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

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 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.

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 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.

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.

Mesenchymal cells engulf and clear apoptotic footplate cells in macrophageless PU.1 null mouse embryos

Development ◽  
2000 ◽  
Vol 127 (24) ◽  
pp. 5245-5252 ◽  
Author(s):  
W. Wood ◽  
M. Turmaine ◽  
R. Weber ◽  
V. Camp ◽  
R.A. Maki ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Body Shape ◽  
Mouse Embryos ◽  
Null Mouse ◽  
Wild Type ◽  
Wild Type Embryo ◽  
Cell Numbers ◽  
Embryonic Tissues ◽  
In The Wild ◽  
Clearance Process

Apoptosis is one of the key tools used by an embryo to regulate cell numbers and sculpt body shape. Although massive numbers of cells die during development, they are so rapidly phagocytosed that very few corpses are ever seen in most embryonic tissues. In this paper, we focus on the catastrophic cell death that occurs as the developing footplate is remodelled to transform webbed regions into free interdigital spaces. In the wild-type embryo, these dead cells are rapidly engulfed and cleared by macrophages. We show that in a macrophageless mouse embryo, null for the haemopoetic-lineage-specific transcription factor, PU.1, the task of phagocytosis is taken over by ‘stand-in’ mesenchymal neighbours in a clear example of cell redundancy. However, it takes three times as many of these mesenchymal phagocytes to complete the task and, at each stage of the clearance process - in the recognition of apoptotic debris, its engulfment and finally its digestion - they appear to be less efficient than macrophages. A molecular explanation for this may be that several of the engulfment genes expressed by macrophages, including the ABC1 transporter (believed to be part of the phagocytic machinery conserved from Caenorhabditis elegans to mouse), are not upregulated by these ‘stand-in’ phagocytes.

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.

Untersuchungen über die Speicherung und Ausscheidung von freiem Tryptophan durch die Malpighischen Gefäße von Drosophila melanogaster

1962 ◽  
Vol 17 (9) ◽  
pp. 620-622 ◽  
Author(s):  
Armin Wessing ◽  
Angelika Bonse
Keyword(s):  
Drosophila Melanogaster ◽  
Larval Stage ◽  
Malpighian Tubules ◽  
Wild Type ◽  
In The Wild

The Malpighian tubules of Drosophila melanogaster accumulate a considerable quantity of Tryptophan as well as Kynurenin and Oxykynurenin especially after pupation, because the histolytical processes begin at this time. In the wild-type this Tryptophan is utilized for the formation of Kynurenin, Oxykynurenin and Ommochromes, while in the mutant r, which is uncapable of forming these compounds, it is stored in the Malpighian tubules and the (Tryptophan) contents reaches 20 times the norm. This accumulated Tryptophan is excreted during the larval stage, after hatching and in the following days, while the meconia and excrements of the wild flies contain no Tryptophan.

Freeze-substituted fungal cells of Nectria haematococca: A comparison of the macroconidial walls of the adhesion-competent wild type with an adhesion-reduced mutant

1990 ◽  
Vol 48 (3) ◽  
pp. 688-689
Author(s):  
Thecan Caesar-Ton That ◽  
Lynn Epstein
Keyword(s):  
Freeze Substitution ◽  
Uranyl Acetate ◽  
Wild Type ◽  
Nectria Haematococca ◽  
Fruit Extract ◽  
Dialysis Tubing ◽  
Tube Emergence ◽  
Contrast Microscopy ◽  
In The Wild ◽  
Freeze Damage

Nectria haematococca mating population I (anamorph, Fusarium solani) macroconidia attach to its host (squash) and non-host surfaces prior to germ tube emergence. The macroconidia become adhesive after a brief period of protein synthesis. Recently, Hickman et al. (1989) isolated N. haematococca adhesion-reduced mutants. Using freeze substitution, we compared the development of the macroconidial wall in the wild type in comparison to one of the mutants, LEI.Macroconidia were harvested at 1C, washed by centrifugation, resuspended in a dilute zucchini fruit extract and incubated from 0 - 5 h. During the incubation period, wild type macroconidia attached to uncoated dialysis tubing. Mutant macroconidia did not attach and were collected on poly-L-lysine coated dialysis tubing just prior to freezing. Conidia on the tubing were frozen in liquid propane at 191 - 193C, substituted in acetone with 2% OsO4 and 0.05% uranyl acetate, washed with acetone, and flat-embedded in Epon-Araldite. Using phase contrast microscopy at 1000X, cells without freeze damage were selected, remounted, sectioned and post-stained sequentially with 1% Ba(MnO4)2 2% uranyl acetate and Reynold’s lead citrate. At least 30 cells/treatment were examined.

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