Effects of a chromosome-3 mutator gene on radiation-induced mutability in Drosophila melanogaster females

A series of X-irradiation experiments was carried out using Drosophila melanogaster females homozygous for a third chromosome mutator gene and females which had a similar genetic background except that the mutator-bearing third chromosomes were substituted by normal wild-type chromosomes. The mutator females had been previously shown by Gold and Green to manifest a higher level of radiation-induced mutability (as measured by the X-ray-induction of sex-linked recessive lethals) in their pre-meiotic germ cells compared to normal females at an exposure of 100 R. In the presence work, the sensitivity of the pre-meiotic germ cells of mutator and normal females to the X-ray induction (2000 R) of sex-linked recessive lethals was studied. In addition, experiments were conducted to examine the sensitivity of the immature (stage 7; prophase I of meiosis) oocytes of both kinds of females to the induction of dominant lethals, X-linked recessive lethals and X-chromosome losses. The result show that in pre-meiotic germ cells, the frequencies of radiation-induced recessive lethals are similar in both kinds of females. However, the proportion of these mutations that occur in clusters of size 3 and higher, is higher in mutator than in normal females. In stage-7 oocytes, the frequencies of radiation-induced dominant lethals and sex-linked recessive lethals were similar in both kinds of females. The X-loss frequencies however, were consistently higher in mutator females although statistical significance was obtained only at higher exposures (3000 and 3750 R) and not at lower ones (750-2250 R). Possible reasons for the discrepancy between the present results and those of Gold and Green with respect to pre-meiotic germ cells are discussed.     

The cytogenetics of mutator gene-induced X-linked lethals in Drosophila melanogaster

A third chromosome mutator gene effectively increases the spontaneous frequency of sex-linked recessive lethals in females but not in females of Drosophila melanogaster. Approximately half the mutator-induced mutants occur as clusters of the same mutant implying a premeiotic origin. An appreciable number of the mutator-induced lethals are associated with comparatively long deficiencies of several salivary gland chromosome bands. The possible modes of mutator gene action are conjectured.     

The effect of caffeine on repair systems in oocytes of Drosophila melanogaster. I

Young Drosophila females were treated with caffeine, then mated for 24 h to males that had been irradiated with 2000 R X-irradiation, so that only mature spermatozoa were sampled. The radiation-induced frequency of dominant lethals and sex chromosome loss in the paternal genome was determined. The results show that treatment of females with caffeine leads to an increase in the frequencies of radiation-induced dominant lethals and to sex-chromosome loss.When young virgin females of the radioresistant stock RöI₂ were treated with caffeine and then irradiated with 3000 R X-irradiation, a striking increasein dominant lethals (in the maternal genome) was observed; caffeine treatment increased the X-ray response of the radioresistant stock to the level of the normal (+60) stock. It is suggested that caffeine reduces the efficiency of a system in Drosophila oocytes that repairs X-ray-produced chromosome breaks in both the paternal and maternal genomes.     

Effect of glyoxal pretreatment on radiation-induced genetic damage in Drosophila melanogaster

The effects of glyoxal and of glyoxal pretreatments on radiation-induced genetic damage were investigated in Drosophila melanogaster mature sperm, by means of sex-linked recessive and dominant lethality, reciprocal translocation and chromosome loss tests. In addition, the possible mutagenic effect of glyoxal was assessed in postmeiotic cells up to 7 days after treatment. The results obtained show: (1) the frequencies of recessive lethals after glyoxal treatment were within control values, (2) no clastogenic effect of glyoxal was observed, (3) glyoxal pretreatment did not modify the frequency of recessive lethals induced by X-rays, (4) after pretreatment with glyoxal a consistent, though not significant, increase was seen in the frequency of reciprocal translocations in 3 replicate experiments, (5) the yield of dominant lethals and of complete and partial chromosome loss induced by radiation was significantly increased by pretreatments with glyoxal. It is suggested that the increase of the frequency of genetic endpoints resulting from chromosome breakage, when glyoxal was administered prior to irradiation, could be ascribed to: (a) a sensitizing action of glyoxal to the clastogenic effect of ionizing radiation; (b) the formation of reactive species by the interaction of glyoxal with radiation; and/or (c) interference of glyoxal with the normal handling of radiation-induced lesions in mature postmeiotic male cells.     

