Staining is first detected at cleavage stage 12, prior to cellularization about 45 minutes prior to gastrulation. The yolk nuclei are strongly stained and remain so. Broad general staining forms first, but bands develop and soon narrow. Staining appears in odd numbered stripes, complementary to that found in Fushi tarazu, in even numbered stripes. Strongest staining appears in the anterior. As germ band elongation begins [Images], seven new bands are added between the seven original ones. The new bands show weaker staining. During elongation, new staining is detected near the posterior end in an area that includes the presumptive proctodeum. FTZ staining appears in clusters, two clusters per segment, one on either side of the ventral midline. In addition, one neuroblast cell in the interior of each segment is stained. Additional neuroblasts become stained later, six or seven on each side of the hemisegment. Only 13-15 neurons are stained by EVE antibody in each of the three thoracic and first seven abdominal ganglia. eve is expressed in segmental clusters of paracardial precursor cells from stage 11 onward (Frasch, 1987).

This study reports the expression pattern of Dll in the genital disc, the requirement of Dll activity for the development of the terminalia and the activation of Dll by the combined action of the morphogenetic signals Wingless (Wg) and Decapentaplegic (Dpp). In Drosophila, the terminalia comprise the entire set of internal and external genitalia (with the exception of the gonads), and includes the hindgut and the anal structures. They arise from a single imaginal disc of ventral origin which is of complex organization and shows bilateral symmetry. The genital disc shows extreme sexual dimorphism. Early in development, the anlage of the genital disc of both sexes consists of three primordia: the female genital primordium (FGP); the male genital primordium (MGP), and the anal primordium (AP). In both sexes, only two of the three primordia develop: the corresponding genital primordium and the anal primordium. These in turn develop, according to the genetic sex, into female or male analia. The undeveloped genital primordium is the repressed primordium (either RFP or RMP, for the respective female and male genital primordia) (Gorfinkiel, 1999).

During the development of the two components of the anal primordium -- the hindgut and the analia -- only the latter is dependent on Dll and hedgehog (hh) function. The hindgut is defined by the expression of the homeobox gene even-skipped. The lack of Dll function in the anal primordia transforms the anal tissue into hindgut by the extension of the eve domain. Meanwhile targeted ectopic Dll represses eve expression and hindgut formation. The Dll requirement for the development of both anal plates in males and only for the dorsal anal plate in females, provides further evidence for the previously held idea that the analia arise from two primordia. In addition, evaluation was made of the requirement for the optomotor-blind (omb) gene which, as in the leg and antenna, is located downstream of Dpp. These results suggest that the terminalia show similar behavior as the leg disc or the antennal part of the eye-antennal disc, consistent with both the proposed ventral origin of the genital disc and the evolutive consideration of the terminalia as an ancestral appendage (Gorfinkiel, 1999).

Both the female and male anal primordia give rise to two different adult structures: the hindgut and the anal plates. These territories are well defined by the complementary expression of the homeotic genes Dll and even-skipped (eve). Adult regions that express Dll and eve were defined by X-Gal staining of Dll-GAL4/UAS-LacZ and eve-lacZ- flies, respectively. These two genes show a complementary expression pattern. Dll is expressed in the anal plates of both females and males but not in the hindgut. In contrast, eve is expressed in the hindgut of both females and males. Some residual Dll expression is detected in the rectal papillae, but these structures are not derived from the genital disc. Thus, the adult analia and hindgut are defined by Dll and eve expression patterns, respectively. Also in the genital disc, eve labels the prospective hindgut that occupies the central part of the anal primordium while Dll marks the primordia of the anal plates located at both ends of the primordia in both females and males. This eve expression both in discs and adults suggests that eve is required for hindgut development (Gorfinkiel, 1999).

