scholarly journals The abnormal oocyte phenotype is correlated with the presence of blood transposon in Drosophila melanogaster.

Genetics ◽  
1989 ◽  
Vol 123 (3) ◽  
pp. 485-494
Author(s):  
G Lavorgna ◽  
C Malva ◽  
A Manzi ◽  
S Gigliotti ◽  
F Graziani
Keyword(s):  
Drosophila Melanogaster ◽  
Sequence Analysis ◽  
Restriction Enzyme ◽  
Polymorphism Analysis ◽  
Restriction Map ◽  
Dna Rearrangement ◽  
Restriction Enzyme Site ◽  
Wild Type ◽  
Chromosome Walking ◽  
In The Wild

Abstract The abnormal oocyte mutation (2;44) originates in the wild: it confers no visible phenotype on homozygous abo males or females, but homozygous abo females produce defective eggs and the probability of their developing into adults is much lower than that of heterozygous sister females. We isolated by chromosome walking 200 kb of DNA from region 32. This paper reports that a restriction enzyme site polymorphism analysis in wild type and mutant stocks allowed us to identify a DNA rearrangement present only in stocks carrying the abo mutation. The rearrangement is caused by a DNA insert on the abo chromosome in region 32E which, by restriction map and sequence analysis, was identified as copia-like blood transposon. The transposon, in strains that had remained in abo homozygous conditions for several generations and had lost the abo maternal-effect, was no longer present in region 32E. Certain features of the abo mutation, discussed in the light of this finding, may be ascribed to the nature of the particular allele studied.

The development of the sensory neuron pattern in the antennal disc of wild-type and mutant (lz3, ssa) Drosophila melanogaster

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 1063-1075
Author(s):  
M.C. Lienhard ◽  
R.F. Stocker
Keyword(s):  
Drosophila Melanogaster ◽  
Sensory Neuron ◽  
Antennal Segment ◽  
Wild Type ◽  
Homeotic Mutant ◽  
In The Wild ◽  
The Brain ◽  
Antennal Disc ◽  
Antennal Nerve

The development of the sensory neuron pattern in the antennal disc of Drosophila melanogaster was studied with a neuron-specific monoclonal antibody (22C10). In the wild type, the earliest neurons become visible 3 h after pupariation, much later than in other imaginal discs. They lie in the center of the disc and correspond to the neurons of the adult aristal sensillum. Their axons join the larval antennal nerve and seem to establish the first connection towards the brain. Later on, three clusters of neurons appear in the periphery of the disc. Two of them most likely give rise to the Johnston's organ in the second antennal segment. Neurons of the olfactory third antennal segment are formed only after eversion of the antennal disc (clusters t1-t3). The adult pattern of antennal neurons is established at about 27% of metamorphosis. In the mutant lozenge3 (lz3), which lacks basiconic antennal sensilla, cluster t3 fails to develop. This indicates that, in the wild type, a homogeneous group of basiconic sensilla is formed by cluster t3. The possible role of the lozenge gene in sensillar determination is discussed. The homeotic mutant spineless-aristapedia (ssa) transforms the arista into a leg-like tarsus. Unlike leg discs, neurons are missing in the larval antennal disc of ssa. However, the first neurons differentiate earlier than in normal antennal discs. Despite these changes, the pattern of afferents in the ectopic tarsus appears leg specific, whereas in the non-transformed antennal segments a normal antennal pattern is formed. This suggests that neither larval leg neurons nor early aristal neurons are essential for the outgrowth of subsequent afferents.

scholarly journals THE α-GLYCEROPHOSPHATE CYCLE IN DROSOPHILA MELANOGASTER

1974 ◽  
Vol 63 (3) ◽  
pp. 864-882 ◽  
Author(s):  
Stephen J. O'Brien ◽  
Yoshio Shimada
Keyword(s):  
Drosophila Melanogaster ◽  
Oxidative Phosphorylation ◽  
Adult Life ◽  
Respiratory Control ◽  
Premature Mortality ◽  
Pyridine Nucleotide ◽  
Null Alleles ◽  
Wild Type ◽  
Relative Viability ◽  
In The Wild

