scholarly journals Temperature sensitivity of negative segregation distortion in Drosophila melanogaster.

Genetics ◽  
1993 ◽  
Vol 135 (3) ◽  
pp. 831-841 ◽  
Author(s):  
Y Hiraizumi
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Segregation Distortion ◽  
Current Model ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Absolute Increase ◽  
Negative Segregation ◽  
Absolute Reduction ◽  
Radical Revision

Abstract Previous work has shown that the direction of segregation distortion in the SD (Segregation Distorter) system in Drosophila melanogaster can sometimes be reversed, but this was found only with rather weak distorters and the effect was not large. The present study reports large negative segregation distortion in a strong distorter, SD-72 chromosome. In the presence of a specific X chromosome, supp-X(SD), the proportion, k, of SD-72 chromosomes recovered from the SD-72/cn bw males ranges from 0.99 at 20 degrees to 0.11 at 28.5 degrees, whereas with a standard-X chromosome, k ranges from 0.99 to 0.95 for the same temperature range. The temperature-sensitive period is during spermiogenesis. Using a mating system in which the sperm supply is nearly exhausted, it was shown that the negative distortion at high temperatures is due to an absolute reduction in the number of SD-72 chromosomes and an absolute increase in the number of cn bw chromosomes recovered. After adjusting for non-SD-related temperature effects, the amount of decrease in the number of SD-72 progeny is nearly the same as the amount of increase in the number of cn bw progeny, suggesting that the dysfunction switches from a spermatid carrying one homolog to one carrying the other. Negative distortion requires a radical revision of current hypotheses for the mechanism of segregation distortion and a possible modification of the current model is suggested, based on differential recovery of dysfunction in the two homologs during spermiogenesis.

SD-72 has a temperature-sensitive period during spermiogenesis

1983 ◽  
Vol 25 (6) ◽  
pp. 662-667 ◽  
Author(s):  
Kathleen Matthews ◽  
Mark A. Mortin
Keyword(s):  
Drosophila Melanogaster ◽  
High Temperature ◽  
Segregation Distortion ◽  
Temperature Treatment ◽  
High Temperature Treatment ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Proximate Cause ◽  
Naturally Occurring ◽  
Segregation Distorter

Segregation distorter (SD) chromosomes in Drosophila melanogaster are naturally occurring second chromosomes which produce greatly altered transmission frequencies when present in heterozygous males (Hartl and Hiraizumi 1976). The proximate cause of segregation distortion is abortion of spermatids carrying the non-SD homologue (Tokuyasu et al. 1977). SD-72, a chromosome previously shown (Mange 1968) to be unaffected by high temperature treatment of spermatocytes, a stage when several SD genotypes are temperature sensitive, has a temperature-sensitive period during spermiogenesis. SD-72/cn bw males exposed to a 24-h pulse of 29 °C, then brooded for 24 h, experience a decrease in segregation distortion of approximately two-thirds. The timing of the reduction in distortion indicates that the temperature-sensitive period is postmeiotic.

scholarly journals Negative segregation distortion in the SD system of Drosophila melanogaster: a challenge to the concept of differential sensitivity of Rsp alleles.

Genetics ◽  
1990 ◽  
Vol 125 (3) ◽  
pp. 515-525
Author(s):  
Y Hiraizumi
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Segregation Distortion ◽  
Experimental Results ◽  
Differential Sensitivity ◽  
Female Transfer ◽  
New Model ◽  
Young Males ◽  
Negative Segregation

Abstract Current models of segregation distortion based on previous experimental results predict that, in the Sd heterozygous Rspi/Rsps male, the chromosome carrying the sensitive Rsps allele is distorted or transmitted in a frequency smaller than that of the expected Mendelian 0.5 relative to the chromosome carrying the insensitive Rspi allele. The present study presents a case where this does not occur, that is, when the genotype of the males is supp-X(SD)/Y; Sd E(SD)Rspi M(SD)+/Sd+ E(SD)+ Rsps M(SD)+ where supp-X(SD) is an X chromosome carrying a strong suppressor or suppressors of SD activity and SD+ E(SD)+ Rsps M(SD)+ is the standard cn bw chromosome. Following the "inseminated female transfer" procedure, young males of the above genotype carrying the standard-X instead of the supp-X(SD) chromosome show k values for the SD chromosome (frequencies of the SD chromosome recovered among progeny) of about 0.75, but with the supp-X(SD) chromosome, the k values are reduced to 0.36-0.41. Several possibilities other than the mechanism of segregation distortion to explain the reduced k values are ruled out. The occurrence of "negative segregation distortion" is clearly demonstrated, where the chromosome carrying the Rspi allele is distorted but the chromosome with the Rsps allele is not. This result requires a major modification of the current models or even a new model for the mechanism of segregation distortion to accommodate Rsp allele sensitivity or insensitivity. The present study also shows that males of the genotype, Sd Rspss M(SD)+/Sd+ Rspss M(SD), are almost completely sterile, but their fertility is considerably increased when SD activity is suppressed by the presence of the supp-X(SD) chromosome. This result suggests that the amount of the Sd product is not limited with respect to the interacting sites available, that is, the amount is large enough to interact with both of the Rspss alleles.

