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

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.

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 45-58 ◽  
Author(s):  
J.L. Brown ◽  
C. Wu

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.


Development ◽  
1988 ◽  
Vol 102 (2) ◽  
pp. 325-338 ◽  
Author(s):  
A. Martinez-Arias ◽  
R.A.H. White

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.


Development ◽  
1989 ◽  
Vol 105 (4) ◽  
pp. 761-767 ◽  
Author(s):  
P.A. Lawrence ◽  
P. Johnston

The first sign of metamerization in the Drosophila embryo is the striped expression of pair-rule genes such as fushi tarazu (ftz) and even-skipped (eve). Here we describe, at cellular resolution, the development of ftz and eve protein stripes in staged Drosophila embryos. They appear gradually, during the syncytial blastoderm stage and soon become asymmetric, the anterior margins of the stripes being sharply demarcated while the posterior borders are undefined. By the beginning of germ band elongation, the eve and ftz stripes have narrowed and become very intense at their anterior margins. The development of these stripes in hairy-, runt-, eve-, ftz- and engrailed- embryos is illustrated. In eve- embryos, the ftz stripes remain symmetric and lack sharp borders. Our results support the hypothesis (Lawrence et al. Nature 328, 440–442, 1987) that individual cells are allocated to parasegments with respect to the anterior margins of the eve and ftz stripes.


It is now possible to monitor directly the pattern of activity of homeotic and segmentation genes in the Drosophila embryo. Precisely bounded domains of expression are established in the blastoderm, at the time when cells became committed to specific segment identities. Some patterns of expression appear in their final form; others evolve rapidly during formation of the blastoderm. Transcripts of the homeotic gene Ultrabithorax accumulate at high levels in a single parasegment of the blastoderm, and in a block of seven parasegments of the extended germ band. The boundaries of these Ubx domains appear to lie precisely at presumptive A -P compartment boundaries. During formation of the germ band, the abundance of Ultrabithorax transcripts shows a transient segment ‘pair-rule’ modulation. I suggest that this reflects an interaction between the Ultrabithorax gene and a segment pair-rule function, which may serve to establish the precise correlation between lineage boundaries and the domains of Ultrabithorax expression.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tim Liebisch ◽  
Armin Drusko ◽  
Biena Mathew ◽  
Ernst H. K. Stelzer ◽  
Sabine C. Fischer ◽  
...  

AbstractDuring the mammalian preimplantation phase, cells undergo two subsequent cell fate decisions. During the first decision, the trophectoderm and the inner cell mass are formed. Subsequently, the inner cell mass segregates into the epiblast and the primitive endoderm. Inner cell mass organoids represent an experimental model system, mimicking the second cell fate decision. It has been shown that cells of the same fate tend to cluster stronger than expected for random cell fate decisions. Three major processes are hypothesised to contribute to the cell fate arrangements: (1) chemical signalling; (2) cell sorting; and (3) cell proliferation. In order to quantify the influence of cell proliferation on the observed cell lineage type clustering, we developed an agent-based model accounting for mechanical cell–cell interaction, i.e. adhesion and repulsion, cell division, stochastic cell fate decision and cell fate heredity. The model supports the hypothesis that initial cell fate acquisition is a stochastically driven process, taking place in the early development of inner cell mass organoids. Further, we show that the observed neighbourhood structures can emerge solely due to cell fate heredity during cell division.


1988 ◽  
Vol 59 (3) ◽  
pp. 437-442 ◽  
Author(s):  
Noel S. Skeef ◽  
John R. Duncan

1. The possibility of an effect of zinc on the rate of tumour cell division, mediated through a regulation of cellular cAMP concentration, was investigated in the present study in rats.2. Dietary Zn deficiency (< 1·5 mg Zn/kg) but not Zn excess (500 mg Zn/kg) resulted in an increased cAMP concentration in transplanted hepatoma cells. Neither treatment had any effect on the cAMP concentration in regenerating liver or normal resting liver. Both the deficient and excess Zn diets resulted in a small reduction in tumour growth (not statistically significant).3. The results seem to indicate that the relation investigated in the present study does not apply in the cell line used.


Genes ◽  
2010 ◽  
Vol 1 (3) ◽  
pp. 335-348 ◽  
Author(s):  
Ban-Hock Toh ◽  
Yugang Tu ◽  
Zemin Cao ◽  
Mark E. Cooper ◽  
Zhonglin Chai

Development ◽  
1989 ◽  
Vol 107 (4) ◽  
pp. 847-853 ◽  
Author(s):  
P.A. Lawrence ◽  
P. Johnston

We report the first attempt of its kind to study genetic interactions using young Drosophila embryos that are mosaic for wildtype and mutant cells. Using nuclear transplantation we make mosaic embryos in which a patch of cells lacks a particular segmentation gene, A. With antibodies, we than look at the expression of another gene that is known to be downstream of gene A, with respect to the cells in the patch. We have examples of patches of hairy cells (where we monitor the effect on fushi tarazu (ftz) expression), even-skipped (monitoring ftz) and ftz (monitoring engrailed and Ultrabithorax). Our main finding is that the dependence of engrailed expression on the ftz gene is strictly cell-autonomous. This result goes some way towards explaining the dependence of Ultrabithorax expression on ftz, a dependence we show to be locally cell-autonomous within parts of parasegments 6 and 8 but non autonomous within parasegment 7.


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