Analysis of gene expression during development in the homeotic mutant Contrabithorax of Drosophila melanogaster

Development ◽  
1975 ◽  
Vol 34 (1) ◽  
pp. 19-31
Author(s):  
Gines Morata
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Normal Level ◽  
X Rays ◽  
Wild Type ◽  
Homeotic Transformation ◽  
Homeotic Mutant ◽  
A Cell ◽  
Final Expression

Contrabithorax, a mutant of the bithorax system in Drosophila melanogaster produces a partial homeotic transformation of mesothorax (wing) into metathorax (haltere). The wing of a fly homozygous or heterozygous for the mutant is a mosaic of wing and haltere structures. A genetic analysis of the mutant suggests that its phenotype is due to some form of derepression in the wing of two other genes of the bithorax system (bithorax and postbithorax) which are not normally active there. This repression is not complete. The activity of the two genes is below the normal level resulting in only a partial transformation of wing into haltere. Clones of marked cells were generated by X-rays and were found to include both transformed (haltere) and untransformed (wing) territory; this was true even for those generated late in development. Thus the final expression of a cell depends not on its immediate ancestry but perhaps on the level of the products of the wild-type alleles of bithorax and postbithorax.

scholarly journals Rel Induces Interferon Regulatory Factor 4 (IRF-4) Expression in Lymphocytes

2000 ◽  
Vol 191 (8) ◽  
pp. 1281-1292 ◽  
Author(s):  
Raelene J. Grumont ◽  
Steve Gerondakis
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Nuclear Factor Κb ◽  
Wild Type ◽  
Cell Type ◽  
Regulatory Factor ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Interferon Regulatory Factor 4

In lymphocytes, the Rel transcription factor is essential in establishing a pattern of gene expression that promotes cell proliferation, survival, and differentiation. Here we show that mitogen-induced expression of interferon (IFN) regulatory factor 4 (IRF-4), a lymphoid-specific member of the IFN family of transcription factors, is Rel dependent. Consistent with IRF-4 functioning as a repressor of IFN-induced gene expression, the absence of IRF-4 expression in c-rel−/− B cells coincided with a greater sensitivity of these cells to the antiproliferative activity of IFNs. In turn, enforced expression of an IRF-4 transgene restored IFN modulated c-rel−/− B cell proliferation to that of wild-type cells. This cross-regulation between two different signaling pathways represents a novel mechanism that Rel/nuclear factor κB can repress the transcription of IFN-regulated genes in a cell type–specific manner.

scholarly journals Functional monopolar spindles caused by mutation in mgr, a cell division gene of Drosophila melanogaster

1988 ◽  
Vol 89 (1) ◽  
pp. 39-47 ◽  
Author(s):  
C. Gonzalez ◽  
J. Casal ◽  
P. Ripoll
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Division ◽  
Genetic Analysis ◽  
Normal Chromosome ◽  
Phenotypic Traits ◽  
Polyploid Cells ◽  
A Cell

Mutation in the gene merry-go-round (mgr) of Drosophila causes a variety of phenotypic traits in somatic and germinal tissues, such as polyploid cells, metaphasic arrest, postmeiotic cysts with 16 nuclei, and spermatids with four times the normal chromosome content. The most characteristic phenotype is the appearance of mitotic and meiotic figures where all chromosomes are arranged in a circle. Treatment with anti-mitotic drugs and the phenotype of double mutants mgr asp (asp being a mutation altering the spindle) show that these circular figures need a functional spindle for their formation. These abnormal figures are caused by monopolar spindles similar to those observed after different treatments in several organisms. All mutant traits indicate that mgr performs a function necessary for the correct behaviour of centrosomes, thus opening this organelle to genetic analysis.

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 DEVELOPMENT IN GENETIC MOSAICS OF ARISTAPEDIA, A HOMOEOTIC MUTANT OF DROSOPHILA MELANOGASTER

Genetics ◽  
1974 ◽  
Vol 76 (4) ◽  
pp. 767-774
Author(s):  
J H Postlethwait ◽  
J R Girton
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Line ◽  
Crossing Over ◽  
Wild Type ◽  
Genetic Mosaics ◽  
X Ray ◽  
A Cell

ABSTRACT Development of the homoeotic mutation, aristapedia (ss  a), was investigated by means of genetic mosaics. The wild-type alleles of aristapedia and the bristle markers yellow, singed, and forked were removed from cells at different times in development by X-ray induced somatic crossing-over. The phenotype of the resulting clones was examined in order to ascertain whether it was leg or antenna. The y sn f; ssa clones showed a leg phenotype if induced before the mid-third instar, but showed an antennal phenotype if induced after this time. Late non-expression of ss  a may be due either to an influence of surrounding ss  + tissues on the small ss  a clones, or to a persistence of the effect of ss  + for one or two cell generations after it is removed from a cell line.