scholarly journals X-linked elements associated with negative segregation distortion in the SD system of Drosophila melanogaster.

Genetics ◽  
1994 ◽  
Vol 138 (1) ◽  
pp. 145-152
Author(s):  
Y Hiraizumi ◽  
J M Albracht ◽  
B C Albracht
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Segregation Distortion ◽  
Recovery Rate ◽  
Considerable Decrease ◽  
Negative Segregation ◽  
The Third ◽  
Switch Mechanism ◽  
Rate Of Recovery

Abstract Three elements, M1, M2 and M3, found in a special X chromosome, supp-X(SD), modify the degree and direction of segregation distortion in the SD system of Drosophila melanogaster. The first element, M1, is located between the y and the cv loci, probably close to the y locus. The second element, M2, is located near the cv locus and the third element, M3, is located between the y and the car loci. The M1 element appears to cause a relatively small amount of reduction in the rate of recovery of the SD-72, but not the cn bw, chromosome from SD-72/cn bw males, when raised at 27.5 degrees. The M2 and the M3 elements cause considerable decrease in the recovery rate of the SD-72 chromosome, whereas they increase the recovery rate of the cn bw chromosome. The amount of decrease is nearly the same as the amount of increase for each element. Some type of "switch" mechanism in the directions of distortion is suggested for each of these two elements and their effects appear to be approximately additive.

scholarly journals THE MECHANISM OF A BROODING EFFECT ASSOCIATED WITH SEGREGATION DISTORTION IN DROSOPHILA MELANOGASTER

Genetics ◽  
1973 ◽  
Vol 74 (4) ◽  
pp. 619-631
Author(s):  
D L Hartl
Keyword(s):  
Drosophila Melanogaster ◽  
Segregation Distortion ◽  
Mature Sperm ◽  
Temperature Sensitive ◽  
Short Time

ABSTRACT The recovery of the SD chromosome from a heterozygous SD male increases with brood. This is independent of the age of the female, occurs during the time the sperm are stored in the females, disappears when the segregation distortion is suppressed, and is temperature-sensitive-temperature shocks above or below 25°C applied to the mature sperm both tend to accelerate the increase in the recovery of SD. All this suggests the existence of a class of sperm affected by SD in which the sperm are able to fertilize eggs for a short time following ejaculation but become dysfunctional thereafter.

scholarly journals Hybrid dysgenesis in Drosophila melanogaster: partial sterility associated with embryo lethality in the P-M system

1984 ◽  
Vol 44 (1) ◽  
pp. 11-28 ◽  
Author(s):  
Margaret G. Kidwell
Keyword(s):  
Drosophila Melanogaster ◽  
Gonadal Dysgenesis ◽  
Gonadal Development ◽  
Hybrid Dysgenesis ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Hybrid Progeny ◽  
Partial Sterility ◽  
Embryo Lethality ◽  
Response To Temperature

SummaryVariable frequencies of unhatched eggs were observed to be produced by a number of F1 interstrain hybrids. This type of partial sterility resulting from F2 embryo death was found to be associated with the P-M system of hybrid dysgenesis. Dysgenic hybrid progeny of crosses between M strain females and P strain males may therefore have reduced fertility due to the disruption of development at two different stages: early F1 gonadal development and early F2 embryo development. These disruptions result in the previously described F1 gonadal dysgenesis (GD sterility) and F2 embryo lethality (EL sterility) respectively. The two morphologically distinct types of P-M-associated sterility differ in their patterns of response to F1 developmental temperature, and the temperature-sensitive period for EL sterility occurs considerably later in F1 development than for GD sterility. EL sterility is similar to SF sterility, which is associated with the I–R system of hybrid dysgenesis in that both result from death during early F2 embryogenesis. However, EL sterility differs from SF sterility in not being restricted to hybrids of the female sex and in showing different patterns of response to temperature and ageing in the F1 generation. Some implications of the existence of EL sterility for methods of strain classification in the I–R system are explored.