Mutation Induction in the Male Recombination Strains of DROSOPHILA MELANOGASTER

One group of the second chromosome lines isolated from a southern Texas population of Drosophila melanogaster, which has been known to show relatively high frequencies of male recombinations, was found to increase the frequency of sex-linked recessive lethal mutations from a control frequency of 0.18% to 1.63%. The second group, which showed a very much reduced frequency of male recombinations, was found to cause a slight increase to 0.48%, although it was not statistically significant. The first group was also tested for the recessive lethal mutation frequency in the second chromosome; the frequency increased from a control frequency of 0.28% to 2.82%. Mapping of a portion of the sex-linked lethals indicated a distribution along the entire X chromosome, although there was a tendency of clustering towards the tip of the X chromosome. One sex-linked lethal line so far tested was found to be associated with an inversion (approximate breakpoints, 14A-18A). It was suggested that the element causing male recombination might be similar to the hi mutator gene studied earlier by Ives (1950).     

Evidence of an essential difference between point mutations and chromosome breaks induced by triethylene melamine inDrosophila spermatozoa

Summary Storing of triethylene melamine-treated mature spermatozoa in untreated females was found to result in increased frequencies of both sex-linked recessive lethals and translocations involving the Y, II and III chromosomes. Frequencies of these mutations in effectively unstored spermatozoa were determined from progenies produced using sperm 2–4 days after treatment. The increase in translocation frequencies was on the order of 12-fold in progenies from sperm utilized 11–13 days after treatment when the sperm were stored at 25°C, and 3- to 6-fold when comparable sperm were stored at 12.5°C. Consistent but much smaller increases in frequencies of sex-linked lethals were found, with the increase in lethals tending to be correlated with relative increase in translocation frequency in a given experiment. On the assumption that sex-linked lethals related to chromosome breakage would be expected to increase in frequency in the same proportion as do translocations, approximate agreement was obtained when the proportions of breakage-related lethals among unstored lethals were estimated from the data in the four experimental series. The data are thus consistent with the hypothesis that chromosome breaks but not point mutations are realized during storage of treated spermatozoa. Possible interpretations of a differential effect of storage on treated chromosomes are discussed.Studies carried out while the author was a guest investigator at the Institute of Animal Genetics on sabbatical leave from the University of Minnesota.     

Increment kinetics of recessive lethal mutations and dominant lethals in offspring of Drosophila melanogaster on storage of methyl-methanesulfonate-treated sperm in females

The frequencies of sex-linked recessive lethal mutations in F1 males after feeding adult male Drosophila melanogaster with 0.25 and 0.5 mM methyl methanesulfonate (MMS) orally for 24 h increased approximately linearly with storage of the treated spermatozoa in females, whereas the number of hits of dominant lethals in the sperm after feeding 0.3 and 0.5 mM MMS increased approximately with the square of the storage time. Chromosome losses and mosaics in F1 males also increased with the dose of MMS to males, but their yields were too low to be analyzed quantitatively, only indicating a slight increase of chromosome loses and a slight decrease of mosaics with the time of storage of sperm. Maternal non-disjunctions (or chromosome losses), detected in F1 males, decreased with the dose of MMS to spermatozoa and their yield decreased with the time of storage of sperm of both MMS-treated and the control groups. A unitary model is proposed to explain the effect of storage on the dominant lethals and recessive lethal mutations.     

Effects of a small X-ray exposure to Drosophila melanogaster females on the recovery of genetic damage from X-irradiated males.

Wild-type (Oregon-K) Drosophila melanogaster males were X-irradiated and mated to Oster females (y sc^s1 In49sc⁸; bw; st p^p) that had received a 20 R X-ray exposure (Group MF) or no irradiation (group M). Mature spermatozoa of the irradiated males were sampled and the frequencies of dominant lethals, sex-linked recessive lethals and 2–3 translocations were measured. In the group in which the irradiated males were mated to irradiated females, the survival of eggs was significantly higher than in the group in which only the males were irradiated. However, there was no consistent and detectable difference between the two groups with respect to the frequencies of recessive lethals and translocations.The relatively higher egg survival in the MF group is amenable to an interpretation based on an inducible repair process in females that acts on radiation damage induced in spermatozoa but, such an explanation is inadequate to explain the other results. It is concluded that the observations considered together preclude a general and unifying interpretation based on a low-dose-X-ray-inducible genetic repair process in females (acting on damage in spermatozoa). Possible reasons for the discrepancy between the expectation of differences in response between the MF and M groups (in sex-linked lethal and translocation frequencies) and the observation of no consistent differences between them are discussed.     