Hh signal is required to form the genital and anal structures but not the hindgut. In the leg and antennal discs, the expression of Dll depends on the Hh signaling pathway. Using the hh ts2 allele, it was observed that in the genital disc, Hh is also required for Dll activation: after 4 days at the restrictive temperature, the genital discs are very small and show no Dll expression. In the same hh ts2 larvae, residual Dll expression can be detected in the trochanter region of the leg disc. However, eve expression in the anal primordia is maintained and occupies most of the reduced genital disc. This result indicates that Dll, but not eve expression, depends on Hh and that all the terminalia with the exception of the hindgut require Hh function. To further analyze this hh requirement for Dll activation, the effect of smoothened (smo) lack of function was examined. In smo2 cells, Hh reception is impeded because smo is a component of the Hh receptor complex. In the genital disc, Dll expression only disappears in smo2 clones when the clone is large enough to cover most of the Dll expression domain. Accordingly, eve expression is also ectopically activated in smo2 mutant cells; although in Dll2 cells eve cannot be activated in certain regions of the clones. These results indicate once again that Dll is dependent on Hh function while eve is not (Gorfinkiel, 1999).

The embryonic heart precursors of Drosophila are arranged in a repeated pattern of segmental units. There is growing evidence that the development of individual elements of this pattern depends on both mesoderm intrinsic patterning information and inductive signals from the ectoderm. Two homeobox genes, ladybird early and ladybird late, are involved in the cardiogenic pathway in Drosophila. At early stage 12, lb genes are expressed in clusters of about four cells per hemisegment in the developing heart region. These cells represent a segmental subset of tinman-expressing heart progenitors, which form a continuous row at the dorsal crest of the mesoderm at this stage. even-skipped expression begins at a slightly earlier time than lb in similar clusters of cells. It appears that two cells from each segmental eve cluster develop into a particular type of pericardial cells, termed e-PCs. Double stainings for lb and eve expression demonstrate that the e-PC progenitors are distinct from the lb-expressing heart progenitors and located posteriorly adjacent to them in each segment. Similar stainings of embryos at later stages show that the lb-expressing cells give rise to a subpopulation of cardioblasts (CBs) and a second type of pericardial cells, termed l-PCs. Cell rearrangements during stage 12, which involve a 90° clockwise rotation of the heart progenitor clusters within each segment, place the lb-expressing cells at the dorsal side and move the eve-expressing cells ventrally to them. This morphogenetic process results in a dorsal row of cardioblasts and ventrolaterally adjacent rows of pericardial cells on either side of the embryo. At stage 14, generally four out of six cardioblasts per hemisegment express both tin and mef-2. Double stainings with Lb antibodies show that the two anterior tin- and mef-2-expressing cardioblasts in each hemisegment co-express lb. In addition, tin and lb are co-expressed in the l-PCs, which are located ventrally below the cardioblasts. However, lb is not expressed in the e-PCs, which are found in more lateral positions at this stage. These results indicate a diversification among cardioblasts of each segment, as well as among the pericardial cells, that is already apparent during stage 11. Overexpression of ladybird causes a hyperplasia of heart precursors and alters the identity of even-skipped-positive pericardial cells. Surprisingly, the number of eve-expressing pericardial cells is strongly reduced in overexpressors (Jagla, 1997).

In Drosophila, central nervous system (CNS) formation starts with the delamination from the neuroectoderm of about 30 neuroblasts (NBs) per hemisegment. These give rise to approximately 350 neurons and 30 glial cells during embryonic development. Understanding the mechanisms leading to cell fate specification and differentiation in the CNS requires the identification of the NB lineages. The embryonic lineages derived from 17 NBs of the ventral (medial) part of the neuroectoderm have previously been described. Thirteen lineages derived from the dorsal (lateral) part of the neuroectoderm are described here and 12 of them are assigned to identified NBs. Together, the 13 lineages comprise approximately 120 neurons and 22 to 27 glial cells which have been included in a systematic terminology. Therefore, NBs from the dorsal neuroectoderm produce about 90% of the glial cells in the embryonic ventral ganglion. Two of the NBs give rise to glial progeny exclusively (NB 6-4A, GP); five NBs give rise to glia as well as neurons (NBs 1-3, 2-5, 5-6, 6-4T, 7-4). These seven NBs are arranged as a group in the most lateral region of the NB layer. The other lineages (NBs 2-4, 3-3, 3-5, 4-3, 4-4, 5-4, clone y) are composed exclusively of neurons (interneurons, motoneurons, or both). It has been possible to link the lateral cluster of even-skipped expressing cells (EL) to the lineage of NB 3-3. Along with the previously described clones, the vast majority (more than 90%) of cell lineages in the embryonic ventral nerve cord (in the thorax and abdomen) are now known. Previously identified neurons and most glial cells are now linked to certain lineages and, thus, to particular NBs. This complete set of data provides a foundation for the interpretation of mutant phenotypes and for future investigations on cell fate specification and differentiation (Schmidt, 1997).