scholarly journals Improved genome assembly of American alligator genome reveals conserved architecture of estrogen signaling

2016 ◽  
Author(s):  
Edward S. Rice ◽  
Satomi Kohno ◽  
John St. John ◽  
Son Pham ◽  
Jonathan Howard ◽  
...  
Keyword(s):  
Sex Determination ◽  
Genome Assembly ◽  
Critical Period ◽  
Incubation Temperature ◽  
Current Model ◽  
Alligator Mississippiensis ◽  
Estrogen Signaling ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
American Alligator

AbstractThe American alligator, Alligator mississippiensis, like all crocodilians, has temperature-dependent sex determination, in which the sex of an embryo is determined by the incubation temperature of the egg during a critical period of development. The lack of genetic differences between male and female alligators leaves open the question of how the genes responsible for sex determination and differentiation are regulated. One insight into this question comes from the fact that exposing an embryo incubated at male-producing temperature to estrogen causes it to develop ovaries. Because estrogen response elements are known to regulate genes over long distances, a contiguous genome assembly is crucial for predicting and understanding its impact.We present an improved assembly of the American alligator genome, scaffolded with in vitro proximity ligation (Chicago) data. We use this assembly to scaffold two other crocodilian genomes based on synteny. We perform RNA sequencing of tissues from American alligator embryos to find genes that are differentially expressed between embryos incubated at male-versus female-producing temperature. Finally, we use the improved contiguity of our assembly along with the current model of CTCF-mediated chromatin looping to predict regions of the genome likely to contain estrogen-responsive genes. We find that these regions are significantly enriched for genes with female-biased expression in developing gonads after the critical period during which sex is determined by incubation temperature. We thus conclude that estrogen signaling is a major driver of female-biased gene expression in the post-temperature sensitive period gonads.

THE DEVELOPMENTAL GENETICS OF THE TEMPERATURE-SENSITIVE LETHAL ALLELE OF THE SUPPRESSOR OF FORKED, l(1)su(f)ts67g, IN DROSOPHILA MELANOGASTER

Genetics ◽  
1974 ◽  
Vol 76 (3) ◽  
pp. 487-510
Author(s):  
Marianne E Dudick ◽  
Theodore R F Wright ◽  
Lynda Lee Brothers
Keyword(s):  
Drosophila Melanogaster ◽  
Ribosomal Protein ◽  
Sensitive Period ◽  
Developmental Genetics ◽  
Temperature Sensitive ◽  
Wild Type Allele ◽  
Wild Type ◽  
Type Allele ◽  
Lethal Allele

ABSTRACT A temperature-sensitive lethal allele of suppressor of forked, l(1)su(f)ts67g (ts67), has been discovered and characterized as follows: Flies which are hemizygous for ts67 live at 18° and 25° but die at 30° primarily as larvae. The temperature-sensitive period for ts67 homozygotes or hemizygotes begins in second instar and ends at pupation. ts67 is lethal at 30° when heterozygous with suppressor of forked (su(f)), a deficiency for suppressor of forked (su(f)  -), and a non-conditional lethal allele of suppressor of forked (3DES). It is viable at 30° when heterozygous with the wild-type allele of suppressor of forked. At 25° but not at 18° forked bristles are suppressed in flies of the following genotypes: fsts67/Y, fsts67/fsts67, fsts67/fssu(f), futs67/fs3DES, futs67/fssu(f)  -, futs67/fssu(f). There is some suppression of forked bristles at 25° in the heterozygote, fsts67/fs+su(f). The forked bristle phenotype is not suppressed at either temperature in flies of the genotypes futs67/Y, futs67/futs67/ (fs and fu indicating suppressible and unsuppressible alleles of forked). The temperature-sensitive period for suppression of forked bristles begins at pupation and extends through the period of bristle synthesis. The deficiency phenotype (bristles reduced in size or absent, wing wrinkled or blistered, eyes rough) typical of flies of the genotype fssu(f)/fssu(f)  - at 18° and 25°, is exhibited by flies of the genotypes fsts67/fssu(f)  - at 25° and futs67/fssu(f) at 29°. An allele of lozenge (lz1) which can be suppressed by su(f) is suppressed at 25° but not at 18° in lz1ts67/Y males. ts67 homozygous females are fertile at 25° but sterile at 30°. The hypothesis is discussed that the su(f) locus codes for a ribosomal protein and that suppression and enhancement are affected by mutations at the locus by mutant ribosome-induced misreading. The possibility is presented that ts67 may be used to determine the translation time in development of any gene.

