Repression of Drosophila pair-rule segmentation genes by ectopic expression of tramtrack

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 45-58 ◽  
Author(s):  
J.L. Brown ◽  
C. Wu
Keyword(s):  
Heat Shock ◽  
Ectopic Expression ◽  
Complex Pattern ◽  
Fushi Tarazu ◽  
Segmentation Genes ◽  
Blastoderm Stage ◽  
Pair Rule ◽  
Drosophila Embryos

The tramtrack (ttk) protein has been proposed as a maternally provided repressor of the fushi tarazu (ftz) gene in Drosophila embryos at the preblastoderm stage. Consistent with this hypothesis, we have detected by immunohistochemistry the presence of ttk protein in preblastoderm embryos. This is followed by a complete decay upon formation of the cellular blastoderm when ftz striped expression is at its peak. In addition, the highly complex pattern of zygotic ttk expression suggests specific functions for ttk late in development that are separate from the regulation of ftz. We have produced ttk protein ectopically in blastoderm-stage embryos transformed with a heat shock-ttk construct. Ectopic ttk caused complete or near-complete repression of the endogenous ftz gene, as well as significant repression of the pair-rule genes even skipped, odd skipped, hairy and runt. These findings suggest that specific repression by ttk (or by undiscovered repressors) may be more than an isolated phenomenon during the rapid cleavage divisions, a period when the need for genetic repression has not been generally anticipated.

Control of segmental asymmetry in Drosophila embryos

Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 785-796 ◽  
Author(s):  
A.S. Manoukian ◽  
H.M. Krause
Keyword(s):  
Double Negative ◽  
Common Theme ◽  
Negative Regulators ◽  
Fushi Tarazu ◽  
Segment Polarity Genes ◽  
Segment Polarity ◽  
Body Patterning ◽  
Blastoderm Stage ◽  
Pair Rule ◽  
Drosophila Embryos

During Drosophila development, an important aspect of body patterning is the division of the embryo into repeating morphological units referred to as parasegments. The parasegmental domains are first defined at the blastoderm stage by alternating stripes of transcripts encoded by the pair-rule genes fushi tarazu (ftz) and even-skipped (eve) and later by stripes encoded by the segment polarity genes engrailed (en) and wingless. Here, we show that the runt gene (run) is required to generate asymmetries within these parasegmental domains. Using a heat-shock-inducible run transgene, we found that ectopic run expression leads to rapid repression of eve stripes and a somewhat delayed expansion of ftz stripes. Unexpectedly, we also found that ectopic run was a rapid and potent repressor of odd-numbered en stripes. Two remarkably different segmental phenotypes were generated as a consequence of these effects. In solving the mechanisms underlying these phenotypes, we discovered that the positioning of en stripes is largely determined by the actions of negative regulators. Our data indicate that run is required to limit the domains of en expression in the odd-numbered parasegments, while the odd-skipped gene is required to limit the domains of en expression in the even-numbered parasegments. Activation of en at the anterior margins of both sets of parasegments requires the repression of run and odd by the product of the eve gene. The spatial restriction of gene expression via negative and double negative pathways such as these is likely to be a common theme during development.

Pattern formation in the Drosophila embryo: allocation of cells to parasegments by even-skipped and fushi tarazu

Development ◽  
1989 ◽  
Vol 105 (4) ◽  
pp. 761-767 ◽  
Author(s):  
P.A. Lawrence ◽  
P. Johnston
Keyword(s):  
Pattern Formation ◽  
Drosophila Embryo ◽  
Germ Band ◽  
Fushi Tarazu ◽  
Cellular Resolution ◽  
Blastoderm Stage ◽  
Pair Rule ◽  
Drosophila Embryos

The first sign of metamerization in the Drosophila embryo is the striped expression of pair-rule genes such as fushi tarazu (ftz) and even-skipped (eve). Here we describe, at cellular resolution, the development of ftz and eve protein stripes in staged Drosophila embryos. They appear gradually, during the syncytial blastoderm stage and soon become asymmetric, the anterior margins of the stripes being sharply demarcated while the posterior borders are undefined. By the beginning of germ band elongation, the eve and ftz stripes have narrowed and become very intense at their anterior margins. The development of these stripes in hairy-, runt-, eve-, ftz- and engrailed- embryos is illustrated. In eve- embryos, the ftz stripes remain symmetric and lack sharp borders. Our results support the hypothesis (Lawrence et al. Nature 328, 440–442, 1987) that individual cells are allocated to parasegments with respect to the anterior margins of the eve and ftz stripes.