Radioprotective effect of six chemicals against X-ray-induced genetic damage in D. melanogaster

In Drosophila melanogater six chemicals were tested for radioprotectiveeffect against X-ray-induced genetic damage such as sex-linked recessive lethals and autosomal translocations using Oster's ring-X chromosome stock. A 2-day brood pattern was followed to score the damage induced at different spermatogenic stages separately. In all cases the chemicals were injected before X-irradiation. 10-mM solution of reduced glutathione (GSH) provided statistically significant protection against sex-linked recessive lethals in all broods. In translocation tests this chemical reduced the frequency in all broods but the result is not statistically significant. Cysteamine (MEA) did not show any protective effect but the frequency of lethals was slightly reduced in the first and fourth broods. 2-Aminoethyl isothiuronium Br·HBr (AET) showed a statistically significant protective effect when the data of the replicate experiments were pooled. Negative results were obtained for 5-hydroxytryptamine (5-HT) in sex-linked lethal tests. Aminoethyl phosphorothioate (AEPT) reduced the frequencies of both sex-linked lethals and autosomal translocations in all broods consistently but the results are not statistically significant. In tests for both lethals and translocations the reduction was largest in the stages with highest radiosensitivity. N(3-Aminopropyl)aminoethyl phosphorothioate (3AP-AEPT) gave no protection.     

Influence of the MR (mutator) factor on X-ray-induced genetic damage

The genetical effects induced by MR, in the progeny of outcrossed MR-males, include very high frequencies of visible and lethal mutations and chromosome aberrations. The hypothesis is that MR causes breaks at specific sites in the DNA where, subsequently, insertion sequences become integrated. To examine whether there exists an interaction between breaks and radiation induced lesions, MRh12/Cy males were crossed to Berlin K females and the male progeny from this cross carrying the MR or Cy chromosome were irradiated. The frequencies of X-linked recessive lethals and II-III translocations were determined. Non-irradiated MR and non-MR (Cy) male progeny were used in concurrent controls. The results show that the frequencies of II-III translocations in the MR-containing males is not significantly higher than in the controls. However, with regard to the production of recessive lethal mutations a clear synergism between MRh12 and X-irradiation was observed.     

Studies on mutagen-sensitive strains of Drosophila melanogaster. IV. Modification of genetic damage induced by X-irradiation of spermatozoa and spermatids in N2 or O2 by mei-9a, mei-41D5 and mus(1)101D1

The influence of defects in DNA repair processes on X-ray-induced genetic damage in post-meiotic male germ cell stages of Drosophila melanogaster was studied using the 'maternal effects approach'. Basc males were irradiated in N2, air or O2 either as 48-h-old pupae (to sample spermatids) or as 3-4-day-old adults (to sample mature spermatozoa) and mated to females of 3 repair-deficient strains (mei-9a: excision-repair-deficient; mei-41D5: post-replication-repair-deficient; mus(1)101D1: post-replication-repair-deficient and impaired in DNA synthesis). Simultaneous controls involving mating of males to repair-proficient females (mei+) were run. The frequencies of sex-linked recessive lethals and of autosomal translocations were determined following standard genetic procedures. The responses elicited in the different crosses with repair-deficient females were compared with those in mei+ crosses. The main findings are the following: with mei-9 females, the frequencies of recessive lethals are higher after irradiation of spermatids in N2, but not after irradiation in air of O2 (relative to those in the mei+ crosses); this result is different from that obtained in earlier work with spermatozoa, in which cell stage, higher yields of recessive lethals were obtained after irradiation of males in either N2 or air; in the mei-9 crosses, there are no significant differences in response (relative to mei+) after irradiation of either spermatozoa or spermatids in O2; the translocation frequencies in the mei-9 crosses are similar to those in the mei+ crosses, irrespective of the treated germ cell stage or the irradiation atmosphere; irradiation of either spermatozoa or spermatids in N2, air or O2 does not result in any differential recovery of recessive lethals in the mei-41 relative to mei+ crosses; irradiation of spermatids in N2 and of spermatozoa in air leads to a higher recovery of translocations in the mei-41 crosses; and after irradiation of spermatids or spermatozoa in any of the gaseous atmospheres, the frequencies of recessive lethals and of translocations are lower in the mus-101 crosses. The differences in responses (between cell stages, in different gaseous atmospheres and with different repair-deficient females) are explained on the basis of both qualitative and quantitative differences in the composition of the initial lesions and the extent to which their repair may be affected by the defects present in the different repair-deficient females. Several discrepancies between expectations based on biochemical results and the genetic results are pointed out.(ABSTRACT TRUNCATED AT 400 WORDS)     

