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.

scholarly journals Odd-paired controls frequency doubling in Drosophila segmentation by altering the pair-rule gene regulatory network

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Erik Clark ◽  
Michael Akam
Keyword(s):  
Gene Expression ◽  
Gene Regulatory Network ◽  
Regulatory Network ◽  
Frequency Doubling ◽  
Drosophila Embryo ◽  
Anteroposterior Patterning ◽  
Regulatory Interactions ◽  
Pair Rule Gene ◽  
Gene Regulatory ◽  
Pair Rule

The Drosophila embryo transiently exhibits a double-segment periodicity, defined by the expression of seven 'pair-rule' genes, each in a pattern of seven stripes. At gastrulation, interactions between the pair-rule genes lead to frequency doubling and the patterning of 14 parasegment boundaries. In contrast to earlier stages of Drosophila anteroposterior patterning, this transition is not well understood. By carefully analysing the spatiotemporal dynamics of pair-rule gene expression, we demonstrate that frequency-doubling is precipitated by multiple coordinated changes to the network of regulatory interactions between the pair-rule genes. We identify the broadly expressed but temporally patterned transcription factor, Odd-paired (Opa/Zic), as the cause of these changes, and show that the patterning of the even-numbered parasegment boundaries relies on Opa-dependent regulatory interactions. Our findings indicate that the pair-rule gene regulatory network has a temporally modulated topology, permitting the pair-rule genes to play stage-specific patterning roles.

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.

The molecular basis for metameric pattern in the Drosophila embryo

Development ◽  
1987 ◽  
Vol 101 (1) ◽  
pp. 1-22 ◽  
Author(s):  
M. Akam
Keyword(s):  
Molecular Basis ◽  
Subsequent Development ◽  
The Body ◽  
Drosophila Embryo ◽  
Homeotic Genes ◽  
Simple Pattern ◽  
Segment Polarity ◽  
Maternal Determinants ◽  
Segment Pattern ◽  
Pair Rule

The metameric organization of the Drosophila embryo is generated in the first 5 h after fertilization. An initially rather simple pattern provides the foundation for subsequent development and diversification of the segmented part of the body. Many of the genes that control the formation of this pattern have been identified and at least twenty have been cloned. By combining the techniques of genetics, molecular biology and experimental embryology, it is becoming possible to unravel the role played by each of these genes. The repeating segment pattern is defined by the persistent expression of engrailed and of other genes of the ‘segment polarity’ class. The establishment of this pattern is directed by a transient molecular prepattern that is generated in the blastoderm by the activity of the ‘pair-rule’ genes. Maternal determinants at the poles of the egg coordinate this prepattern and define the anteroposterior sequence of pattern elements. The primary effect of these determinants is not known, but genes required for their production have been identified and the product of one of these, bicoid is known to be localized at the anterior of the egg. One early consequence of their activity is to define domains along the A-P axis within which a series of ‘cardinal’ genes are transcribed. The activity of the cardinal genes is required both to coordinate the process of segmentation and to define the early domains of homeotic gene expression. Further interactions between the homeotic genes and other classes of segmentation genes refine the initial establishment of segment identities.

Hierarchy of the genetic interactions that specify the anteroposterior segmentation pattern of the Drosophila embryo as monitored by caudal protein expression

Development ◽  
1987 ◽  
Vol 101 (3) ◽  
pp. 421-435 ◽  
Author(s):  
M. Mlodzik ◽  
W.J. Gehring
Keyword(s):  
Protein Product ◽  
The Body ◽  
Drosophila Embryo ◽  
Fate Map ◽  
Gradient Distribution ◽  
Segmentation Genes ◽  
Anteroposterior Axis ◽  
Segmentation Pattern ◽  
Maternal Determinants ◽  
Homeotic Selector

The establishment of the body pattern of Drosophila along the anteroposterior axis requires the coordinated functions of at least three classes of genes. First, the maternally active coordinate genes define the polarity of the embryo and act as primary determinants; second, the segmentation genes divide the developing embryo into the correct number of segments and third, the segments become specified by the homeotic selector genes. We have examined the effects of mutations in the genes of the first two classes on the spatial distribution of the protein product(s) of the caudal (cad) gene, which in wild type shows a graded distribution along the anteroposterior axis during the syncytial blastoderm stage, whereas its persistent zygotic expression is confined to the telson region (the posterior terminal structures). Mutations in maternal genes that specify the spatial coordinates of the egg and the future embryo change the gradient distribution of cad according to the alterations of the fate map which they produce. A second group of maternally expressed genes, the gap genes of the ‘grandchildless-knirps’ group, which are considered to represent posterior activities, do not have any effect on the cad gradient. The same is true for the zygotic segmentation genes that are active after fertilization. However, the same class of zygotic genes partly affects the zygotic cad expression in the telson. Therefore, the two phases of cad expression represent different levels within the genetic hierarchy. The cad protein gradient seems to form in response to the primary maternal determinants independent of the segmentation genes, whereas the latter influence zygotic cad expression in the telson region which corresponds to a homeotic selector gene function.

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.