Analysis of function of the pair-rule genes hairy, even-skipped and fushi tarazu in mosaic Drosophila embryos

Development ◽  
1989 ◽  
Vol 107 (4) ◽  
pp. 847-853 ◽  
Author(s):  
P.A. Lawrence ◽  
P. Johnston
Keyword(s):  
Genetic Interactions ◽  
Nuclear Transplantation ◽  
Fushi Tarazu ◽  
Segmentation Gene ◽  
Hairy Cells ◽  
Analysis Of Function ◽  
Mutant Cells ◽  
Pair Rule ◽  
Drosophila Embryos

We report the first attempt of its kind to study genetic interactions using young Drosophila embryos that are mosaic for wildtype and mutant cells. Using nuclear transplantation we make mosaic embryos in which a patch of cells lacks a particular segmentation gene, A. With antibodies, we than look at the expression of another gene that is known to be downstream of gene A, with respect to the cells in the patch. We have examples of patches of hairy cells (where we monitor the effect on fushi tarazu (ftz) expression), even-skipped (monitoring ftz) and ftz (monitoring engrailed and Ultrabithorax). Our main finding is that the dependence of engrailed expression on the ftz gene is strictly cell-autonomous. This result goes some way towards explaining the dependence of Ultrabithorax expression on ftz, a dependence we show to be locally cell-autonomous within parts of parasegments 6 and 8 but non autonomous within parasegment 7.

Expression of engrailed during segmentation in grasshopper and crayfish

Development ◽  
1989 ◽  
Vol 107 (2) ◽  
pp. 201-212 ◽  
Author(s):  
N.H. Patel ◽  
T.B. Kornberg ◽  
C.S. Goodman
Keyword(s):  
Monoclonal Antibody ◽  
Cell Proliferation ◽  
Cell Division ◽  
Embryonic Stage ◽  
Germ Band ◽  
Segmentation Genes ◽  
Pair Rule ◽  
Drosophila Embryos ◽  
The Way

We have used a monoclonal antibody that recognizes engrailed proteins to compare the process of segmentation in grasshopper, crayfish, and Drosophila. Drosophila embryos rapidly generate metameres during an embryonic stage characterized by the absence of cell division. In contrast, many other arthropod embryos, such as those of more primitive insects and crustaceans, generate metameres gradually and sequentially, as cell proliferation causes caudal elongation. In all three organisms, the pattern of engrailed expression at the segmented germ band stage is similar, and the parasegments are the first metameres to form. Nevertheless, the way in which the engrailed pattern is generated differs and reflects the differences in how these organisms generate their metameres. These differences call into question what role homologues of the Drosophila pair-rule segmentation genes might play in other arthropods that generate metameres sequentially.

Interactions between the pair-rule genes runt, hairy, even-skipped and fushi tarazu and the establishment of periodic pattern in the Drosophila embryo

Development ◽  
1988 ◽  
Vol 104 (Supplement) ◽  
pp. 51-60 ◽  
Author(s):  
Philip Ingham ◽  
Peter Gergen
Keyword(s):  
Double Mutant ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Periodic Pattern ◽  
Fushi Tarazu ◽  
Blastoderm Stage ◽  
Pair Rule

The pair-rule genes of Drosophila play a fundamental role in the generation of periodicity in the early embryo. We have analysed the transcript distributions of runt, hairy, even-skipped and fushi tarazu in single and double mutant ernbryos. The results indicate a complex set of interactions between the genes during the blastoderm stage of embryogenesis.

Effects of ectopic expression of caudal during Drosophila development

Development ◽  
1990 ◽  
Vol 109 (2) ◽  
pp. 271-277 ◽  
Author(s):  
M. Mlodzik ◽  
G. Gibson ◽  
W.J. Gehring
Keyword(s):  
Heat Shock ◽  
Imaginal Disc ◽  
Ectopic Expression ◽  
Homeobox Gene ◽  
Homeotic Genes ◽  
Posterior Half ◽  
Fushi Tarazu ◽  
Drosophila Development ◽  
Head Development ◽  
Cad Protein

The effects of heat-shock-induced ectopic expression of the homeobox gene caudal (cad) at all stages of Drosophila development have been examined. Presence of cad protein (CAD) at the anterior end of cellular blastoderm embryos was found to disrupt head development and segmentation, due to alteration of the expression of segmentation genes such as fushi tarazu and engrailed, as well as repression of head-determining genes such as Deformed. These results support the conclusion that, while CAD is probably required to activate transcription of fushi tarazu in the posterior half of the embryo, it should not be expressed in the anterior half prior to gastrulation, and thus suggest a role for the CAD gradient. Ectopic expression of CAD at later stages of development has no obvious effects on embryogenesis or imaginal disc development, suggesting that the homeotic genes of the Antennapedia and Bithorax Complexes are almost completely epistatic to caudal.

