Regulation of segment polarity genes in the Drosophila blastoderm by fushi tarazu and even skipped

Nature ◽  
1988 ◽  
Vol 331 (6151) ◽  
pp. 73-75 ◽  
Author(s):  
P. W. Ingham ◽  
N. E. Baker ◽  
A. Martinez-Arias
Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 785-796 ◽  
Author(s):  
A.S. Manoukian ◽  
H.M. Krause

During Drosophila development, an important aspect of body patterning is the division of the embryo into repeating morphological units referred to as parasegments. The parasegmental domains are first defined at the blastoderm stage by alternating stripes of transcripts encoded by the pair-rule genes fushi tarazu (ftz) and even-skipped (eve) and later by stripes encoded by the segment polarity genes engrailed (en) and wingless. Here, we show that the runt gene (run) is required to generate asymmetries within these parasegmental domains. Using a heat-shock-inducible run transgene, we found that ectopic run expression leads to rapid repression of eve stripes and a somewhat delayed expansion of ftz stripes. Unexpectedly, we also found that ectopic run was a rapid and potent repressor of odd-numbered en stripes. Two remarkably different segmental phenotypes were generated as a consequence of these effects. In solving the mechanisms underlying these phenotypes, we discovered that the positioning of en stripes is largely determined by the actions of negative regulators. Our data indicate that run is required to limit the domains of en expression in the odd-numbered parasegments, while the odd-skipped gene is required to limit the domains of en expression in the even-numbered parasegments. Activation of en at the anterior margins of both sets of parasegments requires the repression of run and odd by the product of the eve gene. The spatial restriction of gene expression via negative and double negative pathways such as these is likely to be a common theme during development.


Development ◽  
2001 ◽  
Vol 128 (17) ◽  
pp. 3253-3261 ◽  
Author(s):  
Nirupama Deshpande ◽  
Rainer Dittrich ◽  
Gerhard M. Technau ◽  
Joachim Urban

The Drosophila central nervous system derives from neural precursor cells, the neuroblasts (NBs), which are born from the neuroectoderm by the process of delamination. Each NB has a unique identity, which is revealed by the production of a characteristic cell lineage and a specific set of molecular markers it expresses. These NBs delaminate at different but reproducible time points during neurogenesis (S1-S5) and it has been shown for early delaminating NBs (S1/S2) that their identities depend on positional information conferred by segment polarity genes and dorsoventral patterning genes. We have studied mechanisms leading to the fate specification of a set of late delaminating neuroblasts, NB 6-4 and NB 7-3, both of which arise from the engrailed (en) expression domain, with NB 6-4 delaminating first. In contrast to former reports, we did not find any evidence for a direct role of hedgehog in the process of NB 7-3 specification. Instead, we present evidence to show that the interplay of the segmentation genes naked cuticle (nkd) and gooseberry (gsb), both of which are targets of wingless (wg) activity, leads to differential commitment to NB 6-4 and NB 7-3 cell fate. In the absence of either nkd or gsb, one NB fate is replaced by the other. However, the temporal sequence of delamination is maintained, suggesting that formation and specification of these two NBs are under independent control.


Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 1029-1043 ◽  
Author(s):  
M. Peifer ◽  
C. Rauskolb ◽  
M. Williams ◽  
B. Riggleman ◽  
E. Wieschaus

The segment polarity genes of Drosophila were initially defined as genes required for pattern formation within each embryonic segment. Some of these genes also function to establish the pattern of the adult cuticle. We have examined the role of the armadillo (arm) gene in this latter process. We confirmed and extended earlier findings that arm and the segment polarity gene wingless are very similar in their effects on embryonic development. We next discuss the role of arm in pattern formation in the imaginal discs, as determined by using a pupal lethal allele, by analyzing clones of arm mutant tissue in imaginal discs, and by using a transposon carrying arm to produce adults with a reduced level of arm. Together, these experiments established that arm is required for the development of all imaginal discs. The requirement for arm varies along the dorsal-ventral and proximal-distal axes. Cells that require the highest levels of arm are those that express the wingless gene. Further, animals with reduced arm levels have phenotypes that resemble those of weak alleles of wingless. We present a description of the patterns of arm protein accumulation in imaginal discs. Finally, we discuss the implications of these results for the role of arm and wingless in pattern formation.