"Null" mutations previously isolated at the αGpdh-1 locus of Drosophila melanogaster, because of disruption of the energy-producing α-glycerophosphate cycle, severely restrict the flight ability and relative viability of affected individuals. Two "null" alleles, αGpdh-1BO-1-4, and αGpdh-1BO-1-5, when made hemizygous with a deficiency of the αGpdh-1 locus, Df(2L)GdhA, were rendered homozygous by recombination with and selective elimination of the Df(2L)GdhA chromosome. After over 25 generations, a homozygous αGpdh-1BO-1-4 stock regained the ability to fly despite the continued absence of measurable αGPDH activity. Inter se heterozygotes of three noncomplementing αGpdh-1 "null" alleles and the "adapted" αGpdh-1BO-1-4 homozygotes were examined for metabolic enzymatic activities related to the energy-producing and pyridine nucleotide-regulating functions of the α-glycerophosphate cycle in Drosophila. The enzyme functions tested included glyceraldehyde-3-phosphate dehydrogenase, cytoplasmic and soluble malate dehydrogenase, lactate dehydrogenase, mitochondrial NADH oxidation, oxidative phosphorylation, and respiratory control with the substrates α-glycerophosphate, succinate, and pyruvate. These activities in any of the mutant genotypes in early adult life were indistinguishable from those in the wild type. There was, however, a premature deterioration and atrophy of the ultrastructural integrity of flight muscle sarcosomes observed by electron microscopy in the "null" mutants. These observations were correlated with a decrease in state 3 mitochondrial oxidation with α-glycerophosphate, succinate, and pyruvate, as well as with loss of respiratory control in adults as early as 2 wk after eclosion. Such observations, which normally are seen in aged dipterans, were accompanied by premature mortality of the mutant heterozygotes. The adapted αGpdh-1BO-1-4 was identical with wild type in each of the aging characters with the single exception of lowered rates of mitochondrial oxidative phosphorylation.

scholarly journals A Chlamydomonas outer arm dynein mutant missing the alpha heavy chain.

1991 ◽  
Vol 113 (3) ◽  
pp. 615-622 ◽  
Author(s):  
H Sakakibara ◽  
D R Mitchell ◽  
R Kamiya
Keyword(s):  
Cross Section ◽  
Heavy Chain ◽  
Fragment Length Polymorphism ◽  
Beat Frequency ◽  
Polymorphism Analysis ◽  
Wild Type ◽  
Heavy Chains ◽  
Flagellar Beat ◽  
Section Electron ◽  
In The Wild

A novel Chlamydomonas flagellar mutant (oda-11) missing the alpha heavy chain of outer arm dynein but retaining the beta and gamma heavy chains was isolated. Restriction fragment length polymorphism analysis with an alpha heavy chain locus genomic probe indicated that the oda-11 mutation was genetically linked with the structural gene of the alpha heavy chain. In cross-section electron micrographs, the oda-11 axoneme lacked the outermost appendage of the outer arm, indicating that the alpha heavy chain should be located in this region in the wild-type outer arm. This mutant swam at 119 microns/s at 25 degrees C, i.e., at an intermediate speed between those of wild type (194 microns/s) and of oda-1 (62 microns/s), a mutant missing the entire outer dynein arm. The flagellar beat frequency (approximately 50 Hz) was also between those of wild type (approximately 60 Hz) and oda-1 (approximately 26 Hz). These results indicate that the outer dynein arm of Chlamydomonas can be assembled without the alpha heavy chain, and that the outer arm missing the alpha heavy chain retains partial function.

scholarly journals The occurrence of long ribosomal transcripts homologous to type I insertions in bobbed mutants of Drosophila melanogaster

1989 ◽  
Vol 54 (2) ◽  
pp. 127-135 ◽  
Author(s):  
Mohamed Makni ◽  
Mohamed Marrakchi ◽  
Nicole Prud'Homme
Keyword(s):  
Drosophila Melanogaster ◽  
Ribosomal Genes ◽  
Type I ◽  
Wild Type ◽  
Coding Region ◽  
Rdna Genes ◽  
Sandwich Hybridization ◽  
Number Of Genes ◽  
In The Wild ◽  
Two Temperatures

SummaryIn Drosophila melanogaster up to two thirds of the rDNA genes contain insertion sequences of two types in the 28S coding region. Comparison of the ribosomal insertion transcripts in the wild type and in two bobbed mutants reared at two temperatures showed that the level of type I transcripts is dependent on both the number of genes with type I insertions in the bobbed loci and the intensity of bobbed phenotype. Importantly, a long transcript of 8·7 kb hybridized to the ribosomal probe, the INS I probe and also to the restriction fragment of the rDNA downstream of the point of insertion was found in one bobbed mutant. This result and also those from sandwich hybridization indicate that some interrupted ribosomal genes are functional.