scholarly journals Persistent one-way walking in a circular arena in Drosophila melanogaster Canton-S strain

2017 ◽  
Author(s):  
Chengfeng Xiao ◽  
Shuang Qiu ◽  
R Meldrum Robertson
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Y Chromosome ◽  
Genetic Background ◽  
Chromosome 2 ◽  
Wild Type ◽  
Promoting Effect ◽  
Directional Change ◽  
Pleiotropic Function

AbstractWe describe persistent one-way walking of Drosophila melanogaster in a circular arena. Wild-type Canton-S adult flies walked in one direction, counter-clockwise or clockwise, for minutes, whereas white-eyed mutant w1118 changed directions frequently. Locomotion in the circular arena could be classified into four components: counter-clockwise walking, clockwise walking, nondirectional walking and pausing. Genetic analysis revealed that while wild-type genetic background was associated with reduced directional change and reduced numbers of one-way (including counterclockwise and clockwise) and nondirectional walks, the white (w+) locus promoted persistent oneway walking by increasing the maximal duration of one-way episodes. The promoting effect of w+ was further supported by the observations that (1) w+ duplicated to the Y chromosome, (2) four genomic copies of mini-white inserted on the autosomes, and (3) pan-neuronal overexpression of the White protein increased the maximal duration of one-way episodes, and that RNAi knockdown of w+ in the neurons decreased the maximal duration of one-way episodes. These results suggested a pleiotropic function of w+ in promoting persistent one-way walking in the circular arena.

scholarly journals In Vivo and In Vitro Analysis of Baculovirusie-2 Mutants

1999 ◽  
Vol 73 (3) ◽  
pp. 2460-2468 ◽  
Author(s):  
Elena A. Prikhod’ko ◽  
Albert Lu ◽  
Joyce A. Wilson ◽  
Lois K. Miller
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Late Gene ◽  
Wild Type ◽  
Late Gene Expression ◽  
Specific Effects ◽  
Viral Promoters ◽  
Occlusion Bodies ◽  
A Cell ◽  
Budded Virus

ABSTRACT Upon transient expression in cell culture, the ie-2gene of Autographa californica nuclear polyhedrosis virus (AcMNPV) displays three functions: transactivation of viral promoters, direct or indirect stimulation of virus origin-specific DNA replication, and arrest of the cell cycle. The ability of IE2 to trans stimulate DNA replication and coupled late gene expression is observed in a cell line derived fromSpodoptera frugiperda but not in a cell line derived fromTrichoplusia ni. This finding suggested that IE-2 may exert cell line-specific or host-specific effects. To examine the role of ie-2 in the context of infection and its possible influence on the host range, we constructed recombinants of AcMNPV containing deletions of different functional regions within ie-2 and characterized them in cell lines and larvae of S. frugiperda and T. ni. Theie-2 mutant viruses exhibited delays in viral DNA synthesis, late gene expression, budded virus production, and occlusion body formation in SF-21 cells but not in TN-5B1-4 cells. In TN-5B1-4 cells, the ie-2 mutants produced more budded virus and fewer occlusion bodies but the infection proceeded without delay. Examination of the effects of ie-2 and the respective mutants on immediate-early viral promoters in transient expression assays revealed striking differences in the relative levels of expression and differences in responses to ie-2 and its mutant forms in different cell lines. In T. ni and S. frugiperda larvae, the infectivities of the occluded form ofie-2 mutant viruses by the normal oral route of infection was 100- and 1,000-fold lower, respectively, than that of wild-type AcMNPV. The reduction in oral infectivity was traced to the absence of virions within the occlusion bodies. The infectivity of the budded form of ie-2 mutants by hemocoelic injection was similar to that of wild-type virus in both species. Thus,ie-2 mutants are viable but exhibit cell line-specific effects on temporal regulation of the infection process. Due to its effect on virion occlusion, mutants of IE-2 were essentially noninfectious by the normal route of infection in both species tested. However, since budded viruses exhibited normal infectivity upon hemocoelic injection, we conclude that ie-2 does not affect host range per se. The possibility that IE-2 exerts tissue-specific effects has not been ruled out.

Chromatin structure of a P-element-transduced hsp-28 gene in Drosophila melanogaster

1986 ◽  
Vol 6 (11) ◽  
pp. 4126-4129
Author(s):  
J C Eissenberg ◽  
S C Elgin
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Chromatin Structure ◽  
Dnase I ◽  
P Element ◽  
Direct Selection ◽  
Wild Type ◽  
Dnase I Hypersensitive Sites ◽  
Hypersensitive Sites ◽  
Selection For

The Drosophila hsp-28 gene was heat inducible when transduced to novel chromosomal sites even when no direct selection for transduced gene expression was imposed. The pattern of DNase I-hypersensitive sites 5' to the wild type and transduced copy of hsp-28 was similar. In addition, DNase I-hypersensitive sites occurred within the P-element sequences flanking transduced loci.

