Genetic Capacity for Adaptation to Cold Resistance at Different Developmental Stages of Drosophila melanogaster

Evolution ◽  
1979 ◽  
Vol 33 (1) ◽  
pp. 350 ◽  
Author(s):  
Nikola Tucic
Keyword(s):  
Drosophila Melanogaster ◽  
Cold Resistance ◽  
Developmental Stages ◽  
Adaptation To Cold

Genetic characterization of ms (3) K81, a paternal effect gene of Drosophila melanogaster.

Genetics ◽  
1995 ◽  
Vol 140 (1) ◽  
pp. 219-229 ◽  
Author(s):  
G K Yasuda ◽  
G Schubiger ◽  
B T Wakimoto
Keyword(s):  
Drosophila Melanogaster ◽  
Developmental Stages ◽  
Normal Function ◽  
Loss Of Function ◽  
Male Sterile ◽  
Specific Product ◽  
Paternal Effect ◽  
Developmental Arrest ◽  
Effect Gene

Abstract The vast majority of known male sterile mutants of Drosophila melanogaster fail to produce mature sperm or mate properly. The ms(3) K81(1) mutation is one of a rare class of male sterile mutations in which sterility is caused by developmental arrest after sperm entry into the egg. Previous studies showed that males homozygous for the K81(1) mutation produce progeny that arrest at either of two developmental stages. Most embryos arrest during early nuclear cycles, whereas the remainder are haploid embryos that arrest at a later stage. This description of the mutant phenotype was based on the analysis of a single allele isolated from a natural population. It was therefore unclear whether this unique paternal effect phenotype reflected the normal function of the gene. The genetic analysis and initial molecular characterization of five new K81 mutations are described here. Hemizygous conditions and heteroallelic combinations of the alleles were associated with male sterility caused by defects in embryogenesis. No other mutant phenotypes were observed. Thus, the K81 gene acted as a strict paternal effect gene. Moreover, the biphasic pattern of developmental arrest was common to all the alleles. These findings strongly suggested that the unusual embryonic phenotype caused by all five new alleles was due to loss of function of the K81+ gene. The K81 gene is therefore the first clear example of a strict paternal effect gene in Drosophila. Based on the embryonic lethal phenotypes, we suggest that the K81+ gene encodes a sperm-specific product that is essential for the male pronucleus to participate in the first few embryonic nuclear divisions.

Morphological and molecular modifications induced by heat shock in Drosophila melanogaster embryos

Development ◽  
1983 ◽  
Vol 77 (1) ◽  
pp. 167-182
Author(s):  
Giorgio Graziosi ◽  
Franco de Cristini ◽  
Angelo di Marcotullio ◽  
Roberto Marzari ◽  
Fulvio Micali ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Heat Shock ◽  
Dna Synthesis ◽  
Histological Analysis ◽  
Developmental Stages ◽  
Early Embryo ◽  
Direct Relation ◽  
Hsp 70 ◽  
Survival Pattern ◽  
Shock Proteins

The early embryo of Drosophila melanogaster did not survive treatment at 37 °C (heat shock) for 25 min. The histological analysis of eggs treated in this way showed that the heat shock caused disintegration of nuclei and of cytoplasmic islands, displacement and swelling of nuclei and blocked mitoses. These effects were not observed in embryos treatedafter blastoderm formation. After this stage, we noticed that development was slowed down. The heat shock proteins (hsp 83,70 and 68) were, under shock, synthesized at all developmental stages. There was little or no synthesis of hsp 70 and 68 in unfertilized eggs, but synthesis increased in proportion to the number of nuclei present. Most probably, hsp 70 synthesis was directed by zygotic mRNA. DNA synthesis was not blocked by the heat shock though the overall incorporation of [3H]thymidine was substantially reduced, presumably because of the block of mitoses. We did not find a direct relation between survival pattern and hsp synthesis. We concluded that some, at least, of the heat shock genes can be activated at all developmental stages and that heat shock could be used for synchronizing mitoses.

