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.

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.

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.

scholarly journals A role of polycomb group genes in the regulation of gap gene expression in Drosophila.

Genetics ◽  
1994 ◽  
Vol 136 (4) ◽  
pp. 1341-1353 ◽  
Author(s):  
F Pelegri ◽  
R Lehmann
Keyword(s):  
Gene Expression ◽  
Small Region ◽  
Early Embryo ◽  
Polycomb Group ◽  
Drosophila Embryo ◽  
Polycomb Group Genes ◽  
Gap Gene ◽  
Anteroposterior Polarity

Abstract Anteroposterior polarity of the Drosophila embryo is initiated by the localized activities of the maternal genes, bicoid and nanos, which establish a gradient of the hunchback (hb) morphogen. nanos determines the distribution of the maternal Hb protein by regulating its translation. To identify further components of this pathway we isolated suppressors of nanos. In the absence of nanos high levels of Hb protein repress the abdomen-specific genes knirps and giant. In suppressor-of-nanos mutants, knirps and giant are expressed in spite of high Hb levels. The suppressors are alleles of Enhancer of zeste (E(z)) a member of the Polycomb group (Pc-G) of genes. We show that E(z), and likely other Pc-G genes, are required for maintaining the expression domains of knirps and giant initiated by the maternal Hb protein gradient. We have identified a small region of the knirps promoter that mediates the regulation by E(z) and hb. Because Pc-G genes are thought to control gene expression by regulating chromatin, we propose that imprinting at the chromatin level underlies the determination of anteroposterior polarity in the early embryo.

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.

Analysis of maternal effect mutant combinations elucidates regulation and function of the overlap of hunchback and Kruppel gene expression in the Drosophila blastoderm embryo

Development ◽  
1989 ◽  
Vol 107 (3) ◽  
pp. 651-662 ◽  
Author(s):  
U. Gaul ◽  
H. Jackle
Keyword(s):  
Maternal Effect ◽  
Drosophila Embryo ◽  
Homeotic Genes ◽  
Protein Distribution ◽  
Wild Type ◽  
Gap Gene ◽  
Gap Genes ◽  
Underlying Mechanisms ◽  
And Function ◽  
Pair Rule

The metameric organisation of the Drosophila embryo is generated early during development, due to the action of maternal effect and zygotic segmentation and homeotic genes. The gap genes participate in the complex process of pattern formation by providing a link between the maternal and the zygotic gene activities. Under the influence of maternal gene products they become expressed in distinct domains along the anteroposterior axis of the embryo; negative interactions between neighboring gap genes are thought to be involved in establishing the expression domains. The gap gene activities in turn are required for the correct patterning of the pair-rule genes; little is known, however, about the underlying mechanisms. We have monitored the distribution of gap and pair-rule genes in wild-type embryos and in embryos in which the anteroposterior body pattern is greatly simplified due to combinations of maternal effect mutations (staufen exuperantia, vasa exuperantia, vasa exuperantia, bicoid oskar, bicoid oskar torsolike, vasa torso exuperantia). We show that the domains of protein distribution of the gap genes hunchback and Kruppel overlap in wild-type embryos. Based on the analysis of the maternal mutant combinations, we suggest an explanation of how this overlap is generated. Furthermore, our data show that different constellations of gap gene activities provide different input for the pair-rule genes, and thus strongly suggest that the overlap of hunchback and Kruppel in wild-type is functional in the formation of the patterns of pair-rule 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.

Mutually repressive interactions between the gap genes giant and Kruppel define middle body regions of the Drosophila embryo

Development ◽  
1991 ◽  
Vol 111 (2) ◽  
pp. 611-621 ◽  
Author(s):  
R. Kraut ◽  
M. Levine
Keyword(s):  
Gene Expression ◽  
Weak Interactions ◽  
Ectopic Expression ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Regulatory Interactions ◽  
Gap Gene ◽  
Gap Genes ◽  
Body Regions ◽  
Bona Fide

