scholarly journals Transposition of the Responder element (Rsp) of the Segregation distorter system (SD) to the X chromosome in Drosophila melanogaster.

Genetics ◽  
1989 ◽  
Vol 122 (1) ◽  
pp. 81-86 ◽  
Author(s):  
E S Walker ◽  
T W Lyttle ◽  
J C Lucchesi
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
X Chromosome ◽  
Meiotic Drive ◽  
Genetic System ◽  
Drive System ◽  
Potential Utility ◽  
X Chromosomes ◽  
Large Numbers ◽  
Segregation Distorter

Abstract In order to test whether the meiotic drive system Segregation distorter (SD) can operate on the X chromosome to exclude it from functional sperm, we have transposed the Responder locus (Rsp) to this element. This was accomplished by inducing detachments of a compound-X chromosome in females carrying a Y chromosome bearing a Rsps allele. Six Responder-sensitive-bearing X chromosomes, with kappa values ranging from 0.90 to 1.00, were established as permanent lines. Two of these have been characterized more extensively with respect to various parameters affecting meiotic drive. SD males with a Responder-sensitive X chromosome produce almost exclusively male embryos, while those with a Rsp-Y chromosome produce almost exclusively female embryos. This provides a genetic system of great potential utility for the study of early sex-specific differentiation events as it allows the collection of large numbers of embryos of a given sex.

scholarly journals Examination of a mutable system affecting the components of the segregation distorter meiotic drive system of Drosophila melanogaster.

Genetics ◽  
1990 ◽  
Vol 125 (1) ◽  
pp. 51-76
Author(s):  
K G Golic
Keyword(s):  
Drosophila Melanogaster ◽  
Transposable Element ◽  
X Chromosome ◽  
Segregation Distortion ◽  
Chromosomal Rearrangements ◽  
Meiotic Drive ◽  
Drive System ◽  
Partial Loss ◽  
Segregation Distorter ◽  
Relationship Of

Abstract Segregation distortion in Drosophila melanogaster is the result of an interaction between the genetic elements Sd, a Rsp sensitive to Sd, and an array of modifiers, that results in the death of sperm carrying Rsp. A stock (designated M-5; cn bw) has been constructed which has the property of inducing the partial loss of sensitivity from previously sensitive cn bw chromosomes, the partial loss of distorting ability from SD chromosomes, and a concomitant acquisition of modifiers on the X chromosome and possibly also on the autosomes. By several criteria the changes exhibited under the influence of M-5; cn bw are characteristic of the transposable-element systems which produce hybrid dysgenesis. In the first place, the magnitude of these effects depends on the nature of the crosses performed. The analogy is further strengthened by the observation that the changes induced by M-5; cn bw share other stigmata of Drosophila transposable-element systems, including high sterility among the progeny of outcrosses, and the production of chromosomal rearrangements. The possible relationship of this system to the P, I and hobo transposable element systems is discussed, as well as its bearing on aspects of the Segregation Distorter phenomenon which have yet to be explained.

scholarly journals DoesStellateCause Meiotic Drive inDrosophila melanogaster?

Genetics ◽  
2002 ◽  
Vol 161 (4) ◽  
pp. 1551-1559 ◽  
Author(s):  
Massimo Belloni ◽  
Patrizia Tritto ◽  
Maria Pia Bozzetti ◽  
Gioacchino Palumbo ◽  
Leonard G Robbins
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
X Chromosome ◽  
Evolutionary History ◽  
Active Element ◽  
Meiotic Drive