Studies on mutagen-sensitive strains of Drosophila melanogaster VIII. Further data on differences between Canton-S and ebony strains with respect to maternal effects for the X-ray induction of autosomal translocations and ring-X chromosome losses in mature spermatozoa

The influence of the maternal genotype (Canton-S, proficient in the repair of X-ray-induced chromosome breaks and ebony, less proficient in this regard) on the recovery of X-ray-induced autosomal (II–III) translocations and ring-X chromosome losses in mature spermatozoa was studied. In the first series of experiments, males carrying appropriate markers on their second and third chromosomes were irradiated and mated to Canton-S or ebony females and the frequencies of II–III translocations were determined. In the second series of experiments, males carrying ring-X chromosomes were irradiated in N₂ or in O₂, mated to Canton-S or ebony females and the frequencies of XO males were determined; additionally, under similar gas-treatment and radiation conditions, the pattern of egg-mortality was also assessed.

The data on translocations show that the yields are higher with ebony than with Canton-S females; these and earlier results on dominant lethals and sex-linked recessive lethals support the interpretation that the maternal repair system in the ebony strain is less proficient and more error-prone than that of the Canton-S strain.

Those on the losses of ring-X chromosomes demonstrate that (i) the absolute yields of XO males are lower with ebony than with Canton-S females irrespective of whether the parental males are irradiated in N₂ or in O₂; (ii) the exposure-frequency relationships are all linear, but the slopes are higher when the males are irradiated in O₂ and are consistent with an oxygen-enhancement-ratio of about 1.5 and (iii) the relationships between the logarithm of egg-survival and XO male frequency are also linear, but the slopes for the O₂ groups are lower than those for the N₂ groups (slope ratios of 0.86–0.87).

The finding that at given survival levels, the XO frequencies are lower in the O₂ than in the N₂ groups of both the Canton-S and ebony series viewed in the context of the mechanisms that have been postulated to explain the loss of ring-X chromosomes in irradiated mature spermatozoa permits the following interpretation for the observed results: (i) a higher proportion of potential XO zygotes is lost through dominant lethality in the O₂ groups than in the N₂ ones presumably because the chromosome breaks induced in O₂ are qualitatively different in the sense that they have higher probability to undergo reunions relative to restitution, compared with breaks induced under anoxia and (ii) this leads to lower than expected oxygen-enhancement ratios (i.e., expected on the basis of published data on sex-linked recessive lethals, another kind of genetic damage which shows a linear exposure-frequency relationship).     

Studies on mutagen-sensitive strains of Drosophila melanogaster I. The enhanced X-ray sensitivity of a mutant strain (ebony) which is UV-sensitive and also deficient in photorepair

Yegorova and colleagues (1978) showed that a mutant strain of Drosophila melanogaster (ebony) was more sensitive to UV-induced killing of embryos and also less proficient in photoreactivating (PR) ability than a wild-type (Canton-S) strain and that the genes governing UV sensitivity and PR ability were different and presumably located on the autosomes. The experiments reported in the present paper were designed to compare the patterns of sensitivity of these 2 strains and their hybrids to X-irradiation. The sensitivity of the larvae to the killing effects of X-irradiation, and of male and female germ-cell stages to the X-ray induction of genetic damage was studied.It was found that the larvae of the ebony strain are more sensitive to X-ray-induced killing than those of the Canton-S strain. The frequencies of radiation-induced dominant lethals and sex-linked recessive lethals are higher in spermatozoa sampled from ebony males than in those of Canton-S males. In spermatozoa sampled from hybrid males, the yields of dominant lethals are no higher than in those sampled from Canton-S males and do not seem to depend on the origin of the X-chromosome. There are no statistically significant differences between the ebony and Canton-S strains in the sensitivity of their spermatozoa to the induction of autosomal translocations.Stage-7 oocytes sampled from ebony females are more sensitive to the X-ray induction of dominant lethality than are those from Canton-S females; oocytes sampled from hybrid females manifest a level of sensitivity that is significantly lower than that in either parental strain. The frequencies of X-chromosome losses induced in in this germ-cell stage are significantly lower in ebony than in Canton-S females at least at the exposure level of 3000 R at which 3 experiments were carried out. There are no measurable differences in the amount of dominant lethality induced in stage-14 oocytes of ebony, Canton-S and hybrid females.When X-irradiated Berlin-K males are mated to ebony or Canton-S females, the yields of dominant lethals are higher when ebony females are used, showing that there is a “maternal effect” for this kind of damage. Such a maternal effect is also found for sex-linked recessive lethals (irradiated Muller-5 males mated to ebony or Canton-S females). However, when irradiated ring-X-chromosome-carrying males are mated to ebony or Canton-S females, the frequencies of paternal sex-chromosome losses (scored as XO males) are lower when ebony females are used.These results have been interpreted on the assumption that the ebony strain is homozygous for recessive, autosomal genes that confer increased radiosensitivity and that the Canton-S strain carries the normal, wild-type alleles for these genes. The higher yields of dominant and recessive lethals in mature spermatozoa and of dominant lethals in stage-7 oocytes are a consequence of an enhanced sensitivity to the mutagenic (in particular, to the chromosome-breaking) effects of X-irradiation and/or of defective repair of radiation-induced genetic damage. The lower yield of XO males from irradiated stage-7 oocytes of ebony females is probably a consequence of a defect in the repair of chromosome-breakage effects, resulting in the conversion of potential X losses in females into dominant lethals. The “maternal effects” for dominant lethals, sex-linked recessive lethals and for the loss of ring-X chromosomes are assumed to have a common causal basis, namely, a defective repair of chromosome-breakage events in the females of the ebony strain.     

