Correlation between cellular level of gene transcriptional silencing and heterochromatin compartment dragging in case of PEV-producing eu-heterochromatin rearrangement in Drosophila melanogaster

2013 ◽  
Vol 47 (2) ◽  
pp. 252-258 ◽  
Author(s):  
S. A. Lavrov ◽  
A. S. Shatskikh ◽  
M. V. Kibanov ◽  
V. A. Gvozdev
Keyword(s):  
Drosophila Melanogaster ◽  
Transcriptional Silencing ◽  
Cellular Level

A single cell approach to problems of cell lineage and commitment during embryogenesis of Drosophila melanogaster

Development ◽  
1987 ◽  
Vol 100 (1) ◽  
pp. 1-12 ◽  
Author(s):  
G.M. Technau
Keyword(s):  
Drosophila Melanogaster ◽  
Single Cell ◽  
Cell Lineage ◽  
Cellular Level ◽  
Central Importance ◽  
Cell Level ◽  
Combined Application ◽  
A Cell ◽  
Pole Cells ◽  
Drosophila Embryos

The mechanisms leading to the commitment of a cell to a particular fate or to restrictions in its developmental potencies represent a problem of central importance in developmental biology. Both at the genetic and at the molecular level, studies addressing this topic using the fruitfly Drosophila melanogaster have advanced substantially, whereas, at the cellular level, experimental techniques have been most successfully applied to organisms composed of relatively large and accessible cells. The combined application of the different approaches to one system should improve our understanding of the process of commitment as a whole. Recently, a method has been devised to study cell lineage in Drosophila embryos at the single cell level. This method has been used to analyse the lineages, as well as the state of commitment of single cell progenitors from various ectodermal, mesodermal and endodermal anlagen and of the pole cells. The results obtained from a clonal analysis of wild-type larval structures are discussed in this review.

scholarly journals BEHAVIOR OF SOMATIC CELLS HOMOZYGOUS FOR ZYGOTIC LETHALS IN DROSOPHILA MELANOGASTER

Genetics ◽  
1977 ◽  
Vol 86 (2) ◽  
pp. 357-376
Author(s):  
Pedro Ripoll
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Viability ◽  
Epidermal Cell ◽  
Somatic Cells ◽  
Cellular Level ◽  
Drosophila Genome ◽  
Genetic Mosaics ◽  
X Ray ◽  
Cell Parameters ◽  
Derivatives Of

ABSTRACT The behavior in genetic mosaics of 86 EMS-induced sex-linked lethals has been studied. Seventy-five percent of them are autonomous in gynandromorphs. Forty-three lethals nonviable in sex mosaics have been analyzed in X-ray-induced spots in the abdominal tergites and the imaginal wing derivatives. Of the lethals, 90.7% are homozygous viable in mosaic spots, and only 9.3% have been classified as epidermal cell lethal. Thus, the fraction of the Drosophila genome essential for cell viability has been estimated to be about 420 genes. The phenotypes at the cellular level of some cell-viable mutations altering cell parameters (mitotic orientation, differentiation, etc.) are described.

scholarly journals MUTANT GENES REGULATING THE INDUCIBILITY OF KYNURENINE SYNTHESIS

1964 ◽  
Vol 21 (2) ◽  
pp. 203-211 ◽  
Author(s):  
T. M. Rizki
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Regulation ◽  
Suppressor Gene ◽  
Culture Conditions ◽  
Cellular Level ◽  
The Body ◽  
In The Wild ◽  
A Cell ◽  
Normal Feeding ◽  
S Allele

Alterations in the cellular synthesis of kynurenine in the larval fatbody of Drosophila melanogaster may be obtained by feeding the precursor tryptophan or by changing the genotype. In the wild type Ore-R strain, autofluorescent kynurenine globules normally occur in the cells in the anterior regions of the fatbody designated as regions 1, 2, and 3. When tryptophan is included in the larval diet, kynurenine will develop throughout the entire fatbody, thus extending to the cells in regions 4, 5, and 6. In the fatbodies of both the sepia mutant strain and the mutant combinations of the suppressible vermilion alleles with the suppressor gene (su2-s, v1 and su2-s, v2), kynurenine is found in the cells from region 1 through region 4. This involvement of additional cells in the synthesis of kynurenine occurs under the usual culture conditions for Drosophila. When sepia larvae are fed tryptophan, kynurenine appears in all of the cells of the fatbody. However, dietary tryptophan does not induce kynurenine production in cells in regions 5 and 6 in the mutant combination su2-s, v1 or su2-s, v2. In the latter strains, an increase in the quantity of kynurenine in the fatbody is detected, but this increase remains limited to the same cells in which kynurenine production is found under normal feeding conditions. When the v36f allele is combined with the su2-s allele, an extremely faint autofluorescence characteristic of kynurenine is found in some of the anteriormost fat cells of regions 1 and 2. This autofluorescence becomes intensified when tryptophan is fed to su2-s, v36f larvae. The genetic control of kynurenine synthesis in the cells of the fatbody of Drosophila melanogaster has been previously demonstrated. The present observations establish genetic regulation of the ability to induce kynurenine production within a cell through the administration of the inducer tryptophan. Kynurenine production has been considered as a unit function of the cell as a whole rather than of the enzyme alone, and it has been concluded that even though cells in different parts of the body perform this same function (kynurenine production), the gene loci regulating this function may be different for cells in different regions of the body. A phenomenon of overlapping domains of gene actions at the cellular level offers a genetic and cellular basis for developmental and physiological homeostasis.