AbstractDrosophila melanogaster males deficient for the crystal (cry) locus of the Y chromosome that carry between 15 and 60 copies of the X-linked Stellate (Ste) gene are semisterile, have elevated levels of nondisjunction, produce distorted sperm genotype ratios (meiotic drive), and evince hyperactive transcription of Ste in the testes. Ste seems to be the active element in this system, and it has been proposed that the ancestral Ste gene was “selfish” and increased in frequency because it caused meiotic drive. This hypothetical evolutionary history is based on the idea that Ste overexpression, and not the lack of cry, causes the meiotic drive of cry– males. To test whether this is true, we have constructed a Ste-deleted X chromosome and examined the phenotype of Ste–/cry– males. If hyperactivity of Ste were necessary for the transmission defects seen in cry– males, cry– males completely deficient for Ste would be normal. Although it is impossible to construct a completely Ste– genotype, we find that Ste–/cry– males have exactly the same phenotype as Ste+/cry– males. The deletion of all X chromosome Ste copies not only does not eliminate meiotic drive and nondisjunction, but it also does not even reduce them below the levels produced when the X carries 15 copies of Ste.

scholarly journals Distinct spermiogenic phenotypes underlie sperm elimination in the Segregation Distorter meiotic drive system

PLoS Genetics ◽  
2021 ◽  
Vol 17 (7) ◽  
pp. e1009662
Author(s):  
Marion Herbette ◽  
Xiaolu Wei ◽  
Ching-Ho Chang ◽  
Amanda M. Larracuente ◽  
Benjamin Loppin ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Satellite Dna ◽  
Copy Number ◽  
Meiotic Drive ◽  
Drive System ◽  
Sperm Chromatin ◽  
Cellular Mechanisms ◽  
Segregation Distorter ◽  
Sperm Nuclei ◽  
Very High

Segregation Distorter (SD) is a male meiotic drive system in Drosophila melanogaster. Males heterozygous for a selfish SD chromosome rarely transmit the homologous SD+ chromosome. It is well established that distortion results from an interaction between Sd, the primary distorting locus on the SD chromosome and its target, a satellite DNA called Rsp, on the SD+ chromosome. However, the molecular and cellular mechanisms leading to post-meiotic SD+ sperm elimination remain unclear. Here we show that SD/SD+ males of different genotypes but with similarly strong degrees of distortion have distinct spermiogenic phenotypes. In some genotypes, SD+ spermatids fail to fully incorporate protamines after the removal of histones, and degenerate during the individualization stage of spermiogenesis. In contrast, in other SD/SD+ genotypes, protamine incorporation appears less disturbed, yet spermatid nuclei are abnormally compacted, and mature sperm nuclei are eventually released in the seminal vesicle. Our analyses of different SD+ chromosomes suggest that the severity of the spermiogenic defects associates with the copy number of the Rsp satellite. We propose that when Rsp copy number is very high (> 2000), spermatid nuclear compaction defects reach a threshold that triggers a checkpoint controlling sperm chromatin quality to eliminate abnormal spermatids during individualization.

scholarly journals Distinct spermiogenic phenotypes underlie sperm elimination in the Segregation Distorter meiotic drive system

2021 ◽  
Author(s):  
Marion Herbette ◽  
Xiaolu Wei ◽  
Ching-Ho Chang ◽  
Amanda M Larracuente ◽  
Benjamin Loppin ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Satellite Dna ◽  
Copy Number ◽  
Meiotic Drive ◽  
Drive System ◽  
Sperm Chromatin ◽  
Cellular Mechanisms ◽  
Segregation Distorter ◽  
Sperm Nuclei ◽  
Very High

Segregation Distorter (SD) is a male meiotic drive system in Drosophila melanogaster. Males heterozygous for a selfish SD chromosome rarely transmit the homologous SD+ chromosome. It is well established that distortion results from an interaction between Sd, the primary distorting locus on the SD chromosome and its target, a satellite DNA called Rsp, on the SD+ chromosome. However, the molecular and cellular mechanisms leading to post-meiotic SD+ sperm elimination remain unclear. Here we show that SD/SD+ males of different genotypes but with similarly strong degrees of distortion have distinct spermiogenic phenotypes. In some genotypes, SD+ spermatids fail to fully incorporate protamines after the removal of histones, and degenerate during the individualization stage of spermiogenesis. In contrast, in other SD/SD+ genotypes, protamine incorporation appears less disturbed, yet spermatid nuclei are abnormally compacted, and mature sperm nuclei are eventually released in the seminal vesicle. Our analyses of different SD+ chromosomes suggest that the severity of the spermiogenic defects associates with the copy number of the Rsp satellite. We propose that when Rsp copy number is very high (> 2000), spermatid nuclear compaction defects reach a threshold that triggers a checkpoint controlling sperm chromatin quality to eliminate abnormal spermatids during individualization.