Terminal divisions of myogenic lineages in the Drosophila embryo generate sibling myoblasts that act as founders for larval muscles or form precursors of adult muscles. The formation of individual muscle fibers is seeded by a special class of founder myoblasts that fuse with neighboring mesodermal cells to form the syncytial precursors of particular muscle. Alternative fates adopted by sibling myoblasts are associated with distinct patterns of gene expression. During normal development (embryonic stage 11), two ventrally located progenitor cells divide once to produce three muscle founders and the precursor of an adult muscle (known as a persistent Twist cell because of its continued expression of twist). The more dorsal of the two progenitors divides, first giving rise to the founders of muscles VA1 and VA2, followed by the more ventral progenitors which produce the VA3 founder and the ventral adult persistent Twist precursor (VaP). As the progenitors divide, Numb is included in one of the two dorsal progenitors and in one of the two ventral progenitors. Thus the division of a muscle progenitor produces an unequal distribution of Numb between the founders: one contains Numb, the other does not. In numb mutants, some muscles are lost and others are transformed. For example VA1 and VaP are duplicated and VA2 and VA3 are lost. Genes expressed in the progenitor cell are maintained in one sibling and repressed in the other. Kruppel, S59 and even skipped expression mark a subset of the developing muscles. In numb mutants the expression of Kruppel, S59 and even skipped is initiated normally but is lost from both founder cells after they are formed. Thus in numb mutants there are no muscles that express Kr, eve or S59. In contrast, when numb is ectopically expressed throughout the mesoderm, Kr, S59 and eve expression are maintained in both founders and in the muscle precursors to which they give rise. In these embryos, Kr, S59 and eve-expressing muscles are duplicated (Gomez, 1997).

Functions for Drosophila brachyenteron and forkhead in mesoderm specification and cell signalling: Triggering of eve expression in heart lineages

The Drosophila Brachyury homolog brachyenteron (byn) is essential for the development of hindgut, anal pads and Malpighian tubules. byn is activated by the terminal gap gene tailless (tll) in a region of 0%-20% egg length of the syncytium (0% = posterior tip). With completion of cellularization, the byn expression becomes downregulated in the posteriormost cap of the embryo, which will later form the posterior midgut, by the terminal gap gene huckebein (hkb). Thus, the expression of byn is confined to a ring of cells from about 10%-20% egg length. The dorsal and the lateral aspects of that ring correspond to the proctodeum, from which the hindgut, the anal pads and the Malpighian tubules later develop. Intriguingly, hkb also determines the posterior extent of the ventral mesoderm primordium by repressing the mesodermal determinant snail (sna). This suggests that the ventralmost aspect of byn expression might comprise the posterior tip of the mesoderm primordium (Kusch, 1999).

There are a number of mesodermal tissues that do not properly develop in embryos lacking the caudal visceral mesoderm (CVM), as in byn, forkhead or tailless embryos. For instance, the trunk visceral mesoderm (TVM) develops aberrantly in byn mutants during late stages of embryogenesis. Although the inner layer of circular muscles differentiates in the absence of the CVM as in wild type, the morphogenesis of this layer does not proceed properly. The nuclei of the TVM are normally arranged as one broad band on each side of the midgut during germband retraction and subsequently split into two bands when the midgut primordia meet at stage 13. During this movement, the nuclei pass the rows of CVM cells, which are located at the dorsal and the ventral edge of the midgut primordium, respectively. In a byn mutant, however, the movement of the TVM nuclei is irregular, so that their organization into bands is lost and they become distributed over the entire gut circumference. Since byn is never expressed in the TVM, it is concluded that the proper arrangement and integrity of the circular muscle fibers requires the presence of the CVM. The irregular dorsoventral extension of the fibers results in an incomplete closure of the layer and the circular muscle layer of the midgut in byn embryos shows sporadic ruptures. These defects might be the reason why the three constrictions that normally subdivide the midgut tube into four gastric chambers are not formed in byn mutants. It seems rather unlikely that the longitudinal muscle fibers physically participate in the formation of the constrictions, since the fibers are oriented perpendicularly to the constriction planes (Kusch, 1999).

