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.

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.

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.

Gradients of Krüppel and knirps gene products direct pair-rule gene stripe patterning in the posterior region of the drosophila embryo

Cell ◽  
1990 ◽  
Vol 61 (2) ◽  
pp. 309-317 ◽  
Author(s):  
Michael J. Pankratz ◽  
Eveline Seifert ◽  
Nicole Gerwin ◽  
Bettina Billi ◽  
Ulrich Nauber ◽  
...  
Keyword(s):  
Posterior Region ◽  
Drosophila Embryo ◽  
Gene Products ◽  
Pair Rule Gene ◽  
Pair Rule

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.

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.

scholarly journals Differential regulation of gastrulation and neuroectodermal gene expression by Snail in the Drosophila embryo

Development ◽  
1997 ◽  
Vol 124 (19) ◽  
pp. 3683-3691 ◽  
Author(s):  
K. Hemavathy ◽  
X. Meng ◽  
Y.T. Ip
Keyword(s):  
Cell Fate ◽  
Target Genes ◽  
Expression Patterns ◽  
Cell Movement ◽  
Drosophila Embryo ◽  
Intermediate Phenotype ◽  
Gene Products ◽  
Mesodermal Cell ◽  
Possible Cause ◽  
Mesodermal Lineage

The initiation of mesoderm differentiation in the Drosophila embryo requires the gene products of twist and snail. In either mutant, the ventral cell invagination during gastrulation is blocked and no mesoderm-derived tissue is formed. One of the functions of Snail is to repress neuroectodermal genes and restrict their expressions to the lateral regions. The derepression of the neuroectodermal genes into the ventral region in snail mutant is a possible cause of defects in gastrulation and in mesoderm differentiation. To investigate such possibility, we analysed a series of snail mutant alleles. We found that different neuroectodermal genes respond differently in various snail mutant background. Due to the differential response of target genes, one of the mutant alleles, V2, that has reduced Snail function showed an intermediate phenotype. In V2 embryos, neuroectodermal genes, such as single-minded and rhomboid, are derepressed while ventral invagination proceeds normally. However, the differentiation of these invaginated cells into mesodermal lineage is disrupted. The results suggest that the establishment of mesodermal cell fate requires the proper restriction of neuroectodermal genes, while the ventral cell movement is independent of the expression patterns of these genes. Together with the data showing that the expression of some ventral genes disappear in snail mutants, we propose that Snail may repress or activate another set of target genes that are required specifically for gastrulation.

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.

Quantitative Analysis of Gene Function in the Drosophila Embryo

Genetics ◽  
2000 ◽  
Vol 154 (1) ◽  
pp. 273-284
Author(s):  
William D Tracey ◽  
Xiangqun Ning ◽  
Martin Klingler ◽  
Sunita G Kramer ◽  
J Peter Gergen
Keyword(s):  
Gene Function ◽  
Model Systems ◽  
Drosophila Embryo ◽  
Direct Role ◽  
Developmental Context ◽  
Maternal Mrna ◽  
Early Drosophila Embryo ◽  
Segment Polarity ◽  
Pair Rule

Abstract The specific functions of gene products frequently depend on the developmental context in which they are expressed. Thus, studies on gene function will benefit from systems that allow for manipulation of gene expression within model systems where the developmental context is well defined. Here we describe a system that allows for genetically controlled overexpression of any gene of interest under normal physiological conditions in the early Drosophila embryo. This regulated expression is achieved through the use of Drosophila lines that express a maternal mRNA for the yeast transcription factor GAL4. Embryos derived from females that express GAL4 maternally activate GAL4-dependent UAS transgenes at uniform levels throughout the embryo during the blastoderm stage of embryogenesis. The expression levels can be quantitatively manipulated through the use of lines that have different levels of maternal GAL4 activity. Specific phenotypes are produced by expression of a number of different developmental regulators with this system, including genes that normally do not function during Drosophila embryogenesis. Analysis of the response to overexpression of runt provides evidence that this pair-rule segmentation gene has a direct role in repressing transcription of the segment-polarity gene engrailed. The maternal GAL4 system will have applications both for the measurement of gene activity in reverse genetic experiments as well as for the identification of genetic factors that have quantitative effects on gene function in vivo.

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.

scholarly journals A promoter interaction map for cardiovascular disease genetics

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Lindsey E Montefiori ◽  
Debora R Sobreira ◽  
Noboru J Sakabe ◽  
Ivy Aneas ◽  
Amelia C Joslin ◽  
...  
Keyword(s):  
Target Gene ◽  
Target Genes ◽  
Gene Interactions ◽  
Dynamic Changes ◽  
Coding Regions ◽  
Chromatin Interactions ◽  
Disease Loci ◽  
Interaction Map ◽  
Induced Pluripotent ◽  
Promoter Interaction

Over 500 genetic loci have been associated with risk of cardiovascular diseases (CVDs); however, most loci are located in gene-distal non-coding regions and their target genes are not known. Here, we generated high-resolution promoter capture Hi-C (PCHi-C) maps in human induced pluripotent stem cells (iPSCs) and iPSC-derived cardiomyocytes (CMs) to provide a resource for identifying and prioritizing the functional targets of CVD associations. We validate these maps by demonstrating that promoters preferentially contact distal sequences enriched for tissue-specific transcription factor motifs and are enriched for chromatin marks that correlate with dynamic changes in gene expression. Using the CM PCHi-C map, we linked 1999 CVD-associated SNPs to 347 target genes. Remarkably, more than 90% of SNP-target gene interactions did not involve the nearest gene, while 40% of SNPs interacted with at least two genes, demonstrating the importance of considering long-range chromatin interactions when interpreting functional targets of disease loci.

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