Ultrabithorax and engrailed expression in Drosophila embryos mutant for segmentation genes of the pair-rule class

Development ◽  
1988 ◽  
Vol 102 (2) ◽  
pp. 325-338 ◽  
Author(s):  
A. Martinez-Arias ◽  
R.A.H. White
Keyword(s):  
Cell Death ◽  
Molecular Probes ◽  
The Body ◽  
Drosophila Embryo ◽  
Segmentation Genes ◽  
Gene Functions ◽  
Pair Rule Gene ◽  
Molecular Phenotypes ◽  
Pair Rule ◽  
Drosophila Embryos

Mutations in the pair-rule class of segmentation genes cause pattern deletions with a double segment periodicity in the Drosophila embryo. This phenotype is, in part, due to cell death. Using molecular probes for engrailed (en) and Ultrabithorax (Ubx) expression as markers for the body plan, we have studied the phenotype of pair-rule mutants prior to cell death. All these mutants alter the expression of en and Ubx; their molecular phenotypes suggest a pathway whereby pair-rule gene functions construct metameric units.

The effect of the heat shock response on ultrastructure of the centrosome of Drosophila cultured cells in interphase: possible relation with changes in the chemical state of calcium.

1993 ◽  
Vol 71 (11-12) ◽  
pp. 507-517 ◽  
Author(s):  
Christiane Marcaillou ◽  
Alain Debec ◽  
Sylvie Lauverjat ◽  
Armelle Saihi
Keyword(s):  
Heat Shock ◽  
Heat Shock Response ◽  
Cultured Cells ◽  
Chemical State ◽  
Ultrastructural Organization ◽  
Heat Shock Stress ◽  
Shock Response ◽  
Pericentriolar Material ◽  
Functional Inactivation ◽  
Drosophila Embryos

Previous observations have shown that the heat shock response affects the centrosome function. We compared the ultrastructural organization of the centrosome in control (23 °C) and heat-shocked (37 °C, 50 min) interphase Drosophila cells to detect the nature of the lesions that could alter this organelle. The centrosome apparatus showed only minor modifications after the stress and the architecture of the centrioles appeared unaffected. The main difference concerned the organization of pericentriolar material which appeared more condensed and clotted. In extreme cases this material seemed to collapse on the centrioles. Recent reports proposed that Ca2+ concentrations could modify the distribution of pericentriolar material. In this study, we measured the changes in total and bound calcium in control or heat-shocked cell samples. The hyperthermia stress induced an increase of about 80% in global calcium. However, there was a decrease of about 50% in bound calcium. A heat shock stress seemed therefore to promote a change from the bound to the free state for a noticeable proportion of the element. As a preliminary hypothesis, these changes in the chemical state of calcium could be related to alterations in the pericentriolar material and thus with the functional inactivation of the centrosome. This view is also supported by calcium analysis on early Drosophila embryos. Contrary to cultured cells, Drosophila embryos did not present a stress inactivation of centrosomes. Equally, a heat shock did not disturb the bound calcium level in embryos.Key words: Centrosome, ultrastructure, calcium, heat shock, Drosophila.

Positioning adjacent pair-rule stripes in the posterior Drosophila embryo

Development ◽  
1994 ◽  
Vol 120 (10) ◽  
pp. 2945-2955 ◽  
Author(s):  
J.A. Langeland ◽  
S.F. Attai ◽  
K. Vorwerk ◽  
S.B. Carroll
Keyword(s):  
Binding Sites ◽  
Drosophila Embryo ◽  
Regulatory Sequences ◽  
Posterior Border ◽  
Adjacent Pair ◽  
Gap Gene ◽  
Competitive Mechanism ◽  
Pair Rule ◽  
Drosophila Embryos ◽  
Do So

We present a genetic and molecular analysis of two hairy (h) pair-rule stripes in order to determine how gradients of gap proteins position adjacent stripes of gene expression in the posterior of Drosophila embryos. We have delimited regulatory sequences critical for the expression of h stripes 5 and 6 to 302 bp and 526 bp fragments, respectively, and assayed the expression of stripe-specific reporter constructs in several gap mutant backgrounds. We demonstrate that posterior stripe boundaries are established by gap protein repressors unique to each stripe: h stripe 5 is repressed by the giant (gt) protein on its posterior border and h stripe 6 is repressed by the hunchback (hb) protein on its posterior border. Interestingly, Kruppel (Kr) limits the anterior expression limits of both stripes and is the only gap gene to do so, indicating that stripes 5 and 6 may be coordinately positioned by the Kr repressor. In contrast to these very similar cases of spatial repression, stripes 5 and 6 appear to be activated by different mechanisms. Stripe 6 is critically dependent upon knirps (kni) for activation, while stripe 5 likely requires a combination of activating proteins (gap and non-gap). To begin a mechanistic understanding of stripe formation, we locate binding sites for the Kr protein in both stripe enhancers. The stripe 6 enhancer contains higher affinity Kr-binding sites than the stripe 5 enhancer, which may allow for the two stripes to be repressed at different Kr protein concentration thresholds. We also demonstrate that the kni activator binds to the stripe 6 enhancer and present evidence for a competitive mechanism of Kr repression of stripe 6.

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