Strikingly, other mesodermal tissues that are affected in mutants lacking the CVM are not in obvious contact with the CVM during development. For instance, in byn mutants, the two rows of cardiac cells do not unite to form the heart vessel. In addition, pericardial cells are missing and the most dorsal internal muscle (dorsal acute 1: DA1) is absent or might be fused with DA2 in many segments. The progenitors of DA1 and of a subset of pericardial cells develop from a common cluster of dorsal mesodermal cells that can be followed from stage 10 on by their even-skipped (eve) expression. Three cells per hemisegment begin to express eve in each of 11 dorsal clusters in the mesoderm. By stage 12, the number of mesodermal eve cells increases by one in each cluster. This additional eve cell appears in succession from posterior to anterior clusters. Furthermore, it has been noted that the cells of the CVM pass the mesodermal eve clusters at a distance of about one cell diameter as they migrate anteriorly along the TVM. Shortly after the time when the leading edge of the CVM had passed, the fourth eve cell is added to the cluster. This addition occurs toward the CVM and by recruitment from neighboring cells rather than by cell division. Most importantly, the temporal and spatial correlation between the appearance of the fourth eve cell and the migration of the CVM is not a mere coincidence. In byn, tll or zfh-1 mutants in which the CVM fails to migrate anteriorly or is absent, the number of eve cells does not increase during germband retraction. It is proposed that this is the primary defect in the dorsal mesoderm that causes the defects in heart and dorsal muscle development of byn or tll mutants, and that normally an inductive signal emerging from the migrating CVM triggers the addition of the fourth eve cells. This view is supported by the observation that the specific rescue of CVM development in byn mutant embryos restores the dorsal mesodermal structures to a considerable extent. byn is neither expressed in the mesodermal eve cells nor in other dorsal mesodermal derivatives of the experimental embryos, but nevertheless the number and position of pericardial cells is essentially normal, the two rows of cardiac cells join and DA1 muscles are detectable in many segments (Kusch, 1999).

It was of interest to know whether byn is required solely for the early specification and migration of the CVM, or whether it is more directly involved in the signalling to the dorsal mesoderm. byn was therefore expressed outside the CVM, throughout the mesoderm, and the number of mesodermal eve cells was monitored. In such experimental embryos, a drastic increase of eve cells is seen at the dorsal edge of the mesoderm in the proximity to the original eve clusters during stage 11. Initially, these additional cells only appear close to the CVM, i.e. in the posterior half of the experimental embryos. Later, they also fill the gaps between the anterior eve clusters, to which the CVM fails to migrate upon ubiquitous mesodermal byn expression, and then form a band of cells along the entire dorsal mesoderm. Only the dorsal mesoderm appears to be competent to (directly or indirectly) respond to byn. This notion is supported by the finding that, in htl embryos that specifically lack derivatives of the dorsal mesoderm, ubiquitous mesodermal expression of byn does not lead to ectopic eve expression. Thus byn is not directly involved in transcriptionally activating eve in the dorsal mesoderm, since byn is normally never expressed in the eve clusters. Instead, it is proposed that byn regulates the expression of the ligand in the signalling process. byn can only exert this function on mesodermal cells, since a strictly ectodermal misexpression of byn has no effect on mesodermal eve expression. In fact, only cells in the neighborhood of the eve cells begin to express eve upon ubiquitous mesodermal byn expression, indicating that the competence to perceive the byn-mediated signal is dictated by contact with other eve cells (Kusch, 1999).

Specification of Drosophila aCC motoneuron identity by a genetic cascade involving even-skipped, grain and zfh1

During nervous system development, combinatorial codes of regulators act to specify different neuronal subclasses. However, within any given subclass, there exists a further refinement, apparent in Drosophila and C. elegans at single-cell resolution. The mechanisms that act to specify final and unique neuronal cell fates are still unclear. In the Drosophila embryo, one well-studied motoneuron subclass, the intersegmental motor nerve (ISN), consists of seven unique motoneurons. Specification of the ISN subclass is dependent upon both even-skipped (eve) and the zfh1 zinc-finger homeobox gene. ISN motoneurons also express the GATA transcription factor Grain, and grn mutants display motor axon pathfinding defects. Although these three regulators are expressed by all ISN motoneurons, these genes act in an eve->grn->zfh1 genetic cascade unique to one of the ISN motoneurons, the aCC. The results demonstrate that the specification of a unique neuron, within a given subclass, can be governed by a unique regulatory cascade of subclass determinants (Garces, 2006).

