TEMPERATURE-SENSITIVE MUTATIONS IN DROSOPHILA MELANOGASTER: XX. LETHALITY DUE TO TRANSLOCATIONS

1974 ◽  
Vol 16 (3) ◽  
pp. 579-592 ◽  
Author(s):  
Thomas C. Kaufman ◽  
David T. Suzuki

In a group of 10 γ-ray-induced temperature-sensitive (ts) lethal mutations on the X chromosome of Drosophila melanogaster, three were found to inhibit crossing over on this element. Subsequent studies showed that these three ts lethal mutations are associated with X [Formula: see text] autosome translocations. Developmental analysis has revealed that the patterns of temperature-sensitivity and lethality are similar to those found in other ts mutations. One of the mutations (T(X;2)X9ts) is unique, however, in that only males exhibit temperature-sensitive lethality while homozygous females are unaffected by a change in temperature. It is proposed that these three mutations may be exhibiting some new type of "position effect".

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.


Genes ◽  
2019 ◽  
Vol 10 (7) ◽  
pp. 498
Author(s):  
Voigt ◽  
Erpf ◽  
Stephan

Drosophila melanogaster recently spread from its tropical origin in Africa and became a cosmopolitan species that has adapted to a wide range of different thermal environments, including temperate climates. An important limiting factor of temperate climates has probably been their low and varying temperatures. The transcriptional output of genes can vary across temperatures, which might have been detrimental while settling in temperate environments. The reduction of temperature-sensitive expression of functionally important genes to ensure consistent levels of gene expression might have been relevant while adapting to such environments. In this study, we focus on the gene vestigial (vg) whose product is a key factor in wing development. We provide evidence that temperature-sensitivity of vg has been buffered in populations from temperate climates. We investigated temperature-sensitivity of vg gene expression in six natural populations, including four temperate populations (three from Europe and one from high-altitude Africa), and two tropical populations from the ancestral species range. All temperate populations exhibited a lower degree of temperature-induced expression plasticity than the tropical populations.


Genetics ◽  
1992 ◽  
Vol 130 (3) ◽  
pp. 569-583
Author(s):  
D F Eberl ◽  
L A Perkins ◽  
M Engelstein ◽  
A J Hilliker ◽  
N Perrimon

Abstract Polytene section 17 of the X chromosome of Drosophila melanogaster, previously known to contain six putative lethal complementation groups important in oogenesis and embryogenesis, has here been further characterized genetically and developmentally. We constructed fcl+Y, a duplication of this region, which allowed us to conduct mutagenesis screens specific for the region and to perform complementation analyses (previously not possible). We recovered 67 new lethal mutations which defined 15 complementation groups within Df(1)N19 which deletes most of polytene section 17. The zygotic lethal phenotypes of these and preexisting mutations within polytene section 17 were examined, and their maternal requirements were analysed in homozygous germline clones using the dominant female sterile technique. We present evidence that an additional gene, which produces two developmentally regulated transcripts, is located in this region and is involved in embryogenesis, although no mutations in this gene were identified. In this interval of 37 to 43 polytene chromosome bands we have defined 17 genes, 12 (71%) of which are of significance to oogenesis or embryogenesis.


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.


1974 ◽  
Vol 16 (4) ◽  
pp. 713-735 ◽  
Author(s):  
David T. Suzuki

In screening Drosophila melanogaster for mutations which cause paralysis at 29cC and recovery of mobility at 22cC, 11 temperature-sensitive (ts) mutants were detected among 1.35 × 106 flies screened. These mutations fell into 3 loci, paralytic (parats), shibire (shits) and stoned (stnts). All three loci affect neurological development. The best explanation for parats appears to be an effect on the inhibitory neuronal system. The shi alleles affect an array of developmental events from early embryos to adults. The pattern of heat-induced changes in shits1 electroretinograms (ERG) is consistent with a ts membranal defect. This is supported by a ts resistance of shits flies to tetrodotoxin which specifically blocks the sodium channel of nerves.The final locus, stn, causes sensitivity to the trauma of temperature changes. A jump response observed when a light is turned off is related to a large "offtransient" in ERGs which is correlated with a simultaneous muscle spike. The property of temperature-sensitivity allows greater analytic powers in the study of neurological mutants.