scholarly journals The effect of novel chromosome position and variable dose on the genetic behavior of the Responder (Rsp) element of the Segregation distorter (SD) system of Drosophila melanogaster.

Genetics ◽  
1989 ◽  
Vol 121 (4) ◽  
pp. 751-763 ◽  
Author(s):  
T W Lyttle
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Meiotic Drive ◽  
Meiotic Pairing ◽  
Genetic Element ◽  
Chromosome Position ◽  
Segregation Distorter ◽  
Sensitive Allele ◽  
Sperm Dysfunction ◽  
Variable Dose

Abstract In the Segregation distorter (SD) system of meiotic drive, a minimum of two trans-acting elements [Sd and E(SD)] act in concert to cause a certain probability of dysfunction for sperm carrying a sensitive allele at the Responder (Rsp) target locus. By employing a number of insertional translocations of autosomal material into the long arm of the Y chromosome, Rsp can be mapped as the most proximal locus in the 2R heterochromatin as defined both by cytology and lethal complementation tests. Several of these insertional translocations result in the transposition of Rsp to the Y chromosome, where its sensitivity remains virtually unaltered. This argues that Rsp is separable from the second chromosome centromere, that its behavior does not depend on its gross chromosomal position, and that meiotic pairing of the chromosomes carrying the various SD elements is not a prerequisite for sperm dysfunction. Several other translocations apparently leave both resulting chromosomes at least partially sensitive to SD action, suggesting that Rsp is a large subdivisible genetic element. This view is compatible with observations published elsewhere that suggest that Rsp is a cytologically large region of highly repetitive AT-rich DNA. The availability of Y-linked copies of Rsp also allows the construction of SD males carrying two independently segregating Rsp alleles; this in turn allows the production of sperm with zero, one or two Rsp copies from the same male. Examination of the relative recovery proportions of progeny arising from these gametes suggests that sperm with two Rsp copies survive at much lower frequencies than would be predicted if each Rsp acted independently in causing sperm dysfunction. Possible explanations for such behavior are discussed.

Linkage and segregation distortion in Drosophila melanogaster

Genome ◽  
1989 ◽  
Vol 32 (5) ◽  
pp. 840-846 ◽  
Author(s):  
Cecil B. Sharp ◽  
Arthur J. Hilliker
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Segregation Distortion ◽  
Homologous Chromosome ◽  
Meiotic Drive ◽  
Major Effect ◽  
Chromosome 2 ◽  
Genetic Elements ◽  
Segregation Distorter ◽  
Per Se

Segregation distortion is caused by a group of genetic elements in and near the centric heterochromatin of chromosome 2 of Drosophila melanogaster. These elements promote their preferential recovery in heterozygous males by rendering sperm bearing the homologous chromosome dysfunctional. Previous work has shown that numerous Y–autosome translocations are associated with the suppression of the segregation distorter phenotype. The present study examined the effects of translocations between the major autosomes upon the expression of segregation distortion. Autosomal translocations involving either the segregation distorter chromosome or its sensitive homologue had no significant effect upon the expression of segregation distortion. These results argue that linkage arrangement per se may not have a major effect on segregation distortion. The suppression of SD by specific Y–autosomal translocations may be due to the disruption of elements on the Y chromosome that are important for the expression of SD.Key words: segregation distortion, meiotic drive, translocations, Drosophila melanogaster.

scholarly journals Genetic analysis of Stellate elements of Drosophila melanogaster.