Why do these three genes act in a unique fashion in aCC, and why is grn and zfh1 sensitive to Notch specifically in this ISN motoneuron? One explanation may be that the differential input from upstream regulators, such as Ftz, Pdm1, Hkb and Pros, acts to modify the genetic interactions between eve, grn and zfh1. Another possibility is that the relative level of each factor plays an important role in dictating different cellular fates. Studies of the related Isl1 and Isl2 LIM-homeobox genes suggest that their involvement in motoneuron subclass specification is not primarily the result of the unique activity of each gene, but rather by the combined 'generic', tightly temporally controlled, Isl1 and Isl2 levels. Similarly, the different expression levels of the transcription factor Cut have been shown to play instructive roles during the specification of neuronal cell identities within the PNS. Different levels of expression of Grn and Zfh1 have been observed; while Grn is strongly expressed in aCC and weakly in RP2, Zfh1 expression shows an opposite distribution. It is tempting to speculate that these levels may be instructive for ISN motoneuron specification (Garces, 2006).

In the VNC, mutually exclusive expression is observed between Grn and Hb9 (and Islet) in different subsets of interneurons and motoneurons. Cross-inhibitory interactions between eve and Hb9 has been shown to contribute to their mutually exclusive expression patterns, and functional studies demonstrate that eve and Hb9 regulate axonal trajectories of dorsally and ventrally projecting axons, respectively. These observations are reminiscent of the cross-repressive interactions between classes of regulators that act to determine, refine and maintain distinct progenitor domains along the dorsoventral axis of the vertebrate neural tube. eve is important for proper grn and zfh1 expression in aCC, but not in RP2. These results are consistent with previously reported observations that the requirement for eve in axonal guidance is somewhat more stringent in aCC than in RP2, leading the the proposal that there may be different target genes for Eve in these two motoneurons (Garces, 2006).

Zfh1 expression was previously shown to depend upon Notch signaling activity in the aCC/pCC sibling pair as mutations in spdo or mam, members of the Notch signaling pathway, lead to de-repression of Zfh1 in pCC. Using the same allelic combinations, de-repression of grn was also observed in the pCC. Whether or not grn is directly suppressed by the Notch pathway remains to be seen, but it is interesting to note that in vertebrates, gata2/3 have been identified as targets of Notch during the differentiation of specific hematopoietic lineages (Garces, 2006).

Within the ISN subclass, the aCC motoneuron pioneers the ISN to innervate the dorsal-most muscle, muscle 1. A number of genetic and cell-ablation studies have convincingly shown that aCC plays an instructive pioneer role and guides the follower U motoneurons along the ISN nerve. These results lend support for the proposed instructive role of aCC in ISN formation. However, these studies indicate that aCC may not be essential for ISN formation. First, using RN2-GAL4 to visualize aCC and RP2, aberrant innervation of muscle 8 were frequently found (35% of hemisegments) in grn mutants. However, an axonal projection was simultaneously observed at the vicinity of the dorsal muscles 2/10. In grn mutants, zfh1 expression is specifically lost in aCC but maintained in RP2. Given the role for zfh1 in motor axon pathfinding, it is proposed that aberrant innervation of muscle 8 in grn mutants, is caused by aCC and not by RP2, and that RP2 pathfinds normally to the muscles 2/10. If so, RP2 may function as a pioneer motoneuron for muscle 2 and project there without the aCC axon. Second, although the rescue of grn mutants using RN2-GAL4 is complete, it was found that using CQ2-GAL4 to specifically rescue U motoneurons does lead to a partial rescue (54% muscles 1/9 innervated compared with 15% in grn mutants). Thus, even in the absence of aCC pioneer function, the Us (presumably U1) can still project to the dorsal-most muscles. This is in line with previous studies showing that in eve aCC/RP2 mosaic mutants and in aCC/RP2 cell ablation experiments, there is still partial innervation of muscle 1/9 (Garces, 2006).