Calreticulin Mediates Anesthetic Sensitivity in Drosophila melanogaster 

2003 ◽  
Vol 99 (4) ◽  
pp. 867-875 ◽  
Author(s):  
Sumiko Gamo ◽  
Junya Tomida ◽  
Katsuyuki Dodo ◽  
Dai Keyakidani ◽  
Hitoshi Matakatsu ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Double Mutant ◽  
Developmental Stages ◽  
Northern Blotting ◽  
General Anesthetics ◽  
Wild Type ◽  
Mutant Strains ◽  
Low Expression

Background Various species, e.g., Caenorhabditis elegans, Drosophila melanogaster, and mice, have been used to explore the mechanisms of action of general anesthetics in vivo. The authors isolated a Drosophila mutant, ethas311, that was hypersensitive to diethylether and characterized the calreticulin (crc) gene as a candidate of altered anesthetic sensitivity. Methods Molecular analysis of crc included cloning and sequencing of the cDNA, Northern blotting, and in situ hybridization to accomplish the function of the gene and its mutation. For anesthetic phenotype assay, the 50% anesthetizing concentrations were determined for ethas311, revertants, and double-mutant strains (wild-type crc transgene plus ethas311). Results Expression of the crc 1.4-kb transcript was lower in the mutant ethas311 than in the wild type at all developmental stages. The highest expression at 19 h after pupation was observed in the brain of the wild type but was still low in the mutant at that stage. The mutant showed resistance to isoflurane as well as hypersensitivity to diethylether, whereas it showed the wild phenotype to halothane. Both mutant phenotypes were restored to the wild type in the revertants and double-mutant strains. Conclusion ethas311 is a mutation of low expression of the Drosophila calreticulin gene. The authors demonstrated that hypersensitivity to diethylether and resistance to isoflurane are associated with low expression of the gene. In Drosophila, calreticulin seems to mediate these anesthetic sensitivities, and it is a possible target for diethylether and isoflurane, although the predicted anesthetic targets based on many studies in vitro and in vivo are the membrane proteins, such as ion channels and receptors.

scholarly journals Expression and localization of Drosophila melanogaster hsp70 cognate proteins.

1986 ◽  
Vol 6 (4) ◽  
pp. 1187-1203 ◽  
Author(s):  
K B Palter ◽  
M Watanabe ◽  
L Stinson ◽  
A P Mahowald ◽  
E A Craig
Keyword(s):  
Drosophila Melanogaster ◽  
Monoclonal Antibodies ◽  
Heat Shock ◽  
Developmental Stages ◽  
Antigenic Determinants ◽  
Heat Shock Cognate Protein ◽  
Maximal Induction ◽  
Shock Proteins ◽  
Related Proteins

Monoclonal antibodies have been used to identify three proteins in Drosophila melanogaster that share antigenic determinants with the major heat shock proteins hsp70 and hsp68. While two of the proteins are major proteins at all developmental stages, one heat shock cognate protein, hsc70, is especially enriched in embryos. hsc70 is shown to be the product of a previously identified gene, Hsc4. We have examined the levels of hsp70-related proteins in adult flies and larvae during heat shock and recovery. At maximal induction in vivo, hsp70 and hsp68 never reach the basal levels of the major heat shock cognate proteins. Monoclonal antibodies to hsc70 have been used to localize it to a meshwork of cytoplasmic fibers that are heavily concentrated around the nucleus.

scholarly journals The RNA polymerase II 15-kilodalton subunit is essential for viability in Drosophila melanogaster.

1992 ◽  
Vol 12 (3) ◽  
pp. 928-935 ◽  
Author(s):  
D A Harrison ◽  
M A Mortin ◽  
V G Corces
Keyword(s):  
Drosophila Melanogaster ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Gene Product ◽  
Metal Binding ◽  
Developmental Stages ◽  
Larval Instar ◽  
A Subunit ◽  
Transplantation Experiments ◽  
Early Larval Development

A small, divergently transcribed gene is located 500 bp upstream of the suppressor of Hairy-wing locus of Drosophila melanogaster. Sequencing of a full-length cDNA clone of the predominant 850-nucleotide transcript reveals that this gene encodes a 15,100-Da protein with high homology to a subunit of RNA polymerase II. The RpII15 protein is 46% identical to the RPB9 protein of Saccharomyces cerevisiae, one of the smallest subunits of RNA polymerase II from that species. Among those identical residues are four pairs of cysteines whose spacing is suggestive of two metal-binding "finger" domains. The gene is expressed at all developmental stages and in all tissues. Two deletions within the RpII15 gene are multiphasic lethal deletions, with accumulation of dead animals commencing at the second larval instar. Ovary transplantation experiments indicate that survival of mutant animals to this stage is due to the persistence of maternal gene product throughout embryogenesis and early larval development. The RpII15 gene product is thus necessary for viability of D. melanogaster.

scholarly journals COLD TEMPERATURE RESISTANCE, CHROMOSOMAL POLYMORPHISM AND INTERPOPULATION HETEROSIS IN DROSOPHILA PSEUDOOBSCURA

