealectomy, and gonadal atrophy after injection of pineal homogenates or of melatonin. In order to further delineate this relationship the pineals from 5 groups of female rats were studied by electron microscopy:ControlsPregnant ratsAfter 4 weekly injections of 0.1 mg. estradiol benzoate.After 8 daily injections of 150 mcgm. melatonin (pineal hormone).After 8 daily injections of 3 mg. serotonin (melatonin precursor).No ultrastructural differences were evident between the control, and the pregnancy and melatonin groups. However, the estradiol injected animals exhibited a marked increase in the amount and size of rough endoplasmic reticulum within the pineal cells.


Genetics ◽  
1981 ◽  
Vol 98 (3) ◽  
pp. 565-587
Author(s):  
William R Engels

ABSTRACT In its hypermutable state, an unstable singed allele, snw, mutates in the germline to two other alleleic forms at a total frequency usually between 40 and 60%. In its stable state, the mutation rate of snw is essentially zero. Its state depends on an extrachromosomal condition indistinguishable from a property called cytotype previously studied as a component of hybrid dysgenesis. Of the two known systems of hybrid dysgenesis, denoted P-M and I-R, snw hypermutability is determined by the P-M system and appears to be independent of the I-R system. Cytotype, as defined by the control of snw mutability, is self-reproducing in the cytoplasm or nucleoplasm of the germline through at least two generations. However, it is not entirely autonomous, being ultimately determined by the chromosomes after sufficiently many generations of backcrossing. This combination of chromosomal and extrachromosomal transmission agrees well with previous studies on cytotype. Temperature differences have little effect on the mean mutation rates, but they have a pronounced effect on the intrinsic variance among individuals. The latter effect suggests that high temperatures reduce germ-cell survival during the development of dysgenic flies. Chromosomal rearrangements produce no apparent effects on the behavior of snw. Hypermutability is thought to be caused by the excision or other alteration of an inserted genetic element in the snw gene. This element might be a copy of the "P factor," which is though to be a mobile sequence capable of causing female sterility and other dysgenic traits in the P-M system.


Genetics ◽  
1990 ◽  
Vol 124 (3) ◽  
pp. 627-636
Author(s):  
C Q Lai ◽  
T F Mackay

Abstract To determine the ability of the P-M hybrid dysgenesis system of Drosophila melanogaster to generate mutations affecting quantitative traits, X chromosome lines were constructed in which replicates of isogenic M and P strain X chromosomes were exposed to a dysgenic cross, a nondysgenic cross, or a control cross, and recovered in common autosomal backgrounds. Mutational heritabilities of abdominal and sternopleural bristle score were in general exceptionally high-of the same magnitude as heritabilities of these traits in natural populations. P strain chromosomes were eight times more mutable than M strain chromosomes, and dysgenic crosses three times more effective than nondysgenic crosses in inducing polygenic variation. However, mutational heritabilities of the bristle traits were appreciable for P strain chromosomes passed through one nondysgenic cross, and for M strain chromosomes backcrossed for seven generations to inbred P strain females, a result consistent with previous observations on mutations affecting quantitative traits arising from nondysgenic crosses. The new variation resulting from one generation of mutagenesis was caused by a few lines with large effects on bristle score, and all mutations reduced bristle number.


Science ◽  
2008 ◽  
Vol 322 (5906) ◽  
pp. 1299j-1299j
Keyword(s):  

2016 ◽  
Vol 113 (46) ◽  
pp. 13003-13008 ◽  
Author(s):  
Malik Joseph Francis ◽  
Siobhan Roche ◽  
Michael Jeffrey Cho ◽  
Eileen Beall ◽  
Bosun Min ◽  
...  

In Drosophila, P-element transposition causes mutagenesis and genome instability during hybrid dysgenesis. The P-element 31-bp terminal inverted repeats (TIRs) contain sequences essential for transposase cleavage and have been implicated in DNA repair via protein–DNA interactions with cellular proteins. The identity and function of these cellular proteins were unknown. Biochemical characterization of proteins that bind the TIRs identified a heterodimeric basic leucine zipper (bZIP) complex between an uncharacterized protein that we termed “Inverted Repeat Binding Protein (IRBP) 18” and its partner Xrp1. The reconstituted IRBP18/Xrp1 heterodimer binds sequence-specifically to its dsDNA-binding site within the P-element TIRs. Genetic analyses implicate both proteins as critical for repair of DNA breaks following transposase cleavage in vivo. These results identify a cellular protein complex that binds an active mobile element and plays a more general role in maintaining genome stability.


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