scholarly journals Phage Reduce Stability for Regaining Infectivity during Antagonistic Coevolution with Host Bacterium

Viruses ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 118 ◽  
Author(s):  
Yihui Yuan ◽  
Qin Peng ◽  
Shaowen Zhang ◽  
Tingting Liu ◽  
Shuo Yang ◽  
...  
Keyword(s):  
First Generation ◽  
Transmembrane Domain ◽  
Polymorphism Analysis ◽  
Host Bacterium ◽  
Cell Wall Polysaccharide ◽  
Wild Type ◽  
Associated Proteins ◽  
In The Wild ◽  
Bacterial Mutants ◽  
Type Phage

The coevolution between phage and host bacterium is an important force that drives the evolution of the microbial community, yet the coevolution mechanisms have still not been well analyzed. Here, by analyzing the interaction between a Bacillus phage vB_BthS_BMBphi and its host bacterium, the coevolution mechanisms of the first-generation phage-resistant bacterial mutants and regained-infectivity phage mutants were studied. The phage-resistant bacterial mutants showed several conserved mutations as a potential reason for acquiring phage resistance, including the mutation in flagellum synthesis protein FlhA and cell wall polysaccharide synthesis protein DltC. All the phage-resistant bacterial mutants showed a deleted first transmembrane domain of the flagellum synthesis protein FlhA. Meanwhile, the regain-infectivity phage mutants all contained mutations in three baseplate-associated phage tail proteins by one nucleotide, respectively. A polymorphism analysis of the three mutant nucleotides in the wild-type phage revealed that the mutations existed before the interaction of the phage and the bacterium, while the wild-type phage could not infect the phage-resistant bacterial mutants, which might be because the synchronized mutations of the three nucleotides were essential for regaining infectivity. This study for the first time revealed that the synergism mutation of three phage baseplate-associated proteins were essential for the phages’ regained infectivity. Although the phage mutants regained infectivity, their storage stability was decreased and the infectivity against the phage-resistant bacterial mutants was reduced, suggesting the phage realized the continuation of the species by way of “dying to survive”.

Wuchsstoffaktivität der Augenpterine von Drosophila melanogaster bei Crithidia fasciculata

1961 ◽  
Vol 16 (4) ◽  
pp. 260-261 ◽  
Author(s):  
Irmgard Ziegler ◽  
Helene A. Nathan
Keyword(s):  
Drosophila Melanogaster ◽  
Growth Factors ◽  
Wild Type ◽  
Active Growth ◽  
Crithidia Fasciculata ◽  
Type D ◽  
Naturally Occurring ◽  
In The Wild ◽  
Growth Experiments

A tetrahydrobiopterin-derivative and a yellow pteridine, accumulated in the eyes of the sepia mutant of Drosophila melanogaster, are very active growth factors for Crithidia fasciculata. Of the three additional pteridines found in the wild-type D. melanogaster, a dark red pteridine, neodrosopterin, is very active whereas a brick-red pteridine, drosopterin, is moderately active and isodrosopterin, probably the isomer of drosopterin is inactive. The relationships of the results of the growth experiments to the naturally-occurring eye pteridines and to the basic biopterin structure are discussed.

The pattern of proliferation of the neuroblasts in the wild-type embryo of Drosophila melanogaster

1987 ◽  
Vol 196 (8) ◽  
pp. 473-485 ◽  
Author(s):  
Volker Hartenstein ◽  
Eberhard Rudloff ◽  
Jose A. Campos -Ortega
Keyword(s):  
Drosophila Melanogaster ◽  
Wild Type ◽  
Wild Type Embryo ◽  
In The Wild

scholarly journals FRACTIONATION OF THE EYE PIGMENTS OF DROSOPHILA MELANOGASTER

1946 ◽  
Vol 30 (1) ◽  
pp. 41-46 ◽  
Author(s):  
George Wald ◽  
Gordon Allen
Keyword(s):  
Drosophila Melanogaster ◽  
Wild Type ◽  
Chemical Behavior ◽  
General Chemical ◽  
In The Wild