Genetics ◽  
1974 ◽  
Vol 76 (4) ◽  
pp. 807-822
Author(s):  
Margaret C Jefferson ◽  
David W Crumpacker ◽  
James S Williams
Keyword(s):  
Cold Resistance ◽  
Developmental Stages ◽  
Chromosomal Polymorphism ◽  
Drosophila Pseudoobscura ◽  
Temperature Resistance ◽  
Low Humidity ◽  
Reverse Situation ◽  
Chromosomal Polymorphisms ◽  
Better Than ◽  
Third Instar Larvae

ABSTRACT Descendants of two Colorado, U.S.A., populations of D. pseudoobscura, Boulder and La Foret, were exposed to +2° and -2°. In third instar larvae from Boulder AR and PP third chromosome gene arrangements survived better than TL and others, while the reverse situation occurred for La Foret. Deleterious dominant effects were observed for AR from La Foret. In adults from Boulder there was a trend towards greater survival for AR and PP than for other gene arrangements, while AR from La Foret showed relatively poor cold resistance. Survival of Boulder and La Foret flies, and their interpopulation hybrid, was determined after exposure to -2° at two humidities. Order of survival of developmental stages was: adults >> third instar larvae > mixture of first and second instar larvae. Adults survived better at low humidity, while larvae survived better at high humidity. Boulder adults and larvae survived better than those from La Foret. Advantage in survival of hybrids over the midparent ranged from 23% to 138%. Hybrid advantage over the higher parent ranged from 5% to 111%. Order of expression of heterosis was: mixture of first and second instar larvae > third instar larvae > adults. Relation of all results to the chromosomal polymorphisms at Boulder (seasonally constant) and La Foret (seasonally cyclic) is discussed.

scholarly journals DNA REPAIR DEPENDENCE OF SOMATIC MUTAGENESIS OF TRANSPOSON-CAUSED WHITE ALLELES IN DROSOPHILA MELANOGASTER AFTER TREATMENT WITH ALKYLATING AGENTS

Genetics ◽  
1986 ◽  
Vol 112 (3) ◽  
pp. 505-522
Author(s):  
Kazuo Fujikawa ◽  
Sohei Kondo
Keyword(s):  
Dna Repair ◽  
Drosophila Melanogaster ◽  
Dna Sequences ◽  
Common Property ◽  
Developmental Stages ◽  
Excision Repair ◽  
Alkylating Agents ◽  
Dose Range ◽  
Lemon Yellow ◽  
Adult Males

ABSTRACT DNA repair-defective alleles of the mei-9, mei-41, mus-104 and mus-101 loci of Drosophila melanogaster were introduced into stocks bearing the UZ and SZ marker sets. Males with the UZ marker set, z  1 (zeste allele) and w  +(TE) (genetically unstable white allele presumably caused by a transposable element), or the SZ marker set, z  1 and w  +R (semistable white allele caused by partial duplication of the w  + locus plus transposon insert), were exposed to EMS at the first instar. After emergence, adult males bearing red spots on lemon-yellow eyes were scored as flies with somatic reversions of w  +(TE) or w  +R. The relative mutabilities (relative values of reversion frequency at an equal EMS dose) of either w  +(TE) or w  +R in a repair-proficient strain and in mei-9, mei-41, mus-104 and mus-101 strains were 1:?1.2:0.3:0.3:0.7, despite the fact that w  +(TE) reverted two to three times as frequently as w  +R under both the repair-proficient and repair-deficient genetic conditions. Similarly, after treatment with MMS, MNNG and ENNG, w  +(TE) was somatically more mutable in the mei-9 strain and less mutable in the mei-41 and mus-104 strains than in the repair-proficient strain. From these results, we propose that mutagenic lesions produced in DNA by treatment with these chemicals are converted to mutant DNA sequences via the error-prone repair mechanisms dependent on the products of the genes mei-41  + (mei-41 and mus-104 being alleles of the same locus) and mus-101  +, whereas they are eliminated by mei-9  +-dependent excision repair. In contrast to the approximately linear responses of induced reversions of w  +(TE) with ENNG in the repair-proficient, mei-9, and mei-41 strains, seemingly there were dosage insensitive ranges for induced reversion with MNNG in the repair-proficient and mei-41 strains, but not for reversion in the mei-9 strain; w  +(TE) in the mus-104 strain was virtually nonmutable with MNNG and ENNG. These results suggest that O  6-methylguanine (O  6MeG) produced in DNA with MNNG, but not O  6-ethylguanine produced with ENNG, is almost completely repaired in a low dose range by constitutive activity of DNA O  6MeG transmethylase. From the distribution of clone sizes of spontaneous revertant spots and other data, we propose that both w  +(TE) and w  +R have a similar tendency to spontaneously revert more frequently at early rather than at late developmental stages, probably reflecting a common property of their inserted transposons.

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