scholarly journals Heterogeneity in the Response of Different Subtypes of Drosophila melanogaster Midgut Cells to Viral Infections

Viruses ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2284
Author(s):  
João M. F. Silva ◽  
Tatsuya Nagata ◽  
Fernando L. Melo ◽  
Santiago F. Elena
Keyword(s):  
Drosophila Melanogaster ◽  
Cellular Response ◽  
Viral Infections ◽  
Cellular Responses ◽  
Cellular Level ◽  
Viral Rna ◽  
Systemic Response ◽  
Cell Subtype ◽  
Replication Strategy ◽  
Rna Accumulation

Single-cell RNA sequencing (scRNA-seq) offers the possibility to monitor both host and pathogens transcriptomes at the cellular level. Here, public scRNA-seq datasets from Drosophila melanogaster midgut cells were used to compare the differences in replication strategy and cellular responses between two fly picorna-like viruses, Thika virus (TV) and D. melanogaster Nora virus (DMelNV). TV exhibited lower levels of viral RNA accumulation but infected a higher number of cells compared to DMelNV. In both cases, viral RNA accumulation varied according to cell subtype. The cellular heat shock response to TV and DMelNV infection was cell-subtype- and virus-specific. Disruption of bottleneck genes at later stages of infection in the systemic response, as well as of translation-related genes in the cellular response to DMelNV in two cell subtypes, may affect the virus replication.

scholarly journals Peculiarities of piRNA-mediated post-transcriptional silencing of Stellate repeats in testes of Drosophila melanogaster

2009 ◽  
Vol 37 (10) ◽  
pp. 3254-3263 ◽  
Author(s):  
Roman N. Kotelnikov ◽  
Mikhail S. Klenov ◽  
Yakov M. Rozovsky ◽  
Ludmila V. Olenina ◽  
Mikhail V. Kibanov ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Transcriptional Silencing

scholarly journals Drosophila melanogaster Responses against Entomopathogenic Nematodes: Focus on Hemolymph Clots

Insects ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 62 ◽  
Author(s):  
Alexis Dziedziech ◽  
Sai Shivankar ◽  
Ulrich Theopold
Keyword(s):  
Drosophila Melanogaster ◽  
Entomopathogenic Nematodes ◽  
Coagulation Factor ◽  
Coagulation Factors ◽  
Body Cavity ◽  
Cellular Level ◽  
Primary Phase ◽  
The Body ◽  
Infection Models ◽  
Two Phases

Several insect innate immune mechanisms are activated in response to infection by entomopathogenic nematodes (EPNs). In this review, we focus on the coagulation of hemolymph, which acts to stop bleeding after injury and prevent access of pathogens to the body cavity. After providing a general overview of invertebrate coagulation systems, we discuss recent findings in Drosophila melanogaster which demonstrate that clots protect against EPN infections. Detailed analysis at the cellular level provided insight into the kinetics of the secretion of Drosophila coagulation factors, including non-classical modes of secretion. Roughly, clot formation can be divided into a primary phase in which crosslinking of clot components depends on the activity of Drosophila transglutaminase and a secondary, phenoloxidase (PO)-dependent phase, characterized by further hardening and melanization of the clot matrix. These two phases appear to play distinct roles in two commonly used EPN infection models, namely Heterorhabditis bacteriophora and Steinernema carpocapsae. Finally, we discuss the implications of the coevolution between parasites such as EPNs and their hosts for the dynamics of coagulation factor evolution.

scholarly journals Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway

2017 ◽  
Author(s):  
Douglas J. Brusich ◽  
Ashlyn M. Spring ◽  
Thomas D. James ◽  
Catherine J. Yeates ◽  
Timothy H. Helms ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Model ◽  
Fruit Fly ◽  
Familial Hemiplegic Migraine ◽  
Cellular Level ◽  
Gain Of Function ◽  
Hemiplegic Migraine ◽  
Intracellular Ca