scholarly journals Insertion of the retroposable element, jockey, near the Adh gene of Drosophila melanogaster is associated with altered gene expression

1996 ◽  
Vol 68 (3) ◽  
pp. 203-209 ◽  
Author(s):  
Lisa D. White ◽  
James W. Jacobson
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Alcohol Dehydrogenase ◽  
Insertion Mutation ◽  
Activity Levels ◽  
Mrna Levels ◽  
Wild Type ◽  
Reporter System ◽  
Wild Type Counterpart ◽  
Altered Gene

SummaryThe alcohol dehydrogenase (Adh) gene of Drosophila melanogaster is well suited to be a gene expression reporter system. Adh produces a measurable phenotype at both the enzyme and mRNA levels. We recovered a spontaneous transposable element (TE) insertion mutation near the Adh gene. The insertion is a truncated retroposable element, jockey, inserted upstream of the adult Adh enhancer region. Comparisons between the Adhjockey allele and its direct wild-type ancestral allele were made in an isogenic background (i.e. identical cis and trans factors). Differences in Adhjockey expression compared with the wild-type can be attributed solely to the presence of the jockey element. This jockey insertion results in a decrease in adult mRNA transcript levels in the Adhjockey homozygous lines relative to the wild-type counterpart and accounts for a correlated decrease in alcohol dehydrogenase (ADH) enzyme activity. The larval ADH activity levels are not detectably different.

Genetic Analysis of theHybrid male rescueLocus of Drosophila

Genetics ◽  
2000 ◽  
Vol 155 (1) ◽  
pp. 225-231 ◽  
Author(s):  
H Allen Orr ◽  
Shannon Irving
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Wild Type Allele ◽  
Wild Type ◽  
Hybrid Male ◽  
Gain Of Function ◽  
Hybrid Inviability ◽  
Type Allele ◽  
Proximate Causes

AbstractSeveral hybrid rescue mutations—alleles that restore the viability of normally lethal hybrids—have been discovered in Drosophila melanogaster and its relatives. Here we analyze one of these genes, Hybrid male rescue (Hmr), asking two questions about its role in hybrid inviability. (1) Does the wild-type allele from D. melanogaster (Hmrmel) cause hybrid embryonic inviability? (2) Does Hmrmel cause hybrid larval inviability? Our results show that the wild-type product of Hmr is neither necessary nor sufficient for hybrid embryonic inviability. Hmrmel does, however, appear to lower the viability of hybrid larvae. The data further suggest (though do not prove) that Hmrmel acts as a gain-of-function poison in hybrids. These findings support previous claims that hybrid embryonic and larval lethalities are genetically distinct and suggest that Hmrmel is at least one of the proximate causes of hybrid larval inviability.

scholarly journals DOG-1 Is the Caenorhabditis elegans BRIP1/FANCJ Homologue and Functions in Interstrand Cross-Link Repair

2007 ◽  
Vol 28 (5) ◽  
pp. 1470-1479 ◽  
Author(s):  
Jillian L. Youds ◽  
Louise J. Barber ◽  
Jordan D. Ward ◽  
Spencer J. Collis ◽  
Nigel J. O'Neil ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Analysis ◽  
Replication Fork ◽  
Cancer Susceptibility ◽  
X Rays ◽  
Wild Type ◽  
Cross Link ◽  
Focus Formation ◽  
C Elegans ◽  
Functional Conservation

ABSTRACT Fanconi anemia (FA) is a cancer susceptibility syndrome characterized by defective DNA interstrand cross-link (ICL) repair. Here, we show that DOG-1 is the Caenorhabditis elegans homologue of FANCJ, a helicase mutated in FA-J patients. DOG-1 performs a conserved role in ICL repair, as dog-1 mutants are hypersensitive to ICL-inducing agents, but not to UVC irradiation or X rays. Genetic analysis indicated that dog-1 is epistatic with fcd-2 (C. elegans FANCD2) but is nonepistatic with brc-1 (C. elegans BRCA1), thus establishing the existence of two distinct pathways of ICL repair in worms. Furthermore, DOG-1 is dispensable for FCD-2 and RAD-51 focus formation, suggesting that DOG-1 operates downstream of FCD-2 and RAD-51 in ICL repair. DOG-1 was previously implicated in poly(G)/poly(C) (G/C) tract maintenance during DNA replication. G/C tracts remain stable in the absence of ATL-1, CLK-2 (FA pathway activators), FCD-2, BRC-2, and MLH-1 (associated FA components), implying that DOG-1 is the sole FA component required for G/C tract maintenance in a wild-type background. However, FCD-2 is required to promote deletion-free repair at G/C tracts in dog-1 mutants, consistent with a role for FA factors at the replication fork. The functional conservation between DOG-1 and FANCJ suggests a possible role for FANCJ in G/C tract maintenance in human cells.

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