Genetics ◽  
1986 ◽  
Vol 113 (2) ◽  
pp. 367-389
Author(s):  
Theodore Homyk ◽  
Donald A R Sinclair ◽  
David T L Wong ◽  
Thomas A Grigliatti

ABSTRACT Temperature-sensitive (ts) autonomous cell-lethal mutations have been used extensively to study important developmental phenomena, such as pattern formation, in Drosophila. Their utility would be enhanced considerably if it were possible to establish which cell type is primarily affected by each lesion. To facilitate such an approach we have isolated and characterized 21 EMS- induced X-linked adult-lethal (adl) mutants, 16 of which are ts. Most of these lesions also elicit ts lethal effects during preimaginal development. They represent 19 different loci distributed randomly along the X chromosome. The general properties of these mutations are described. In addition, results of an in-depth analysis (focus mapping and, in some cases, temperature shift and heat-pulse studies) of four strains, adl-1ts  1, sesE, adl-2ts  1 and rex are reported. Two major temperature-sensitive periods (TSPs) of adl-1 lethality were resolved: one during the second half of embryogenesis and the other coinciding with pupariation. Mosaic analysis revealed separate mesodermal foci for leg paralysis. Developmental analysis of adl-1 embryos suggest that the adl-1 product may be required for maintenance of muscle tissue. Two discrete TSPs of sesE lethality exist: one during the second instar and the other extending from late third instar to early pupation. Mosaic analysis of sesE lethality resolved a pair of neural foci, each of which appears to incorporate three separate foci for leg paralysis. Mosaic analysis of adl-2ts  1 revealed the existence of paired lethal foci that appear to map to the vicinity of the subesophageal ganglion. Analysis of rex mosaics resolved separate mesodermal foci for leg paralysis.


Genetics ◽  
1975 ◽  
Vol 80 (3) ◽  
pp. 519-537
Author(s):  
Robert Arking

ABSTRACT One hundred and twenty-one temperature-sensitive (ts) sex-linked lethals were screened by means of X-ray-induced somatic crossing over to determine if any were ts cell-lethal mutants. Cell-lethal mutations were identified by their ability to block the development of homozygous clones when raised under restrictive conditions (29°). Twenty-two ts cell-lethal mutants were isolated and categorized into three classes, depending upon the patterns of damage observed in larval and imaginal tissues. The phenotypes produced by these mutations ranged from those which affected only a limited set of structures (i.e., genital discs only) to those which affected diverse tissues at all stages of the life cycle. Each mutation has its own characteristic time-dependent pattern, frequency, and type of damage. All the mutations affect imaginal tissue, but only one-third of the mutations affect both larval and imaginal tissue. The fastest-acting lethals need 15 hours at the restrictive temperature to kill the cells and the slowest-acting lethals require at least 48 hours. By choosing the appropriate mutant and by manipulating the times of exposure to the restrictive temperature, it has proven possible to produce duplications and deficiencies in specific structures of the adult. A mechanism by which lethality might yield such structures is suggested. In addition, 15 of the mutants are ts female sterile mutants. Only one of these 15 mutants can recover its fertility when shifted back down to the permissive temperature (22°).


Genetics ◽  
2003 ◽  
Vol 163 (3) ◽  
pp. 931-937 ◽  
Author(s):  
Stefan U Åström ◽  
Thomas W Cline ◽  
Jasper Rine

Abstract Five Drosophila melanogaster genes belong to the highly conserved sir2 family, which encodes NAD+-dependent protein deacetylases. Of these five, dsir2+ (CG5216) is most similar to the Saccharomyces cerevisiae SIR2 gene, which has profound effects on chromatin structure and life span. Four independent Drosophila strains were found with P-element insertions near the dsir2 transcriptional start site as well as extraneous linked recessive lethal mutations. Imprecise excision of one of these P elements (PlacW 07223) from a chromosome freed of extraneous lethal mutations produced dsir217, a null intragenic deletion allele that generates no DSIR2 protein. Contrary to expectations from the report by Rosenberg and Parkhurst on their P-mobilization allele dSir2ex10, homozygosity for dsir217 had no apparent deleterious effects on viability, developmental rate, or sex ratio, and it fully complemented sir2ex10. Moreover, through a genetic test, we ruled out the reported effect of dSir2ex10 on Sex-lethal expression. We did observe a modest, strictly recessive suppression of whitem4 position-effect variegation and a shortening of life span in dsir2 homozygous mutants, suggesting that dsir2 has some functions in common with yeast SIR2.


Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 195-207
Author(s):  
M A Pultz ◽  
G S Carson ◽  
B S Baker

Abstract Sex determination in Drosophila is controlled by a cascade of regulatory genes. Here we describe hermaphrodite (her), a new component of this regulatory cascade with pleiotropic zygotic and maternal functions. Zygotically, her+ function is required for female sexual differentiation: when zygotic her+ function is lacking, females are transformed to intersexes. Zygotic her+ function may also play a role in male sexual differentiation. Maternally, her+ function is needed to ensure the viability of female progeny: a partial loss of her+ function preferentially kills daughters. In addition, her has both zygotic and maternal functions required for viability in both sexes. Temperature sensitivity prevails for all known her alleles and for all of the her phenotypes described above, suggesting that her may participate in an intrinsically temperature-sensitive process. This analysis of four her alleles also indicates that the zygotic and maternal components of of her function are differentially mutable. We have localized her cytologically to 36A3-36A11.


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