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.

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.

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.

fushi tarazu protein expression in the cellular blastoderm of Drosophila detected using a novel imaging technique

Development ◽  
1989 ◽  
Vol 106 (1) ◽  
pp. 95-103 ◽  
Author(s):  
T.L. Karr ◽  
T.B. Kornberg
Keyword(s):  
Transcriptional Regulation ◽  
Protein Expression ◽  
Transcriptional Control ◽  
Imaging Technique ◽  
Drosophila Embryo ◽  
Immunoperoxidase Technique ◽  
Fushi Tarazu ◽  
Post Transcriptional Regulation ◽  
Blastoderm Stage ◽  
Anterior Posterior

The fushi tarazu (ftz) gene is essential for segmentation of the Drosophila embryo. This requirement is reflected at the cellular blastoderm stage of embryogenesis by seven transverse stripes of ftz expression. These stripes correspond to the missing segments of ftz mutant embryos. We describe here novel intermediate patterns of ftz protein expression which were detected in younger embryos by using anti-ftz antibodies and a sensitive fluorescence/immunoperoxidase technique (‘filtered fluorescence imaging’, FFI). Striped patterns of ftz protein evolved continuously, and the different stripes appeared in an ordered sequence, involving both anterior-posterior (A/P) and dorsal-ventral (D/V) progressions. Comparison of these patterns of ftz protein with those of ftz RNA suggests that these novel aspects of the patterning process involve post-transcriptional regulation in addition to the transcriptional control known to be involved in expression of this gene.

Drosophila hairy pair-rule gene regulates embryonic patterning outside its apparent stripe domains

Development ◽  
1993 ◽  
Vol 118 (1) ◽  
pp. 255-266 ◽  
Author(s):  
M. Lardelli ◽  
D. Ish-Horowicz
Keyword(s):  
Transcription Initiation ◽  
Transcriptional Regulators ◽  
Early Embryo ◽  
Embryonic Patterning ◽  
Gene Deletions ◽  
Head Development ◽  
Pair Rule Gene ◽  
Blastoderm Stage ◽  
Embryonic Viability ◽  
Pair Rule

The hairy (h) segmentation gene of Drosophila regulates segmental patterning of the early embryo, and is expressed in a set of anteroposterior stripes during the blastoderm stage. We have used a set of h gene deletions to study the h promoter and the developmental requirements for individual h stripes. The results confirm upstream regulation of h striping but indicate that expression in the anterodorsal head domain depends on sequences downstream of the two transcription initiation sites. Surprisingly, the two anterior-most h domains appear to be dispensable for head development and embryonic viability. One partial promoter deletion expresses ectopic h, leading to misexpression of other segmentation genes and embryonic pattern defects. We demonstrate that h affects patterning outside its apparent stripe domains, supporting a model in which primary pair-rule genes act as concentration-dependent transcriptional regulators, i.e. as local morphogens.

scholarly journals Comparison of the Structure and Expression of odd-skipped and Two Related Genes That Encode a New Family of Zinc Finger Proteins in Drosophila

Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 171-182 ◽  
Author(s):  
Marilyn C Hart ◽  
Lei Wang ◽  
Douglas E Coulter
Keyword(s):  
Amino Acid ◽  
Zinc Finger ◽  
Zinc Fingers ◽  
Functional Divergence ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Amino Acid Substitutions ◽  
New Family ◽  
Segment Polarity ◽  
Pair Rule

Abstract The odd-skipped (odd) gene, which was identified on the basis of a pair-rule segmentation phenotype in mutant embryos, is initially expressed in the Drosophila embryo in seven pair-rule stripes, but later exhibits a segment polarity-like pattern for which no phenotypic correlate is apparent. We have molecularly characterized two embryonically expressed odd-cognate genes, sob and bowel (bowl), that encode proteins with highly conserved C2H2 zinc fingers. While the Sob and Bowl proteins each contain five tandem fingers, the Odd protein lacks a fifth (C-terminal) finger and is also less conserved among the four common fingers. Reminiscent of many segmentation gene paralogues, the closely linked odd and sob genes are expressed during embryogenesis in similar striped patterns; in contrast, the less-tightly linked bowlgene is expressed in a distinctly different pattern at the termini of the early embryo. Although our results indicate that odd and sob are more likely than bowl to share overlapping developmental roles, some functional divergence between the Odd and Sob proteins is suggested by the absence of homology outside the zinc fingers, and also by amino acid substitutions in the Odd zinc fingers at positions that appear to be constrained in Sob and Bowl.

Two distinct mechanisms for differential positioning of gene expression borders involving the Drosophila gap protein giant

Development ◽  
1998 ◽  
Vol 125 (19) ◽  
pp. 3765-3774 ◽  
Author(s):  
X. Wu ◽  
R. Vakani ◽  
S. Small
Keyword(s):  
Target Genes ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Anterior Border ◽  
Gap Gene ◽  
Gap Genes ◽  
Pair Rule Gene ◽  
Differential Positioning ◽  
Pair Rule

We have combined genetic experiments and a targeted misexpression approach to examine the role of the gap gene giant (gt) in patterning anterior regions of the Drosophila embryo. Our results suggest that gt functions in the repression of three target genes, the gap genes Kruppel (Kr) and hunchback (hb), and the pair-rule gene even-skipped (eve). The anterior border of Kr, which lies 4–5 nucleus diameters posterior to nuclei that express gt mRNA, is set by a threshold repression mechanism involving very low levels of gt protein. In contrast, gt activity is required, but not sufficient for formation of the anterior border of eve stripe 2, which lies adjacent to nuclei that express gt mRNA. We propose that gt's role in forming this border is to potentiate repressive interaction(s) mediated by other factor(s) that are also localized to anterior regions of the early embryo. Finally, gt is required for repression of zygotic hb expression in more anterior regions of the embryo. The differential responses of these target genes to gt repression are critical for the correct positioning and maintenance of segmentation stripes, and normal anterior development.