Eye pigments of normal and mutant types of D. melanogaster have been extracted with water and fractionated by chromatographic adsorption on powdered talc. Spectra of all the fractions obtainable in solution have been measured and the general chemical behavior of the pigments is described. Two chemically distinct groups of pigments are found, to be identified with the earlier designated red and brown components. The red component in the wild-type eye contains three well defined pigments, two of them capable of further subdivision so that the total number of fractions obtained is five. There is also present a brown component pigment which could not be treated quantitatively by the methods employed. All members of the wild-type red component are found in cinnabar eyes, unaccompanied by the brown component. Conversely, brown eyes contain a pigment indistinguishable from the wild-type brown component, virtually alone. In sepia eyes, one red component and two brown component pigments can be distinguished, all three pigments differing from those of wild-type eyes. Pigments apparently identical with those found in wild-type melanogaster eyes have also been found in D. virilis.

Temporally restricted expression of transcription factor betaFTZ-F1: significance for embryogenesis, molting and metamorphosis in Drosophila melanogaster

Development ◽  
2000 ◽  
Vol 127 (23) ◽  
pp. 5083-5092 ◽  
Author(s):  
M. Yamada ◽  
T. Murata ◽  
S. Hirose ◽  
G. Lavorgna ◽  
E. Suzuki ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Larval Instar ◽  
Ectopic Expression ◽  
Wild Type ◽  
Specific Expression ◽  
Molting Process ◽  
In The Wild ◽  
Time Specific ◽  
Almost All ◽  
Exact Timing

FTZ-F1, a member of the nuclear receptor superfamily, has been implicated in the activation of the segmentation gene fushi tarazu during early embryogenesis of Drosophila melanogaster. We found that an isoform of FTZ-F1, betaFTZ-F1, is expressed in the nuclei of almost all tissues slightly before the first and second larval ecdysis and before pupation. Severely affected ftz-f1 mutants display an embryonic lethal phenotype, but can be rescued by ectopic expression of betaFTZ-F1 during the period of endogenous betaFTZ-F1 expression in the wild type. The resulting larvae are not able to molt, but this activity is rescued again by forced expression of betaFTZ-F1, allowing progression to the next larval instar stage. On the other hand, premature expression of betaFTZ-F1 in wild-type larvae at mid-first instar or mid-second instar stages causes defects in the molting process. Sensitive periods were found to be around the time of peak ecdysteroid levels and slightly before the start of endogenous betaFTZ-F1 expression. A hypomorphic ftz-f1 mutant that arrests in the prepupal stage can also be rescued by ectopic, time-specific expression of betaFTZ-F1. Failure of salivary gland histolysis, one of the phenotypes of the ftz-f1 mutant, is rescued by forced expression of the ftz-f1 downstream gene BR-C during the late prepupal period. These results suggest that betaFTZ-F1 regulates genes associated with ecdysis and metamorphosis, and that the exact timing of its action in the ecdysone-induced gene cascade is important for proper development.

Cloning and transcriptional control of a eucaryotic permease gene

1982 ◽  
Vol 2 (8) ◽  
pp. 977-984
Author(s):  
M R Chevallier
Keyword(s):  
Transcriptional Control ◽  
Dna Probes ◽  
Yeast Cells ◽  
Restriction Map ◽  
Wild Type ◽  
Yeast Saccharomyces Cerevisiae ◽  
In The Wild ◽  
Dna Fragment ◽  
Uptake Velocity ◽  
Cloned Gene

The uracil permease gene of the yeast Saccharomyces cerevisiae was cloned on a hybrid plasmid which replicates autonomously in both yeast and Escherichia coli. Cloning was carried out by complementation in yeast. The smallest DNA fragment found to complement the uracil permease deficiency in recipient yeast cells measured approximately 2.3 kilobases. In strains transformed by the plasmid with the uracil permease gene inserted, initial rates of uracil uptake increased up to 25 times more than the rates found in the wild type. Using DNA probes carrying several regions of the cloned gene, I showed that a strain carrying the dhul-I mutation, which is not linked to the permease structural gene and is responsible for enhanced uptake velocity of uracil, had enhanced transcription of the permease gene. By using DNA probes recloned in phage M13 mp7, the direction of transcription of the permease gene relative to the restriction map was deduced. A half-life of 2 min was found for the permease mRNA in labeling kinetics experiments.

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