Segmentation gene expression in the housefly Musca domestica

Development ◽  
1991 ◽  
Vol 113 (2) ◽  
pp. 419-430 ◽  
Author(s):  
R. Sommer ◽  
D. Tautz
Keyword(s):  
Gene Expression ◽  
Musca Domestica ◽  
Segmentation Gene ◽  
Gap Genes ◽  
Segment Polarity ◽  
Pair Rule Gene ◽  
Segmentation Gene Expression ◽  
Early Expression ◽  
Early Developmental ◽  
Pair Rule

Drosophila and Musca both belong to the group of higher dipteran flies and show morphologically a very similar early development. However, these two species are evolutionary separated by at least 100 million years. This presents the opportunity for a comparative analysis of segmentation gene expression across a large evolutionary distance in a very similar embryonic background. We have analysed in detail the early expression of the maternal gene bicoid, the gap genes hunchback, Kruppel, knirps and tailless, the pair-rule gene hairy, the segment-polarity gene engrailed and the homoeotic gene Ultrabithorax. We show that the primary expression domains of these genes are conserved, while some secondary expression aspects have diverged. Most notable is the finding of hunchback expression in 11–13 stripes shortly before gastrulation, as well as a delayed expression of terminal domains of various genes. We conclude that the early developmental gene hierarchy, as it has been defined in Drosophila, is evolutionary conserved in Musca domestica.

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.

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.

scholarly journals Mis-regulating segmentation gene expression in Drosophila

Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 1121-1135 ◽  
Author(s):  
S.M. Parkhurst ◽  
D. Ish-Horowicz
Keyword(s):  
Gene Expression ◽  
Fusion Gene ◽  
Ectopic Expression ◽  
Gene Promoter ◽  
Normal Function ◽  
Gap Gene ◽  
Pair Rule Gene ◽  
Segmentation Gene Expression ◽  
Regulated Gene Expression ◽  
Pair Rule

We have used the hunchback (hb) gap-gene promoter to drive ectopic expression of the pair-rule genes fushi tarazu (ftz), even-skipped (eve) and hairy (h). Unexpectedly, flies transformed with such constructs are viable, despite spatial and temporal mis-regulation of pair-rule expression caused by the fusion genes. We show that fusion gene expression is transcriptionally regulated, such that ectopic expression is suppressed when pattern is established, and present evidence indicating that interstripe hb-ftz expression is repressed by eve. These results are considered in terms of redundant control of pair-rule gene striping. We also discuss the potential dangers of using mis-regulated gene expression to analyse normal function.

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.

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.

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.

scholarly journals Conservation and variation in pair-rule gene expression and function in the intermediate-germ beetleDermestes maculatus

Development ◽  
2017 ◽  
Vol 144 (24) ◽  
pp. 4625-4636 ◽  
Author(s):  
Jie Xiang ◽  
Katie Reding ◽  
Alison Heffer ◽  
Leslie Pick
Keyword(s):  
Gene Expression ◽  
Pair Rule Gene ◽  
And Function ◽  
Pair Rule

scholarly journals 18-P004 Complex movements of segmentation gene expression domains in Drosophila homozygous Krüppel mutants

2009 ◽  
Vol 126 ◽  
pp. S286
Author(s):  
Svetlana Surkova ◽  
Manu ◽  
Maria Samsonova ◽  
John Reinitz
Keyword(s):  
Gene Expression ◽  
Segmentation Gene ◽  
Segmentation Gene Expression
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