Genetics ◽  
1994 ◽  
Vol 138 (4) ◽  
pp. 1181-1197 ◽  
Author(s):  
G Palumbo ◽  
S Bonaccorsi ◽  
L G Robbins ◽  
S Pimpinelli
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Copy Number ◽  
Meiotic Drive ◽  
Genetic System ◽  
Male Meiosis ◽  
Meiotic Abnormalities ◽  
Y Chromosomes ◽  
Sperm Development ◽  
Dependent Failure

Abstract Repeated elements are remarkably important for male meiosis and spermiogenesis in Drosophila melanogaster. Pairing of the X and Y chromosomes is mediated by the ribosomal RNA genes of the Y chromosome and X chromosome heterochromatin, spermiogenesis depends on the fertility factors of the Y chromosome. Intriguingly, a peculiar genetic system of interaction between the Y-linked crystal locus and the X-linked Stellate elements seem to be also involved in male meiosis and spermiogenesis. Deletion of the crystal element of the Y, via an interaction with the Stellate elements of the X, causes meiotic abnormalities, gamete-genotype dependent failure of sperm development (meiotic drive), and deposition of protein crystals in spermatocytes. The current hypothesis is that the meiotic abnormalities observed in cry- males is due to an induced overexpression of the normally repressed Ste elements. An implication of this hypothesis is that the strength of the abnormalities would depend on the amount of the Ste copies. To test this point we have genetically and cytologically examined the relationship of Ste copy number and organization to meiotic behavior in cry- males. We found that heterochromatic as well as euchromatic Ste repeats are functional and that the abnormality in chromosome condensation and the frequency of nondisjunction are related to Ste copy number. Moreover, we found that meiosis is disrupted after synapsis and that cry-induced meiotic drive is probably not mediated by Ste.

X-4 Translocations and Meiotic Drive in Drosophila melanogaster Males: Role of Sex Chromosome Pairing

Genetics ◽  
1987 ◽  
Vol 116 (3) ◽  
pp. 409-413
Author(s):  
Bruce McKee
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
X Chromosome ◽  
Chromosome Pairing ◽  
Sex Chromosome ◽  
Meiotic Drive ◽  
Meiotic Pairing ◽  
Size Dependent ◽  
Chromosome Breakpoint

ABSTRACT Males carrying certain X-4 translocations exhibit strongly skewed sperm recovery ratios. The XP4D half of the translocation disjoins regularly from the Y chromosome and the 4PXD half disjoins regularly from the normal 4. Yet the smaller member of each bivalent is recovered in excess of its pairing partner, apparently due to differential gametic lethality. Chromosome recovery probabilities are multiplicative; the viability of each genotype is the product of the recovery probability of its component chromosomes. Meiotic drive can also be caused by deficiency for X heterochromatin. In(1)sc4Lsc8R males show the same size dependent chromosome recoveries and multiplicative recovery probabilities found in T(1;4)BS males. Meiotic drive in In(1)sc4Lsc8R males has been shown to be due to X-Y pairing failure. Although pairing is regular in the T(X;4) males, the striking phenotypic parallels suggest a common explanation. The experiments described below show that the two phenomena are, in fact, one and the same. X-4 translocations are shown to have the same effect on recovery of independently assorting chromosomes as does In(1)sc4Lsc8R. Addition of pairing sites to the 4PXD half of the translocation eliminates drive. A common explanation—failure of the distal euchromatic portion of the X chromosome to participate in X:Y meiotic pairing—is suggested as the cause for drive. The effect of X chromosome breakpoint on X-4 translocation induced meiotic drive is investigated. It is found that translocations with breakpoints distal to 13C on the salivary map do not cause drive while translocations broken proximal to 13C cause drive. The level of drive is related to the position of the breakpoint—the more proximal the breakpoint the greater the drive.

scholarly journals HETEROCHROMATIC EFFECTS ON THE BEHAVIOR OF REVERSED ACROCENTRIC COMPOUND-X CHROMOSOMES IN DROSOPHILA MELANOGASTER

