Manual Genetic Regulatory Hierarchies in Development

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New Orleans, LA Program Reference Code s :. Text Only Version. The former had clear wing-like morphology Fig. The failure of ectopic vg expression to significantly alter haltere morphology and the distinct haltere-like character of the outgrowths formed in third thoracic legs suggests that Ubx acts on genes that are downstream of or parallel to vg in the genetic hierarchy. Targeted expression of Ubx-regulated genes. A Transformation of a T2 leg to wing as a consequence of ectopic Vg expression.

B Transformation of a T3 leg towards haltere. Magnification is the same as in A. The ectopic structure is much smaller than that formed on the T2 leg and the hair morphology and density are like those found on a haltere. In addition, a cluster of what appears to be capitellar sensillae appear that are characteristic for the haltere magnified in inset. C T2 leg imaginal disc of a wild-type third instar larva stained for Sal protein. No expression is detected. Sal is also not expressed in T1 and T3 leg discs not shown. D Upon targeted expression of Vg, Sal is ectopically induced in T2 legs in a broad stripe along the AP axis arrow similar to its expression pattern in the developing wing pouch compare to Fig.


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In addition, Sal is ectopically induced in smaller domains towards the periphery proximal region of the disc arrowheads that may correspond to Sal expression domains in the presumptive hinge and notal regions of the wing disc. The corresponding pattern is normally repressed by Ubx in the developing haltere. Therefore, targeted expression of Vg is unable to override the Ubx-regulation of the downstream gene sal.

F Distal part of a wing. Anterior is to the top, distal to the right. Extra bristles, resembling double row margin bristles developed along the distal AP boundary. The two bristles marked by the arrowhead are magnified in I. H More proximlly on the wing, mainly campaniform sensillae are induced. The region of the anterior crossvein where four instead of only one arrowhead campaniform sensilla developed. G Haltere; same orientation and magnification as F.

On the proximal haltere, ectopic capitellar sensillae are induced arrow, magnified in J ; on the distal haltere, ectopic bristles resembling double row wing margin bristles developed arrowhead, magnified in K. To test whether Ubx regulates genes downstream of vg, we first searched for candidate genes whose expression depended upon Vg. We found that the sal Fig. The patterns of ectopic induction of sal and DSRF not shown in T1 and T2 leg discs are reminiscent of their normal expression patterns in wing discs cf.

In contrast to T3 leg discs, which also express Ubx, the central domains of ectopic induction of Sal and DSRF expression are suppressed cf. These results demonstrate that downstream targets of Vg are also regulated by Ubx, independent of the Ubx regulation of Vg itself. The repression of these and other targets by Ubx would then suggest why the deregulation of Vg expression in the developing haltere is insufficient to reprogram haltere development towards wing development and to alter the morphology of the adult haltere.

Averof, pers. These results imply that there are genes downstream of DSRF and Sal whose expressions are necessary for the realization of a phenotype but which are repressed by Ubx in the haltere disc. In contrast, ectopic expression of the sc gene in the developing haltere is sufficient to induce ectopic sensory organs Fig.


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Interestingly, near the DV boundary, large bristles resembling those of the wing margin are induced Fig. K with F and I , whereas in more proximal regions, sense organs characteristic of the haltere form Fig. J and H. This result suggests that the repression of sensory organ formation by Ubx at the DV boundary is largely at the level of the sc gene, whereas the character of the proximal sense organs is modified by Ubx action downstream of or parallel to scute. Thus, all three outcomes outlined above are obtained in these ectopic expression experiments which reveal that Ubx acts independently upon the five genes we have identified as well as upon genes further downstream of or parallel to these regulators in the wing patterning hierarchy.

The differentiation of the Drosophila haltere from the wing through the action of the Ubx gene is a classic example of Hox regulation of serial homology, and has served as the paradigm for understanding the nature of homeotic gene function Lewis ; Garcia-Bellido ; Morata and Garcia-Bellido ; Lewis This study reveals several features of the control of haltere development by Ubx which, in principle, are likely to apply to the Hox -regulated differential development of other serially homologous structures in other animals.

Specifically, we have shown that Ubx acts: 1 at many levels of regulatory hierarchies, upon long-range signaling proteins, their target genes, as well as genes further downstream, 2 selectively upon a subset of downstream target genes of signals common to both wing and haltere, and 3 independently upon these diverse targets. Below, we discuss these features of the Ubx-regulated gene hierarchy in the haltere and how they expand our general understanding of the Hox-regulated development of homologous structures. Unexpectedly, Ubx does not act solely on genes that are downstream of the global coordinate systems, but also regulates the expression of at least one global organizing signal.

Along the DV boundary, Ubx represses the expression of the Wg signal in the posterior of the haltere field Fig. Ubx also regulates genes downstream of Wg, for example, the sc proneural gene, and downstream of the Dpp signal including salr and the vg quadrant enhancer Fig.

Ubx must also control genes downstream of or parallel to Vg, DSRF, and Sal because the ectopic expression of these genes is not sufficient to alter haltere size or cell morphology Fig. The architecture of the Ubx-regulated gene hierarchy in the haltere. The products of the Ap and En selector genes and the Hh and Dpp signaling proteins are expressed similarly in the wing and haltere. Ser and Wg are expressed similarly in the anterior of the wing and haltere but not in the posterior.