scholarly journals Studies on male recombination in a Southern Greek Drosophila melanogaster population: (a) Effect of temperature. (b) Suppression of male recombination in reciprocal crosses

1977 ◽  
Vol 29 (3) ◽  
pp. 231-238 ◽  
Author(s):  
George Yannopoulos ◽  
Michael Pelecanos
Keyword(s):  
Drosophila Melanogaster ◽  
Germ Cells ◽  
Larval Stage ◽  
Effect Of Temperature ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Cytoplasmic Factor ◽  
Male Recombination ◽  
The City ◽  
North Western

SUMMARYA second chromosome of Drosophila melanogaster (symbol 31.1) isolated from a natural population of North-Western Peloponnesus (at a distance of 8 km from the city of Patras) was found to induce recombination in heterozygous males, both in the second and third chromosomes. The present study also revealed the following points. (1) The phenomenon is temperature-sensitive with higher male recombination at 29 °C than at 25 or 15 °C. (2) The temperature-sensitive period is during the larval stage where premeiotic divisions of germ cells take place. (3) Suppression of male recombination in both the second and third chromosomes occurred when 31.1/CyL4 females were used in the matings, and (4) the suppression of male recombination is caused by a cytoplasmic factor of the CyL4/Pm stock.

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 Evidence of a dual function in fl(2)d, a gene needed for Sex-lethal expression in Drosophila melanogaster.

Genetics ◽  
1992 ◽  
Vol 130 (3) ◽  
pp. 597-612 ◽  
Author(s):  
B Granadino ◽  
A San Juán ◽  
P Santamaria ◽  
L Sánchez
Keyword(s):  
Drosophila Melanogaster ◽  
Germ Cells ◽  
Sensitive Period ◽  
Dual Function ◽  
Temperature Sensitive ◽  
Permissive Temperature ◽  
Loss Of Function ◽  
Germline Development ◽  
Suppression Effect ◽  
Pole Cells

Abstract In Drosophila melanogaster, the female sexual development of the soma and the germline requires the activity of the gene Sxl. The somatic cells need the function of the gene fl(2)d to follow the female developmental pathway, due to its involvement in the female-specific splicing of Sxl RNA. Here we report the analysis of both fl(2)d1 and fl(2)d2 mutations: (1) fl(2)d1 is a temperature-sensitive mutation lethal in females and semilethal in males; (2) fl(2)d2 is lethal in both sexes; (3) the fl(2)d1/fl(2)d2 constitution is temperature-sensitive and lethal in females, while semilethal in males. The temperature-sensitive period of fl(2)d1 in females expands the whole development. SxlM1 partially suppresses the lethality of fl(2)d1 homozygous females and that of fl(2)d1/fl(2)d2 constitution, whereas it does not suppress the lethality of fl(2)d2 homozygous females. The addition of extra Sxl+ copies does not increase the suppression effect of SxlM1. The fl(2)d1 mutation in homozygosis and the fl(2)d1/fl(2)d2 constitution, but not the fl(2)d2 in homozygosis, partially suppress the lethality of SxlM1 males. This suppression is not prevented by the addition of extra Sxl+ copies. The semilethality of both fl(2)d1 and fl(2)d1/fl(2)d2 males, and the lethality of fl(2)d2 males, is independent of Sxl function. There is no female synergistic lethality between mutations at fl(2)d and neither at sc or da. However, the female synergistic lethality between mutations at Sxl and either sc or da is increased by fl(2)d mutations. We have analyzed the effect of the fl(2)d mutations on the germline development of both females and males. For that purpose, we carried out the clonal analysis of fl(2)d1 in the germline. In addition, pole cells homozygous for fl(2)d2 were transplanted into wild-type host embryos, and we checked whether the mutant pole cells were capable of forming functional gametes. The results indicated that fl(2)d mutant germ cells cannot give rise to functional oocytes, while they can form functional sperm. Moreover, SxlM1 suppresses the sterility of the fl(2)d1 homozygous females developing at the permissive temperature. Thus, with respect to the development of the germline the fl(2)d mutations mimic the behavior of loss-of-function mutations at the gene Sxl. Females double heterozygous for fl(2)d and snf1621 are fully viable and fertile. fl(2)d2 in heterozygosis partially suppresses the phenotype of female germ cells homozygous for snf1621; however, this is not the case with the fl(2)d1 mutation. The fl(2)d mutations partially suppress the phenotype of the female germ cells homozygous for ovoDIrSI.(ABSTRACT TRUNCATED AT 400 WORDS)

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