Dynamic changes in the functions of Odd-skipped during early Drosophila embryogenesis

Development ◽  
1998 ◽  
Vol 125 (23) ◽  
pp. 4851-4861 ◽  
Author(s):  
B. Saulier-Le Drean ◽  
A. Nasiadka ◽  
J. Dong ◽  
H.M. Krause
Keyword(s):  
Target Gene ◽  
Target Genes ◽  
Drosophila Embryo ◽  
Gene Products ◽  
Dynamic Changes ◽  
Stage Of Development ◽  
Segment Polarity ◽  
Pair Rule Gene ◽  
Candidate Target ◽  
Pair Rule

Although many of the genes that pattern the segmented body plan of the Drosophila embryo are known, there remains much to learn in terms of how these genes and their products interact with one another. Like many of these gene products, the protein encoded by the pair-rule gene odd-skipped (Odd) is a DNA-binding transcription factor. Genetic experiments have suggested several candidate target genes for Odd, all of which appear to be negatively regulated. Here we use pulses of ectopic Odd expression to test the response of these and other segmentation genes. The results are complex, indicating that Odd is capable of repressing some genes wherever and whenever Odd is expressed, while the ability to repress others is temporally or spatially restricted. Moreover, one target gene, fushi tarazu, is both repressed and activated by Odd, the outcome depending upon the stage of development. These results indicate that the activity of Odd is highly dependent upon the presence of cofactors and/or overriding inhibitors. Based on these results, and the segmental phenotypes generated by ectopic Odd, we suggest a number of new roles for Odd in the patterning of embryonic segments. These include gap-, pair-rule- and segment polarity-type functions.

Concentration-dependent patterning by an ectopic expression domain of the Drosophila gap gene knirps

Development ◽  
1997 ◽  
Vol 124 (7) ◽  
pp. 1343-1354 ◽  
Author(s):  
D. Kosman ◽  
S. Small
Keyword(s):  
Target Genes ◽  
Ectopic Expression ◽  
Drosophila Embryo ◽  
Asymmetric Distribution ◽  
Protein Diffusion ◽  
Expression Domain ◽  
Gap Gene ◽  
Pair Rule Gene ◽  
Transgenic Lines ◽  
Pair Rule

The asymmetric distribution of the gap gene knirps (kni) in discrete expression domains is critical for striped patterns of pair-rule gene expression in the Drosophila embryo. To test whether these domains function as sources of morphogenetic activity, the stripe 2 enhancer of the pair-rule gene even-skipped (eve) was used to express kni in an ectopic position. Manipulating the stripe 2-kni expression constructs and examining transgenic lines with different insertion sites led to the establishment of a series of independent lines that displayed consistently different levels and developmental profiles of expression. Individual lines showed specific disruptions in pair-rule patterning that were correlated with the level and timing of ectopic expression. These results suggest that the ectopic domain acts as a source for morphogenetic activity that specifies regions in the embryo where pair-rule genes can be activated or repressed. Evidence is presented that the level and timing of expression, as well as protein diffusion, are important for determining the specific responses of target genes.

scholarly journals Gap gene properties of the pair-rule gene runt during Drosophila segmentation

Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1671-1683 ◽  
Author(s):  
C. Tsai ◽  
J.P. Gergen
Keyword(s):  
Transcriptional Activation ◽  
Expression Patterns ◽  
Normal Component ◽  
Ectopic Expression ◽  
Antagonistic Effect ◽  
Drosophila Embryo ◽  
Gap Gene ◽  
New Family ◽  
Pair Rule Gene ◽  
Pair Rule

The Drosophila Runt protein is a member of a new family of transcriptional regulators that have important roles in processes extending from pattern formation in insect embryos to leukemogenesis in humans. We used ectopic expression to investigate runt's function in the pathway of Drosophila segmentation. Transient over-expression of runt under the control of a Drosophila heat-shock promoter caused stripe-specific defects in the expression patterns of the pair-rule genes hairy and even-skipped but had a more uniform effect on the secondary pair-rule gene fushi tarazu. Surprisingly, the expression of the gap segmentation genes, which are upstream of runt in the segmentation hierarchy was also altered in hs/runt embryos. A subset of these effects were interpreted as due to an antagonistic effect of runt on transcriptional activation by the maternal morphogen bicoid. In support of this, expression of synthetic reporter gene constructs containing oligomerized binding sites for the Bicoid protein was reduced in hs/runt embryos. Finally, genetic experiments demonstrated that regulation of gap gene expression by runt is a normal component of the regulatory program that generates the segmented body pattern of the Drosophila embryo.

scholarly journals Integration of the head and trunk segmentation systems controls cephalic furrow formation in Drosophila

Development ◽  
1997 ◽  
Vol 124 (19) ◽  
pp. 3747-3754 ◽  
Author(s):  
A. Vincent ◽  
J.T. Blankenship ◽  
E. Wieschaus
Keyword(s):  
Initial Step ◽  
Drosophila Embryo ◽  
Germ Band ◽  
Molecular Analyses ◽  
Single Row ◽  
Gap Gene ◽  
Pair Rule Gene ◽  
Integrated Regulation ◽  
Morphogenetic Fields ◽  
Pair Rule

Genetic and molecular analyses of patterning of the Drosophila embryo have shown that the process of segmentation of the head is fundamentally different from the process of segmentation of the trunk. The cephalic furrow (CF), one of the first morphological manifestations of the patterning process, forms at the juxtaposition of these two patterning systems. We report here that the initial step in CF formation is a change in shape and apical positioning of a single row of cells. The anteroposterior position of these initiator cells may be defined by the overlapping expression of the head gap gene buttonhead (btd) and the primary pair-rule gene even-skipped (eve). Re-examination of the btd and eve phenotypes in live embryos indicated that both genes are required for CF formation. Further, Eve expression in initiator cells was found to be dependent upon btd activity. The control of eve expression by btd in these cells is the first indication of a new level of integrated regulation that interfaces the head and trunk segmentation systems. In conjunction with previous data on the btd and eve embryonic phenotypes, our results suggest that interaction between these two genes both controls initiation of a specific morphogenetic movement that separates two morphogenetic fields and contributes to patterning the hinge region that demarcates the procephalon from the segmented germ band.

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