ABSTRACTGain-of-function mutations in the human CaV2.1 gene CACNA1A cause familial hemiplegic migraine type 1 (FHM1). To characterize cellular problems potentially triggered by CaV2.1 gains of function, we engineered mutations encoding FHM1 amino-acid substitutions S218L (SL) and R192Q (RQ) into transgenes of Drosophila melanogaster CaV2/cacophony. We expressed the transgenes pan-neuronally. Phenotypes were mild for RQ-expressing animals. By contrast, single mutant SL- and complex allele RQ,SL-expressing animals showed overt phenotypes, including sharply decreased viability. By electrophysiology, SL- and RQ,SL-expressing neuromuscular junctions (NMJs) exhibited enhanced evoked discharges, supernumerary discharges, and an increase in the amplitudes and frequencies of spontaneous events. Some spontaneous events were gigantic (10-40 mV), multi-quantal events. Gigantic spontaneous events were eliminated by application of TTX – or by lowered or chelated Ca2+ – suggesting that gigantic events were elicited by spontaneous nerve firing. A follow-up genetic approach revealed that some neuronal hyperexcitability phenotypes were reversed after knockdown or mutation of Drosophila homologs of phospholipase Cβ (PLCβ), IP3 receptor, or ryanodine receptor (RyR) – all factors known to mediate Ca2+ release from intracellular stores. Pharmacological inhibitors of intracellular Ca2+ store release produced similar effects. Interestingly, however, the decreased viability phenotype was not reversed by genetic impairment of intracellular Ca2+ release factors. On a cellular level, our data suggest inhibition of signaling that triggers intracellular Ca2+ release could counteract hyperexcitability induced by gains of CaV2.1 function.AUTHOR SUMMARYPrior research has demonstrated that gain-of-function mutations in a gene important for neurotransmission (CACNA1A) are known to cause migraine in humans. We attempted to mimic some of those gain-of-function mutations in a simple genetic model organism and to examine neurotransmission by electrophysiology. Our findings yield potential clues as to how particular migraine-causing mutations may impact neurophysiology on a cellular level. We used the fruit fly Drosophila melanogaster and its model synapse, the neuromuscular junction (NMJ) to perform our studies. We document three main advances: 1) characterization of fruit fly models harboring gain-of-function calcium channel alterations known to cause human familial hemiplegic migraine type 1 (FHM1); 2) characterization of hyperactive neurotransmission caused by one of these alterations; and 3) an ability to quell hyperactive neurotransmission by impairing intracellular Ca2+ store release, through both genetic and pharmacological means. Our work contributes to a broader understanding of how pathological mutations could impact cellular physiology. More generally, the utilization of genetic model organisms promises to uncover potential ways to reverse those impacts.

scholarly journals Post-transcriptional Silencing and Functional Characterization of the Drosophila melanogaster Homolog of Human Surf1

Genetics ◽  
2005 ◽  
Vol 172 (1) ◽  
pp. 229-241 ◽  
Author(s):  
Mauro A. Zordan ◽  
Paola Cisotto ◽  
Clara Benna ◽  
Alessandro Agostino ◽  
Giorgia Rizzo ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Functional Characterization ◽  
Transcriptional Silencing

scholarly journals Heterogeneity in the response of different subtypes of Drosophila melanogaster enteroendocrine cells to viral infections

2020 ◽  
Author(s):  
João M. F. Silva ◽  
Tatsuya Nagata ◽  
Fernando L. Melo ◽  
Santiago F. Elena
Keyword(s):  
Drosophila Melanogaster ◽  
Cellular Response ◽  
Viral Infections ◽  
Fruit Fly ◽  
Cellular Level ◽  
Enteroendocrine Cells ◽  
Systemic Response ◽  
Down Regulation ◽  
Replication Strategy ◽  
Systemic Level

SummarySingle cell RNA sequencing (scRNA-seq) offers the possibility to monitor both host and pathogens transcriptomes at the cellular level. Here, public scRNA-seq data from Drosophila melanogaster have been used to compare the differences in replication strategy and cellular response between two viruses, Thika virus (TV) and D. melanogaster Nora virus (DMelNV) in enteroendocrine cells (EEs). TV and DMelNV exhibited different patterns of replication and for TV, accumulation varied according to cell subtype. Cells infected with TV underwent down-regulation of genes that represent bottlenecks in the fruit fly interactome, while cells infected with DMelNV went through a down-expression of translation-related genes that represent both hubs and bottlenecks in the host interactome. In contrast, flies infected with DMelNV show only a systemic level down-regulation of bottleneck genes. Here, we use scRNA-seq to highlight the differences and commonalities between cellular response to TV and DMelNV and between cellular and systemic response to DMelNV.

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