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 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)

scholarly journals Studies on the sterility induced by the male recombination factor 31.1 MRF in Drosophila melanogaster

1978 ◽  
Vol 32 (3) ◽  
pp. 239-247 ◽  
Author(s):  
George Yannopoulos
Keyword(s):  
Drosophila Melanogaster ◽  
Male Sterility ◽  
Germ Cells ◽  
Optical Microscope ◽  
The Body ◽  
Female Sterility ◽  
Male Recombination ◽  
Homologous Chromosomes

SUMMARYThe sterility which is associated with male recombination induced by 31.1 MRF was studied genetically and cytologically. In all crosses it was found that female sterility mainly involves failure of the heterozygous females to lay eggs because their ovaries are atrophic. Under the optical microscope, the atrophic ovaries were seen to contain only germaria in their ovarioles. It was also found that in some cases 31.1 MRF affects only one of the two ovaries of the same female. This observation suggests that defective development of atrophic ovaries is not due to influences from the rest of the body but should be attributed to the inability of the germ cells to differentiate. Moreover, various stocks as well as homologous chromosomes were found to react differently to 31.1 MRF with respect to female sterility. In their effect on male sterility it was observed that some strains behave as neutral and others as reactive when mated with 31.1/Cy L4 males.

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.

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 HYBRID DYSGENESIS IN DROSOPHILA MELANOGASTER: THE BIOLOGY OF FEMALE AND MALE STERILITY

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 161-174
Author(s):  
William R Engels ◽  
Christine R Preston
Keyword(s):  
Male Sterility ◽  
Germ Cells ◽  
Germ Line ◽  
Hybrid Sterility ◽  
Primordial Germ Cells ◽  
Wild Strain ◽  
Hybrid Dysgenesis ◽  
Sensitive Period ◽  
Male Recombination ◽  
Larval Stages

ABSTRACT High levels of female and male sterility were observed among the hybrids from one of the two reciprocal crosses between a wild strain of D. melanogaster known as π2 and laboratory strains. The sterility, which is part of a common syndrome called hybrid dysgenesis, was found to be associated with the rudimentary condition of one or both of the ovaries or testes. All other tissues, including those of the reproductive system were normal, as were longevity and mating behavior. The morphological details of the sterility closely mimic the agametic condition occurring when germ cells are destroyed by irradiation or by the maternal-effect mutation, grandchildless. We suggest that sterility in hybrid dysgenesis is also caused by failure in the early development of germ cells. There is a thermo-sensitive period beginning at approximately the time of initiation of mitosis among primordial germ cells a few hours before the egg hatches and ending during the early larval stages. Our results suggest that hybrid dysgenesis, which also includes male recombination, mutation and other traits, may be limited to the germ line, and that each of the primordial germ cells develops, or fails to develop, independently of the others. This hypothesis is consistent with the observed frequencies of unilateral and bilateral sterility, with the shape of the thermo-sensitivity curves and with the fact that males are less often sterile than females. The features of this intraspecific hybrid sterility are found to resemble those seen in some interspecific Drosophila hybrids, especially those from the cross D. melanogasfer × D. simulans.

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.

scholarly journals The recovery and preliminary examination of a temperature sensitive suppressor of the cryptocephal mutant of Drosophila melanogaster

1981 ◽  
Vol 38 (3) ◽  
pp. 297-314 ◽  
Author(s):  
John C. Sparrow
Keyword(s):  
Drosophila Melanogaster ◽  
Temperature Shift ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Induced Mutations ◽  
Chitin Synthesis ◽  
Preliminary Examination

SUMMARYThe recovery of two EMS induced mutations which are dominant suppressors of the lethality of cryptocephal in Drosophila melanogaster are described. One of these mutations Su(crc)1 is described in detail. It maps very close to cryptocephal at 54·7 on the second chromosome and its suppression of cryptocephal is temperature-sensitive. Temperature shift experiments show that the temperature-sensitive period is from before the pupariation until 12 h post pupariation. The temperature-sensitive period of Su(crc)1 is discussed in relation to the expression of l(2)crc, head eversion and the timing of pupal chitin synthesis.

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.

TEMPERATURE-DEPENDENT EXPRESSION OF THE APTEROUS PHENOTYPE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1986 ◽  
Vol 112 (2) ◽  
pp. 217-228
Author(s):  
Mary E Stevens ◽  
Peter J Bryant
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Gene Product ◽  
Constant Temperature ◽  
Temperature Shift ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Temperature Dependent ◽  
Developmental Defects ◽  
Per Se

ABSTRACT Mutations at the apterous (ap) locus in Drosophila melanogaster produce a variety of developmental defects, including several classes of wing abnormalities. We describe the wing phenotype produced by homozygotes and hemizygotes of three different temperature-sensitive apterous alleles grown at 16, 18, 20, 22, 25, and 29°. We also describe the phenotype produced by each of these three alleles when heteroallelic with the non-temperature-sensitive apc allele. Constant-temperature and temperature-shift experiments show that each of the heteroallelic genotypes can produce several of the previously described apterous phenotypes and that the length of the temperature-sensitive period for a given phenotype depends on the allelic combinations used to measure it. We suggest that the stage-specific requirements of the tissue for gene product, rather than the time of gene expression per se, determine the temperature-sensitive periods for apterous and other loci. The results support the hypothesis that the various wing phenotypes produced by apterous mutations are due to quantitative reductions in the activity of gene product and that failure to meet specific threshold requirements for gene product can lead to qualitatively different phenotypes.

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