Dose-dependent regulation of pair-rule stripes by gap proteins and the initiation of segment polarity

Development ◽  
1990 ◽  
Vol 110 (3) ◽  
pp. 759-767 ◽  
Author(s):  
R. Warrior ◽  
M. Levine
Keyword(s):  
Expression Patterns ◽  
Gene Products ◽  
Embryonic Cells ◽  
Periodic Patterns ◽  
Threshold Response ◽  
Gap Gene ◽  
Relative Placement ◽  
Segment Polarity ◽  
Pair Rule Gene ◽  
Pair Rule

A key step in Drosophila segmentation is the establishment of periodic patterns of pair-rule gene expression in response to gap gene products. From an examination of the distribution of gap and pair-rule proteins in various mutants, we conclude that the on/off periodicity of pair-rule stripes depends on both the exact concentrations and combinations of gap proteins expressed in different embryonic cells. It has been suggested that the distribution of gap gene products depends on cross-regulatory interactions among these genes. Here we provide evidence that autoregulation also plays an important role in this process since there is a reduction in the levels of Kruppel (Kr) RNA and protein in a Kr null mutant. Once initiated by the gap genes each pair-rule stripe is bell shaped and has ill-defined margins. By the end of the fourteenth nuclear division cycle, the stripes of the pair-rule gene even-skipped (eve) sharpen and polarize, a process that is essential for the precisely localized expression of segment polarity genes. This sharpening process appears to depend on a threshold response of the eve promoter to the combinatorial action of eve and a second pair-rule gene hairy. The eve and hairy expression patterns overlap but are out of register and the cells of maximal overlap form the anterior margin of the polarized eve stripe. We propose that the relative placement of the eve and hairy stripes may be an important factor in the initiation of segment polarity.

Grasshopper hunchback expression reveals conserved and novel aspects of axis formation and segmentation

Development ◽  
2001 ◽  
Vol 128 (18) ◽  
pp. 3459-3472 ◽  
Author(s):  
Nipam H. Patel ◽  
David C. Hayward ◽  
Sabbi Lall ◽  
Nicole R. Pirkl ◽  
Daniel DiPietro ◽  
...  
Keyword(s):  
Expression Patterns ◽  
Axis Formation ◽  
Embryonic Cells ◽  
Embryonic Patterning ◽  
Axial Patterning ◽  
Gap Gene ◽  
Segment Polarity ◽  
Pair Rule Gene ◽  
Set Up ◽  
Pair Rule

While the expression patterns of segment polarity genes such as engrailed have been shown to be similar in Drosophila melanogaster and Schistocerca americana (grasshopper), the expression patterns of pair-rule genes such as even-skipped are not conserved between these species. This might suggest that the factors upstream of pair-rule gene expression are not conserved across insect species. We find that, despite this, many aspects of the expression of the Drosophila gap gene hunchback are shared with its orthologs in the grasshoppers S. americana and L. migratoria. We have analyzed both mRNA and protein expression during development, and find that the grasshopper hunchback orthologs appear to have a conserved role in early axial patterning of the germ anlagen and in the specification of gnathal and thoracic primordia. In addition, distinct stepped expression levels of hunchback in the gnathal/thoracic domains suggest that grasshopper hunchback may act in a concentration-dependent fashion (as in Drosophila), although morphogenetic activity is not set up by diffusion to form a smooth gradient. Axial patterning functions appear to be performed entirely by zygotic hunchback, a fundamental difference from Drosophila in which maternal and zygotic hunchback play redundant roles. In grasshoppers, maternal hunchback activity is provided uniformly to the embryo as protein and, we suggest, serves a distinct role in distinguishing embryonic from extra-embryonic cells along the anteroposterior axis from the outset of development – a distinction made in Drosophila along the dorsoventral axis later in development. Later hunchback expression in the abdominal segments is conserved, as are patterns in the nervous system, and in both Drosophila and grasshopper, hunchback is expressed in a subset of extra-embryonic cells. Thus, while the expected domains of hunchback expression are conserved in Schistocerca, we have found surprising and fundamental differences in axial patterning, and have identified a previously unreported domain of expression in Drosophila that suggests conservation of a function in extra-embryonic patterning.

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.

The zygotic control of Drosophila pair-rule gene expression. II. Spatial repression by gap and pair-rule gene products

Development ◽  
1989 ◽  
Vol 107 (3) ◽  
pp. 673-683 ◽  
Author(s):  
S.B. Carroll ◽  
S.H. Vavra
Keyword(s):  
Gene Expression ◽  
Expression Patterns ◽  
Control Mechanisms ◽  
Gap Gene ◽  
Gap Genes ◽  
Gene Mutant ◽  
Pair Rule Gene ◽  
Regulatory Effects ◽  
Pair Rule ◽  
Zygotic Control

We examined gene expression patterns in certain single and double pair-rule mutant embryos to determine which of the largely repressive pair-rule gene interactions are most likely to be direct and which interactions are probably indirect. From these studies we conclude that: (i) hairy+ and even-skipped (eve+) regulate the fushi tarazu (ftz) gene; (ii) eve+ and runt+ regulate the hairy gene; (iii) runt+ regulates the eve gene; but, (iv) runt does not regulate the ftz gene pattern, and hairy does not regulate the eve gene pattern. These pair-rule interactions are not sufficient, however, to explain the periodicity of the hairy and eve patterns, so we examined specific gap gene mutant combinations to uncover their regulatory effects on these two genes. Our surprising observation is that the hairy and eve genes are expressed in embryos where the three key gap genes hunchback (hb), Kruppel (Kr), and knirps (kni) have been removed, indicating that these gap genes are not essential to activate the pair-rule genes. In fact, we show that in the absence of either hb+ or kni+, or both gap genes, the Kr+ product represses hairy expression. These results suggest that gap genes repress hairy expression in the interstripe regions, rather than activate hairy expression in the stripes. The molecular basis of pair-rule gene regulation by gap genes must involve some dual control mechanisms such that combinations of gap genes affect pair-rule transcription in a different manner than a single gap gene.