1995 ◽  
Vol 51 (2-3) ◽  
pp. 227-234 ◽  
Author(s):  
Ashim Mukherjee ◽  
S.C. Lakhotia ◽  
J.K. Roy

2008 ◽  
Vol 5 (suppl_1) ◽  
Author(s):  
Madalena Chaves ◽  
Réka Albert

The segment polarity gene family, and its gene regulatory network, is at the basis of Drosophila embryonic development. The network's capacity for generating and robustly maintaining a specific gene expression pattern has been investigated through mathematical modelling. The models have provided several useful insights by suggesting essential network links, or uncovering the importance of the relative time scales of different biological processes in the formation of the segment polarity genes' expression patterns. But the developmental pattern formation process raises many other questions. Two of these questions are analysed here: the dependence of the signalling protein sloppy paired on the segment polarity genes and the effect of cell division on the segment polarity genes' expression patterns. This study suggests that cell division increases the robustness of the segment polarity network with respect to perturbations in biological processes.


Gigabyte ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Sherry Miller ◽  
Teresa D. Shippy ◽  
Prashant S. Hosmani ◽  
Mirella Flores-Gonzalez ◽  
Lukas A. Mueller ◽  
...  

Insects have a segmented body plan that is established during embryogenesis when the anterior–posterior (A–P) axis is divided into repeated units by a cascade of gene expression. The cascade is initiated by protein gradients created by translation of maternally provided mRNAs, localized at the anterior and posterior poles of the embryo. Combinations of these proteins activate specific gap genes to divide the embryo into distinct regions along the anterior–posterior axis. Gap genes then activate pair-rule genes, which are usually expressed in parts of every other segment. The pair-rule genes, in turn, activate expression of segment polarity genes in a portion of each segment. The segmentation genes are generally conserved among insects, although there is considerable variation in how they are deployed. We annotated 25 segmentation gene homologs in the Asian citrus psyllid, Diaphorina citri. Most of the genes expected to be present in D. citri based on their phylogenetic distribution in other insects were identified and annotated. Two exceptions were eagle and invected, which are present in at least some hemipterans, but were not found in D. citri. Many of the segmentation pathway genes are likely to be essential for D. citri development, and thus they may be useful targets for gene-based pest control methods.


Development ◽  
1993 ◽  
Vol 119 (2) ◽  
pp. 501-517 ◽  
Author(s):  
A. Bejsovec ◽  
E. Wieschaus

Each segment of a Drosophila larva shows a precisely organized pattern of cuticular structures, indicating diverse cellular identities in the underlying epidermis. Mutations in the segment polarity genes alter the cuticle pattern secreted by the epidermal cells; these mutant patterns provide clues about the role that each gene product plays in the development of wild-type epidermal pattern. We have analyzed embryos that are multiply mutant for five key patterning genes: wingless, patched, engrailed, naked and hedgehog. Our results indicate that wild-type activity of these five segment polarity genes can account for most of the ventral pattern elements and that their gene products interact extensively to specify the diverse cellular identities within the epidermis. Two pattern elements can be correlated with individual gene action: wingless is required for formation of naked cuticle and engrailed is required for formation of the first row of denticles in each abdominal denticle belt. The remaining cell types can be produced by different combinations of the five gene activities. wingless activity generates the diversity of cell types within the segment, but each specific cell identity depends on the activity of patched, engrailed, naked and hedgehog. These molecules modulate the distribution and interpretation of wingless signalling activity in the ventral epidermal cells and, in addition, each can contribute to pattern through a pathway independent of the wingless signalling pathway.


Development ◽  
1997 ◽  
Vol 124 (7) ◽  
pp. 1393-1403 ◽  
Author(s):  
R. Namba ◽  
T.M. Pazdera ◽  
R.L. Cerrone ◽  
J.S. Minden

The product of the maternal effect gene, bicoid (bcd), is a transcription factor that acts in a concentration-dependent fashion to direct the establishment of anterior fates in the Drosophila melanogaster embryo. Embryos laid by mothers with fewer or greater than the normal two copies of bcd show initial alterations in the expression of the gap, segmentation and segment polarity genes, as well as changes in early morphological markers. In the absence of a fate map repair system, one would predict that these initial changes would result in drastic changes in the shape and size of larval and adult structures. However, these embryos develop into relatively normal larvae and adults. This indicates that there is plasticity in Drosophila embryonic development along the anterior-posterior axis. Embryos laid by mothers with six copies of bcd have reduced viability, indicating a threshold for repairing anterior-posterior mispatterning. We show that cell death plays a major role in correcting expanded regions of the fate map. There is a concomitant decrease of cell death in compressed regions of the fate map. We also show that compression of the fate map does not appear to be repaired by the induction of new cell divisions. In addition, some tissues are more sensitive to fate map compression than others.


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