scholarly journals A COLD-SENSITIVE ZYGOTIC LETHAL CAUSING HIGH FREQUENCIES OF NONDISJUNCTION DURING MEIOSIS I IN DROSOPHILA MELANOGASTER FEMALES

Genetics ◽  
1974 ◽  
Vol 76 (3) ◽  
pp. 511-536
Author(s):  
Theodore R F Wright

ABSTRACT The X-linked, cold-sensitive zygotic lethal, l(1)TW-6cs, both in homozygous and heterozygous females, induces nondisjunction of all four chromosomes at Meiosis I at both 25° and 17°. Nondisjunction frequencies approaching 0.5 for the X and fourth chromosomes have been observed at 16°–18°. The disjunction of the X chromosomes in males is not affected. The mutant causes mitotic irregularities in zygotes at both 25° and 17°. Mortality of all zygotes produced by the crosses 6cs/6cs × 6cs/BsY and FM7/6cs × 6cs/BsY is respectively 86% and 67–74% at 25° and 99.8–99.9% and 94% at 17°. The mortality of 6cs hemizygotes derived from females carrying no doses of 6cs (C(1)DX,y f/y × 6cs/BsY) is 45–55% at 25° and 98% at 17°. The length of the temperature-sensitive period for 6cs homo- and hemizygotes is affected by the maternal dosage of 6cs; the shortest TSP is for zero and the longest is for two maternal doses. Mortality takes place primarily during embryogenesis with some larval and little pupal mortality. Analysis of sectioned embryos indicates that the large array of different patterns of damage observed could have arisen from abnormal cleavage divisions and the incomplete population of the blastoderm with nuclei.

1973 ◽  
Vol 15 (2) ◽  
pp. 237-254 ◽  
Author(s):  
Helen Mayoh ◽  
David T. Suzuki

Among 3,919 EMS-treated X chromosomes, 25 were retained as cold-sensitive (cs) lethals. That is, more than 20% of flies carrying a cs lethal survive at 22 °C and none at 17 °C and for cs semi-lethals, >30% at 22 °C and <13% at 17 °C. The cs mutations are not randomly distributed, seven being located at the X tip and three being alleles to the right of car. Over half exhibited female sterility or reduced fertility and seven exhibited visible phenotypes characteristic of bobbed and Minute mutations. The possible enrichment for ribosomal protein defects by screening for cold-sensitivity is discussed.


1984 ◽  
Vol 44 (1) ◽  
pp. 11-28 ◽  
Author(s):  
Margaret G. Kidwell

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.


Genetics ◽  
1973 ◽  
Vol 74 (3) ◽  
pp. 509-520
Author(s):  
S Elaine Tasaka ◽  
David T Suzuki

ABSTRACT Ethyl methanesulfonate-treated third chromosome of Drosophila melanogaster were tested for the presence of dominant and recessive temperature-sensitive lethal mutations at 17°, 22° and 29°C. Out of 1,176 chromosomes tested, no dominant ts lethals, 21 heat-sensitive, 22 cold-sensitive and 10 heat-cold-sensitive lethals were recovered. Heat-cold sensitivity was produced by a single mutation in all cases. Sixty-two percent of the ts lethals were fertile as homozygotes in both sexes. Surprisingly, 88% of the ts lethals mapped between st and Sb, a region straddling the centromere and estimated to comprise 12.9% of the genetic length and 55% of the physical length of chromosome 3. All but one of the heat- and cold-sensitive lethals complemented with each other at their respective restrictive temperatures.


Genetics ◽  
1974 ◽  
Vol 76 (3) ◽  
pp. 487-510
Author(s):  
Marianne E Dudick ◽  
Theodore R F Wright ◽  
Lynda Lee Brothers

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.


1977 ◽  
Vol 29 (3) ◽  
pp. 231-238 ◽  
Author(s):  
George Yannopoulos ◽  
Michael Pelecanos

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.


Genetics ◽  
1992 ◽  
Vol 130 (3) ◽  
pp. 597-612 ◽  
Author(s):  
B Granadino ◽  
A San Juán ◽  
P Santamaria ◽  
L Sánchez

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)


Genetics ◽  
1972 ◽  
Vol 70 (1) ◽  
pp. 75-86
Author(s):  
Raja Rosenbluth ◽  
Dean Ezell ◽  
David T Suzuki

ABSTRACT Ethyl methanesulfonate-treated autosomes were screened for the presence of dominant cold-sensitive (DCS) lethal mutations in Drosophila melanogaster. None was found among 6,552 treated and 168 untreated third chromosomes. Twenty-three DCS-L chromosomes which caused death at 17°C but survived at 22°C and 29°C were recovered from 5,046 mutagenized chromosome 2's.—The DCS-L mutations all mapped around dp and appeared to be functionally allelic. Lethality of heterozygotes for most of the DCS-L's occurred over a prolonged interval from the embryonic through the larval instars. Prolonged incubation at 17°C did not demonstrate any maternal effect on zygotic survival.


Genetics ◽  
1993 ◽  
Vol 135 (3) ◽  
pp. 831-841 ◽  
Author(s):  
Y Hiraizumi

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.


1981 ◽  
Vol 38 (3) ◽  
pp. 297-314 ◽  
Author(s):  
John C. Sparrow

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.


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