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.

The zygotic control of Drosophila pair-rule gene expression. I. A search for new pair-rule regulatory loci

Development ◽  
1989 ◽  
Vol 107 (3) ◽  
pp. 663-672 ◽  
Author(s):  
S.H. Vavra ◽  
S.B. Carroll
Keyword(s):  
Gene Expression ◽  
Regulatory System ◽  
Wild Type ◽  
Periodic Patterns ◽  
Pair Rule Gene ◽  
New Type ◽  
Regulatory Loci ◽  
Direct Inspection ◽  
Pair Rule ◽  
Zygotic Control

The examination of pair-rule gene expression in wild-type and segmentation mutant embryos has identified many, but not necessarily all, of the elements of the regulatory system that establish their periodic patterns. Here we have conducted a new type of search for previously unknown regulators of these genes by examining pair-rule gene expression in blastoderm embryos lacking parts of or entire chromosomes. This method has the advantage of direct inspection of abnormal pair-rule gene patterns without relying upon mutagenesis or interpretation of larval phenotypes for the identification of segmentation genes. From these experiments we conclude that: (i) most zygotically required regulators of the fushi tarazu (ftz), even-skipped (eve) and hairy (h) pair-rule genes have been identified, except for one or more loci we have uncovered on chromosome arm 2L; (ii) the repression of the ftz and eve genes in the anterior third of the embryo is under maternal, not zygotic control; and (iii) there are no general zygotically required activators of pair-rule gene expression. The results suggest that the molecular basis of pair-rule gene regulation can be pursued with greater confidence now that most key trans-acting factors are already in hand.

Decoding positional information: regulation of the pair-rule gene hairy

Development ◽  
1990 ◽  
Vol 110 (4) ◽  
pp. 1223-1231 ◽  
Author(s):  
K.R. Howard ◽  
G. Struhl
Keyword(s):  
Transcriptional Activation ◽  
Transcriptional Repression ◽  
Expression Patterns ◽  
Positional Information ◽  
Regulatory Elements ◽  
Regulatory Factors ◽  
Cis Acting ◽  
Pair Rule Gene ◽  
Necessary And Sufficient ◽  
Pair Rule

In the series of local gene activations that occur during early Drosophila development, the striped expression patterns of the pair-rule genes provide the first indication of segmental periodicity. The experiments that we report here address the question of how these patterns arise, by studying the regulation of one of these genes, hairy. We show that each of the seven stripes of hairy expression is controlled by a distinct subset of cis-acting regulatory elements, some mediating transcriptional activation and others transcriptional repression. In general, elements necessary and sufficient for triggering a particular stripe response are clustered on the DNA and appear to overlap or be interspersed with elements involved in at least one other stripe response. Our results extend previous findings suggesting that periodic hairy expression arises by a decoding process in which each stripe is triggered by particular combinations or concentrations of regulatory factors. These regulatory factors are likely to include the products of the gap class of segmentation genes that are required for activating or positioning particular subsets of hairy stripes and are expressed with overlapping distributions during early embryogenesis.

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 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.

Anterior repression of a Drosophila stripe enhancer requires three position-specific mechanisms

Development ◽  
2002 ◽  
Vol 129 (21) ◽  
pp. 4931-4940 ◽  
Author(s):  
Luiz Paulo Moura Andrioli ◽  
Vikram Vasisht ◽  
Ekaterina Theodosopoulou ◽  
Adam Oberstein ◽  
Stephen Small
Keyword(s):  
Binding Sites ◽  
Positional Information ◽  
Common Mechanism ◽  
Sequence Repeat ◽  
Conserved Sequence ◽  
Gap Gene ◽  
Embryo Formation ◽  
Pair Rule Gene ◽  
Specific Position ◽  
Pair Rule

The striped expression pattern of the pair-rule gene even skipped(eve) is established by five stripe-specific enhancers, each of which responds in a unique way to gradients of positional information in the earlyDrosophila embryo. The enhancer for eve stripe 2(eve 2) is directly activated by the morphogens Bicoid (Bcd) and Hunchback (Hb). As these proteins are distributed throughout the anterior half of the embryo, formation of a single stripe requires that enhancer activation is prevented in all nuclei anterior to the stripe 2 position. The gap genegiant (gt) is involved in a repression mechanism that sets the anterior stripe border, but genetic removal of gt (or deletion of Gt-binding sites) causes stripe expansion only in the anterior subregion that lies adjacent to the stripe border. We identify a well-conserved sequence repeat, (GTTT)4, which is required for repression in a more anterior subregion. This site is bound specifically by Sloppy-paired 1 (Slp1),which is expressed in a gap gene-like anterior domain. Ectopic Slp1 activity is sufficient for repression of stripe 2 of the endogenous eve gene,but is not required, suggesting that it is redundant with other anterior factors. Further genetic analysis suggests that the(GTTT)4-mediated mechanism is independent of the Gt-mediated mechanism that sets the anterior stripe border, and suggests that a third mechanism, downregulation of Bcd activity by Torso, prevents activation near the anterior tip. Thus, three distinct mechanisms are required for anterior repression of a single eve enhancer, each in a specific position. Ectopic Slp1 also represses eve stripes 1 and 3 to varying degrees,and the eve 1 and eve 3+7 enhancers each contain GTTT repeats similar to the site in the eve 2 enhancer. These results suggest a common mechanism for preventing anterior activation of three different eve enhancers.

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