The gap genes play a key role in establishing pair-rule and homeotic stripes of gene expression in the Drosophila embryo. There is mounting evidence that overlapping gradients of gap gene expression are crucial for this process. Here we present evidence that the segmentation gene giant is a bona fide gap gene that is likely to act in concert with hunchback, Kruppel and knirps to initiate stripes of gene expression. We show that Kruppel and giant are expressed in complementary, non-overlapping sets of cells in the early embryo. These complementary patterns depend on mutually repressive interactions between the two genes. Ectopic expression of giant in early embryos results in the selective repression of Kruppel, and advanced-stage embryos show cuticular defects similar to those observed in Kruppel- mutants. This result and others suggest that the strongest regulatory interactions occur among those gap genes expressed in nonadjacent domains. We propose that the precisely balanced overlapping gradients of gap gene expression depend on these strong regulatory interactions, coupled with weak interactions between neighboring genes.

Head versus trunk patterning in the Drosophila embryo; collier requirement for formation of the intercalary segment

Development ◽  
1999 ◽  
Vol 126 (19) ◽  
pp. 4385-4394 ◽  
Author(s):  
M. Crozatier ◽  
D. Valle ◽  
L. Dubois ◽  
S. Ibnsouda ◽  
A. Vincent
Keyword(s):  
Molecular Mechanisms ◽  
Drosophila Embryo ◽  
Phenotypic Analysis ◽  
Gap Genes ◽  
Segment Polarity ◽  
Pair Rule Gene ◽  
Combinatorial Model ◽  
Hlh Transcription Factors ◽  
Head Skeleton ◽  
Pair Rule

Whereas the segmental nature of the insect head is well established, relatively little is known about the genetic and molecular mechanisms governing this process. In this paper, we report the phenotypic analysis of mutations in collier (col), which encodes the Drosophila member of the COE family of HLH transcription factors and is activated at the blastoderm stage in a region overlapping a parasegment (PS0: posterior intercalary and anterior mandibular segments) and a mitotic domain, MD2. col mutant embryos specifically lack intercalary ectodermal structures. col activity is required for intercalary-segment expression both of the segment polarity genes hedgehog, engrailed, and wingless, and of the segment identity gene cap and collar. The parasegmental register of col activation is controlled by the combined activities of the head-gap genes buttonhead and empty spiracles and the pair-rule gene even skipped; it therefore integrates inputs from both the head and trunk segmentation systems, which were previously considered as being essentially independent. After gastrulation, positive autoregulation of col is limited to cells of anterior PS0. Conversely, heat-pulse induced ubiquitous expression of Col leads to disruption of the head skeleton. Together, these results indicate that col is required for establishment of the PS(−1)/PS0 parasegmental border and formation of the intercalary segment. Our data support neither a simple combinatorial model for segmental patterning of the head nor a direct activation of segment polarity gene expression by head-gap genes, but rather argue for the existence of parasegment-specific second order regulators acting in the head, at a level similar to that of pair-rule genes in the trunk.

Autonomous concentration-dependent activation and repression of Kruppel by hunchback in the Drosophila embryo

Development ◽  
1994 ◽  
Vol 120 (10) ◽  
pp. 3043-3049 ◽  
Author(s):  
C. Schulz ◽  
D. Tautz
Keyword(s):  
Target Gene ◽  
Target Genes ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Gap Gene ◽  
Low Concentrations ◽  
Localization Signal ◽  
Regulatory Effects ◽  
High Concentrations

The subdivision of the anterior-posterior axis in Drosophila is achieved by a cascade of spatially regulated transcription factors which form short-range gradients at the syncytial blastoderm stage. These factors are assumed to have concentration-dependent regulatory effects on their target genes. However, there is so far little direct in vivo evidence that a single factor can autonomously activate and repress a given target gene. We have analysed here the regulatory capabilities of the gap gene hunchback by creating an artificial gradient of hunchback in the early embryo. This was achieved by providing the maternally expressed mRNA of hunchback with the anterior localization signal of the bicoid RNA. The effects of this artificial hunchback gradient were then studied in different types of mutant background. We show that under these conditions hb is autonomously capable of activating the target gene Kruppel at low concentrations and repressing it at high concentrations. In addition, we show that the artificially created hunchback gradient can organize a large part of the segment pattern, although it is expressed at a different position and in a different shape than the wild-type gradient of hunchback.

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