Ftz-F1 is a cofactor in Ftz activation of the Drosophila engrailed gene

Development ◽  
1997 ◽  
Vol 124 (4) ◽  
pp. 839-847 ◽  
Author(s):  
B. Florence ◽  
A. Guichet ◽  
A. Ephrussi ◽  
A. Laughon
Keyword(s):  
Transcriptional Activation ◽  
Binding Sites ◽  
Direct Contact ◽  
Regulatory Element ◽  
Drosophila Embryo ◽  
Homeodomain Protein ◽  
Reporter Expression ◽  
Fushi Tarazu ◽  
Pair Rule Gene ◽  
Pair Rule

The fushi tarazu pair-rule gene is required for the formation of alternating parasegmental boundaries in the Drosophila embryo. fushi tarazu encodes a homeodomain protein necessary for transcription of the engrailed gene in even-numbered parasegments. Here we report that, within an engrailed enhancer, adjacent and conserved binding sites for the Fushi tarazu protein and a cofactor are each necessary, and together sufficient, for transcriptional activation. Footprinting shows that the cofactor site can be bound specifically by Ftz-F1, a member of the nuclear receptor superfamily. Ftz-F1 and the Fushi tarazu homeodomain bind the sites with 4- to 8-fold cooperativity, suggesting that direct contact between the two proteins may contribute to target recognition. Even parasegmental reporter expression is dependent on Fushi tarazu and maternal Ftz-F1, suggesting that these two proteins are indeed the factors that act upon the two sites in embryos. The two adjacent binding sites are also required for continued activity of the engrailed enhancer after Fushi tarazu protein is no longer detectable, including the period when engrailed, and the enhancer, become dependent upon wingless. We also report the existence of a separate negative regulatory element that apparently responds to odd-skipped.

Dax, a locust Hox gene related to fushi-tarazu but showing no pair-rule expression

Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1561-1572 ◽  
Author(s):  
R. Dawes ◽  
I. Dawson ◽  
F. Falciani ◽  
G. Tear ◽  
M. Akam
Keyword(s):  
Schistocerca Gregaria ◽  
Posterior Part ◽  
Homeobox Gene ◽  
Early Embryo ◽  
Neural Precursor Cells ◽  
Germ Band ◽  
Fushi Tarazu ◽  
Hox Gene ◽  
Two Phases ◽  
Pair Rule

We describe an unusual Antennapedia class homeobox gene from the grasshopper Schistocerca gregaria (Orthoptera, African Plague Locust). Its sequence is not sufficiently similar to that of any other insect Hom-Hox gene to identify it unambiguously, but short conserved elements suggest a relationship to the segmentation gene fushi-tarazu, (ftz). We term it Sg Dax (divergent Antennapedia class homeobox gene). Antibodies raised against the protein encoded by this gene reveal two phases of expression during embryogenesis. In the early embryo, it is a marker for the posterior part of the forming embryonic primordium, and subsequently for the posterior part of the growing germ band. In older embryos, it labels a subset of neural precursor cells in each trunk segment, very similar to that defined by the expression of fushi tarazu (ftz) in Drosophila. We suggest that Schistocerca Dax and Drosophila ftz are homologous members of a gene family whose members are diverging relatively rapidly, both in terms of sequence and role in early development.

Theoretical aspects of stripe formation in relation to Drosophila segmentation

Development ◽  
1988 ◽  
Vol 104 (1) ◽  
pp. 105-113
Author(s):  
T.C. Lacalli ◽  
D.A. Wilkinson ◽  
L.G. Harrison
Keyword(s):  
Hierarchical Control ◽  
Reaction Diffusion ◽  
Positional Information ◽  
Kinetic Mechanism ◽  
Periodic Pattern ◽  
Linear Pattern ◽  
Pattern Forming ◽  
Gradient Models ◽  
Blastoderm Stage ◽  
Pair Rule

Many aspects of Drosophila segmentation can be discussed in one-dimensional terms as a linear pattern of repeated elements or cell states. But the initial metameric pattern seen in the expression of pair-rule genes is fully two-dimensional, i.e. a pattern of stripes. Several lines of evidence suggest a kinetic mechanism acting globally during the syncytial blastoderm stage may be responsible for generating this pattern. The requirement that the mechanism should produce stripes, not spots or some other periodic pattern, imposes preconditions on this act, namely (1) sharp anterior and posterior boundaries that delimit the pattern-forming region, and (2) an axial asymmetrizing influence in the form of an anteroposterior gradient. Models for Drosophila segmentation generally rely on the gradient to provide positional information in the form of concentration thresholds that cue downstream elements of a hierarchical control system. This imposes restrictions on how such models cope with experimental disturbances to the gradient. A shallower gradient, for example, means fewer pattern elements. This need not be the case if the gradient acts through a kinetic mechanism like reaction-diffusion that involves the whole system. It is then the overall direction of the gradient that is important rather than specific concentration values.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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