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.

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.

scholarly journals A Screen for Genes That Interact With the Drosophila Pair-Rule Segmentation Gene fushi tarazu

Genetics ◽  
2004 ◽  
Vol 168 (1) ◽  
pp. 161-180 ◽  
Author(s):  
Mark W. Kankel ◽  
Dianne M. Duncan ◽  
Ian Duncan
Keyword(s):  
Fushi Tarazu ◽  
Segmentation Gene ◽  
Pair Rule

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.

The evolving role of the orphan nuclear receptorftz-f1, a pair-rule segmentation gene

2013 ◽  
Vol 15 (6) ◽  
pp. 406-417 ◽  
Author(s):  
Alison Heffer ◽  
Nathaniel Grubbs ◽  
James Mahaffey ◽  
Leslie Pick
Keyword(s):  
Segmentation Gene ◽  
Pair Rule

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.

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.

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.

The pattern of cell death in fushi tarazu, a segmentation gene of Drosophila

Development ◽  
1988 ◽  
Vol 104 (3) ◽  
pp. 447-451 ◽  
Author(s):  
L. Magrassi ◽  
P.A. Lawrence
Keyword(s):  
Cell Death ◽  
Wild Type ◽  
Germ Band ◽  
Fushi Tarazu ◽  
Larval Cuticle ◽  
Dividing Cells ◽  
In The Wild ◽  
Indirect Consequence ◽  
Dying Cells ◽  
Pair Rule

The pair-rule mutant, fushi tarazu, causes deletion of alternate metameres. Here we show that there is cell death in the mutant which begins at the completion of germ band extension. We map the dying cells in the epidermis; they occur scattered all over those regions that, in the wild type, would form the even-numbered parasegments and are also found in posterior parts of the odd-numbered parasegments. In the affected zones, dying and dividing cells are intermingled; we suggest that cells from these zones may still give descendents that contribute to the larval cuticle. Cell death is not limited to those cells that would normally express ftz+, suggesting that it is some indirect consequence of the abnormal situation in the mutant embryo.

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