Nucleocytoplasmic Relations in a Mutator-Suppressor System of DROSOPHILA ANANASSAE

A partially characterized mutator-suppressor system, previously identified in the ca; stw stock of Drosophila ananassae, was shown to exist in the ca ancestral stock; it consists of a clastogenic mutator of sperm chromosomes and a supressor that functions in the oöcyte soon after fertilization. Transmission of these components was monitored by Minute mutation frequencies produced by the progeny of recurrently backcrossed hybrid females derived from reciprocal outcrosses of the ca stock. In this way, the mutator was shown to be an extrachromosomally transmitted element whose propagation depends upon nuclear genes. Suppressivity was found to be determined by nuclear genes, some of which are expressed only after a delay of several generations. Neither the mutator nor its suppressor appear to be infectious. Measurement of dominant lethal frequencies showed that the suppressor is completely effective in repair of premutational lesions induced by the mutator. The properties of this mutator-suppressor system were compared with those of hybrid dysgenesis in Drosophila melanogaster.     

Farm-grade chlorpyrifos (Durmet) is genotoxic in somatic and germ-line cells of Drosophila.

The mutagenic potential of Durmet, a farm-grade formulation of chlorpyrifos, was studied in the Drosophila wing mosaic and sex-linked recessive lethal tests. Larvae of the 2nd or 3rd instar carrying suitable recessive genetic markers on chromosome 3 were exposed to different concentrations of the insecticide and the frequency of induction of mutant mosaic spots on the wings was noted. The Basc technique was followed to study the induction of sex-linked recessive lethals. On the basis of the frequency of induction of mosaic wing spots and sex-linked recessive lethals, it is concluded that Durmet is genotoxic in somatic cells as well as germ cells of Drosophila.     

Radiosensitivity of Drosophila lines. VII. The effect of the maternal genotype on the yield of recessive and dominant lethal mutations induced by the gamma irradiation of males

The effect of material repair on induction of paternal mutations was tested with radiosensitive rad(2)201G1 mutant. Basc males were irradiated at doses from 0 to 60 Gy of gamma-rays and mated to the radiosensitive mutant or control females. Frequencies of sex-linked recessive lethals and dominant lethals (induced in the paternal genome) were determined. With control females, the rate of recessive lethals increased linearly from 0 to 60 Gy. With rad(2)201G1 mutant, an increase in spontaneous and induced rates of paternal dominant lethals was observed; the rate of sex-linked recessive lethals increased non-linearly from 0 to 60 Gy.     