Genetics ◽  
1979 ◽  
Vol 91 (3) ◽  
pp. 537-551
Author(s):  
L Sandler ◽  
Joseph O'Tousa
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
X Chromosome ◽  
Egg Production ◽  
Heterochromatic Region ◽  
Meiotic Behavior ◽  
X Chromosomes ◽  
General Properties ◽  
Single Exchange

ABSTRACT Previous studies of reversed acrocentric compound-X chromosomes suggested peculiar influences of heterochromatin on both the synthesis and meiotic behavior of such compounds. It seemed, with respect to synthesis, that the long arm of the Y chromosome on an X.YL chromosome was necessary in order for the heterochromatic exchange giving rise to reversed acrocentrics to occur, even though YL itself did not participate in the compound-generating event. With respect to behavior, the resulting compounds appeared, presumably as a consequence of their singular generation, to contain an interstitial heterochromatic region that caused the distribution of exchanges between the elements of the compound to be abnormal (many zero and two-exchange tetrads with few, if any, single-exchange tetrads). Removing the interstitial heterochromatin (or, curiously, appending YL as a second arm of the compound) eliminated the recombinational anomalies and resulted in typical tetrad distributions.—We provide evidence that these peculiarities, while presumably real, were likely the consequence of a special X.YL chromosome that was used to synthesize the reversed acrocentrics examined in the early studies and are not general properties of either reversed acrocentric compounds or of interstitial heterochromatin. However, we show that specific heterochromatic regions do, in fact, profoundly influence the behavior of (apparently all) reversed acrocentric compound-X chromosomes. In particular, we demonstrate that specific portions of the Y chromosome and of the basal X-chromosome heterochromatin, when present as homologs for reversed acrocentric compounds, markedly and coordinately increase bath the frequency of exchange between the elements of the compound and the fertility (egg production) of compound-bearing females. It is, we suppose, some aspect of this heterochromatic effect, produced by the% special X.YL chromosome, that caused the earlier-analyzed compounds to exhibit the observed anomalies.

scholarly journals SITE-SPECIFIC INSTABILITY IN DROSOPHILA MELANOGASTER: EVIDENCE FOR TRANSPOSITION OF DESTABILIZING ELEMENT

Genetics ◽  
1982 ◽  
Vol 101 (3-4) ◽  
pp. 461-476
Author(s):  
Todd R Laverty ◽  
J K Lim
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Lethal Mutation ◽  
Chromosome Rearrangements ◽  
Chromosome Break ◽  
Secondary Mutation ◽  
X Chromosomes ◽  
Site Specific ◽  
Normal Sequence ◽  
Lethal Mutations

ABSTRACT In this study, we show that at least one lethal mutation at the 3F-4A region of the X chromosome can generate an array of chromosome rearrangements, all with one chromosome break in the 3F-4A region. The mutation at 3F-4A (secondary mutation) was detected in an X chromosome carrying a reverse mutation of an unstable lethal mutation, which was mapped in the 6F1-2 doublet (primary mutation). The primary lethal mutation at 6F1-2 had occurred in an unstable chromosome (Uc) described previously (Lim 1979). Prior to reversion, the 6F1-2 mutation had generated an array of chromosome rearrangements, all having one break in the 6F1-2 doublet (Lim 1979, 1980). In the X chromosomes carrying the 3F-4A secondary lethal mutation the 6F1-2 doublet was normal and stable, as was the 3F-4A region in the X chromosome carrying the primary lethal mutation. The disappearance of the instability having a set of genetic properties at one region (6F1-2) accompanied by its appearance elsewhere in the chromosome (3F-4A) implies that a transposition of the destabilizing element took place. The mutant at 3F-4A and other secondary mutants exhibited all but one (reinversion of an inversion to the normal sequence) of the eight properties of the primary lethal mutations. These observations support the view that a transposable destabilizing element is responsible for the hypermutability observed in the unstable chromosome and its derivaties.

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