A selected subset of the target genes activated by Dpp, Wg, or other pathways are regulated by Ubx shown boxed. Note that some target genes are also upstream activators or coactivators of genes which are also Ubx-regulated. The Salr, Vg, Sc, and DSRF products in turn affect the differentiation of veins, wing and haltere cells, sensory organs, and intervein cells. Ubx regulation can operate selectively upon different enhancers of the same gene. The vg quadrant enhancer vg Q is Ubx-regulated; the vg boundary enhancer vg B is not.

We found that the Wg, Dpp, and Notch signal transduction pathways are active and competent throughout the haltere field and that Ubx selectively prevents activation of targets of these pathways. For example, Ubx prevents Notch -mediated Wg activation but not vg boundary activation on the DV boundary in the posterior of the haltere. Similarly, Ubx represses Dpp-mediated activation of salr and the vg quadrant enhancer, but not of the omb gene. Repression is therefore gene or enhancer-specific, not pathway-specific.

The picture emerging from this work is that there are different tiers of target genes that are regulated by Ubx independently of each other. For example, Ubx represses the expression of the vg quadrant enhancer and two downstream targets of Vg, salr and DSRF, in the haltere. Similarly, the repression of scute in the anterior of the haltere is independent of the repression of Wg. The independent regulation of these five genes or enhancers by Ubx may be either direct or indirect.

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Several observations are more consistent with direct control by Ubx. The simplest explanation for the repression of wg, salr, DSRF, sc, and the vg quadrant enhancer is that Ubx is directly blocking their activation by these pathways. Regardless of whether Ubx regulation of any individual gene is direct or not, the independent regulation of these target genes by Ubx has several important implications.

First, because there is independent regulation of genes at different levels of the same pathway, it reveals that Ubx is not acting on just a few genes at the top of regulatory hierarchies. Second, it explains why the deregulation of any individual Ubx target gene may be insufficient to transform particular haltere characters towards the wing. That is, it is difficult to break the grip of Ubx repression of wing characters because repression is operating on genes at multiple levels. And third, for repression to operate at these different levels, it implies that the evolution of the haltere progressed through the accumulation of a complex network of Ubx-regulated interactions.

One unpredictable and very informative finding of this work was that the ectopic expression of certain Ubx-regulated genes that have fairly dramatic effects on other tissues did not perturb haltere development. One conclusion that might be drawn from these results is that the repression of these genes is not significant for haltere development.

Yet, there is no doubt that the Ubx-regulated genes we have identified are developmentally significant in that they are required for the formation or patterning of major wing characters. This concept, forwarded by Waddington in the s Waddington , , , recognized that regulatory interactions in developmental processes may constrain the extent or direction of morphological change in response to environmental or genetic perturbation. An explanation for the canalization of certain developmental pathways in the haltere may lie in the evolution and architecture of the Ubx-regulated hierarchies.

The evolution of the haltere was a gradual transformation of a full-sized hindwing into a balancing organ, involving the modification, reduction, or elimination of many characters. If we consider just one feature, such as the relative size of the flight appendage, we can extrapolate from mutational studies to infer that there were many genes and pathways upon which selection could act to reduce the size of the hindwing. It is likely that the reduction of hindwing cell number and volume involved changes in the regulation of multiple genes acting at different developmental stages with the vg and wg genes being two of many potentially affected genes.

If Ubx regulation thus evolved at many loci, then we should find that perturbation of single genes in these networks may have no overt effects. Although it is not obvious why Ubx regulation would be maintained on targets whose derepression has no clear consequences, we must acknowledge that our resolution in these experiments is relatively low and we may not be able to perceive minor effects. Over evolutionary time selection against even the slightest deleterious effects that may arise from derepression of target genes would stabilize Ubx repression throughout a hierarchy.

The null allele Kerridge and Morata Ubx 6.

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Antibodies were provided by M. Skeath Sc Washington University, St. Louis, MO , and R. Immunohistochemistry was performed as previously described Carroll et al. Using a Distal-less Dll —GAL4 driver that directs ectopic expression in a large area of the developing leg including the region distal to the presumptive tibia ectopic, Vg expression was examined in developing leg discs. Ectopic expression of Sc in the wing and haltere was targeted by the Decapentaplegic Dpp -GAL4 driver that directs ectopic expression along the AP boundary of imaginal discs.

We thank M. Affolter, J.

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Montagne, R. Barrio, S. Cumberledge, N. Patel, J. Skeath, and R. White for antibodies and other reagents; M. Morata for the Dll-Gal4 stock; J. Skeath for the UAS-scute stock; J. Kennison for the slide of the four-winged fly; M. Hoffmann, J.

Gene regulatory network

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Gene regulatory network - Wikipedia

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Researchers identify genetic regulatory networks that influence poplar wood formation

Cabrera C. CrossRef Google Scholar. Carroll S. Science : — Nature : 58 — Casanova J. Cell 42 : — Castelli-Gair J. Genetics : — Couso J. Diaz-Benjumea F. Garcia-Bellido A. Ciba Found. Google Scholar. Gibson-Brown J. Grimm S. Irvine K. Cell Biol.