Studies on mutagen-sensitive strains of Drosophila melanogaster. II. Detection of qualitative differences between genetic damage induced by X-irradiation of mature spermatozoa in oxygenated and anoxic atmospheres through the use of the repair-deficient mutant mei-9a

Muller-5 males were irradiated with X-rays in nitrogen, in air or in oxygen (followed by nitrogen or oxygen post-treatments in the nitrogen and oxygen series) and were mated to females of a repair-proficient strain (mei+) or to those of a strain known to be deficient in excision repair of UV damage (in somatic cells). The latter strain, designated as mei-9a, is also known to be sensitive, in the larval stages, to the killing effects of UV, X-rays and to a number of chemical mutagens. The frequencies of sex-linked recessive lethals and autosomal translocations induced in the spermatozoa of males were determined and compared. The frequencies of sex-linked recessive lethals in the mei-9 control groups were consistently higher than in the mei+ groups. Irradiation in air or in nitrogen led to significantly higher yields of recessive lethals when the irradiated males were mated to mei-9 females, whereas, after irradiation in oxygen, the yields were similar with both kinds of female. No significant differences in the frequencies of reciprocal translocations were observed between the mei+ and mei-9 groups after irradiation of the males in nitrogen, in air or in oxygen. Likewise, no differential effects of the contrasting post-treatments (nitrogen versus oxygen), either for recessive lethals or for translocations, could be discerned. These results are considered to support the notion that the kinds of genetic damage induced in mature spermatozoa in air or in nitrogen are qualitatively similar (at least with respect to the component(s) that lead to the production of recessive lethal mutations), but clearly different when induced in an oxygen atmosphere. The enhanced yields of recessive lethals with mei-9 females (after irradiation of the males either in air or in nitrogen) has been interpreted on the assumption that the mei-9 mutant is also deficient for the repair of X-ray-induced, recessive lethal-generating premutational lesions. Possible reasons for the lack of differences between the mei+ and mei-9 groups with respect to translocation yields and for the absence of measurable differences in response between the contrasting post-treatments (after irradiation of the males in nitrogen) are discussed.     

Temperature-sensitive autosomal dominant lethal mutations in Drosophila melanogaster induced by ethylmethane sulfonate

Cold- and heat-sensitive dominant autosome and recessive sex-linked lethals were scored using C(1)RM, y; vg bw; e ss tester stock. The frequencies of heat-sensitive mutations were 1.43, 0.30, 0.07% and of cold-sensitive ones were 0.39, 0.16 and 0.09% in the 1-st, 2-nd and 3-rd chromosomes, respectively. For the first time, dominant cold-sensitive lethals were obtained in chromosome 3. The data from genetic analysis point to the fact that penetrance of such mutations strongly depends on the genetic background. That may be the reason, why they were not obtained using some of the balancer-3 chromosomes. Also, "cryptic" dominant autosome mutants were found which were not conditional but only revealed in the F2 generation. Their possible origin as gonado-somatic mosaics is discussed.     

Genetic control of mutability in laboratory mice. I. Genetic analysis of the sensitivity of mice of strains 101/H and C57BL/6 to the mutagenic effect of thio-TEPA]

The distribution of male mice of the BC1 generation was analysed with respect to the frequency of chromosome aberrations in bone marrow cells induced by thio-TEPA. The BC1 descendants were derived from the F1 of the cross (C3H X 101) X 101 and the F1 of the cross (CBA X B6) X B6. With respect to mutability the BC1 descendants of both types could be divided into two classes. The average frequencies of the cells with chromosome aberrations in the BC1 descendants of the 101 line were in the two classes 33.4 and 64.2 percent respectively. The corresponding values for the two classes of the BC1 descendants of the B6 line were 24 percent and 33.2 percent respectively. These data suggest that each of the lines studied has one recessive mutator gene. Preliminary symbols are proposed: mut-1 for the gene of the line 101/H and mut-2 for the gene of the line B6. The gene mut-2 is linked with the gene a (nonagouti) (Vth linkage group, chromosome 2).     

Effects of storing x-rayed spermatozoa on the frequency of translocations and sex-linked lethalsin Drosophila melanogaster

Summary x-rayed adult males ofDrosophila melanogaster were left with untreated females from 2 to 3 days after which the males were discarded. Sex-linked recessive lethals and translocations were scored in progeny produced during the first 2 or 3 days following irradiation, and after storage of the spermatozoa in the females for 6 days.The results obtained show that the frequencies of sex-linked lethals and of translocation involving the two large autosomes and the x-chromosome were unchanged by storage. In experiments in which Y, 2, 3 translocations were scored both the 2–3, and the Y translocations showed a slight increase. These experiments show that the strong storage effect on translocations produced by certain alkylating agents is peculiar to chromosomes treated by these chemicals.Guest investigator at the Institute of Animal Genetics, Edinburgh, on leave from Assuit University Egypt.