grn is part of an eve --> grn --> zfh1 transcriptional cascade crucial for specification of aCC motoneuron identity. However, the failure of grn to rescue eve, and of zfh1 to completely rescue grn, combined with the misexpression results, indicate additional roles for both eve and grn. These roles could be either in the regulation of other aCC determinants and/or in the regulation of genes directly involved in aCC axon pathfinding. Although there are no obvious candidates for additional aCC determinants, recent studies point to a candidate axon pathfinding gene. The Drosophila unc-5 gene encodes a netrin receptor and is expressed in subsets of neurons in the VNC. Misexpression of unc-5 is sufficient to trigger ectopic VNC exit in subsets of interneurons. Recent studies now show that unc-5 is specifically expressed in eve motoneurons, and that eve is necessary, but only partly sufficient for unc-5 expression. In line with these findings, it was found that whereas single misexpression of eve or grn in dMP2 neurons has very minor effects, co-misexpression of eve and grn can efficiently trigger dMP2 lateral axonal exit. This combinatorial effect of eve/grn occurs without apparent activation of zfh1. However, misexpression of zfh1 can also trigger dMP2 lateral exit. Thus, these genes appear to be able to act in an independent manner to trigger VNC exit, but in a highly context-dependent manner. A speculative explanation for not only the mutant and rescue results, but also these misexpression results, would be that all three regulators are needed for robust and context-independent activation of axon pathfinding genes such as, for example, unc-5 (Garces, 2006).

grn encodes a GATA Zn-finger transcription factor and is the ortholog of the closely related vertebrate gata2 and gata3 genes. In vertebrates, gata2/3 are expressed in overlapping domains in the nervous system, but relatively little is known about their function. Expression data and evidence from gene targeting suggest an involvement in neurogenesis, neuronal migration and axon projection. A role in specifying neuronal subtypes within the context of neural tube patterning is emerging and recently a role for gata2/3 during 5-HT neuron development has been reported. The role of gata3 in the development of the inner ear has been of particular interest, and in humans, mutations in this gene have been linked to HDR syndrome, which is characterized by hypoparathyroidism, deafness and renal defects. In the mouse, gata3 is expressed in auditory but not vestibular ganglion neurons during development. The mouse gata3 mutant shows auditory ganglion neuron loss and efferent nerve misrouting, revealing that gata3 regulates molecules associated with neural differentiation and guidance. These vertebrate studies, combined with the current results, suggest that gata2/3 genes, similar to other transcription factors specifying neuronal identities, such as islet1/2, evx1/2 or Hb9, and their respective orthologs in Drosophila, have maintained similar functions throughout evolution (Garces, 2006).

Differential and overlapping functions of two closely related Drosophila FGF8-like growth factors in mesoderm development: Regulation of Eve expression

Thisbe (Ths) and Pyramus (Pyr), two closely related Drosophila homologues of the vertebrate fibroblast growth factor (FGF) 8/17/18 subfamily, are ligands for the FGF receptor Heartless (Htl). Both ligands are required for mesoderm development, but their differential expression patterns suggest distinct functions during development. Single mutants were generated and it was found that ths or pyr loss-of-function mutations are semi-lethal and mutants exhibit much weaker phenotypes as compared with loss of both ligands or htl. Thus, pyr and ths display partial redundancy in their requirement in embryogenesis and viability. Nevertheless, it was found that pyr and ths single mutants display defects in gastrulation and mesoderm differentiation. Localised expression of pyr is required for normal cell protrusions and high levels of MAPK activation in migrating mesoderm cells. The results support the model that Pyr acts as an instructive cue for mesoderm migration during gastrulation. Consistent with this function, mutations in pyr affect the normal segmental number of cardioblasts. Furthermore, Pyr is essential for the specification of even-skipped-positive mesodermal precursors and Pyr and Ths are both required for the specification of a subset of somatic muscles. The results demonstrate both independent and overlapping functions of two FGF8 homologues in mesoderm morphogenesis and differentiation. It is proposed that the integration of Pyr and Ths function is required for robustness of Htl-dependent mesoderm spreading and differentiation, but that the functions of Pyr have become more specific, possibly representing an early stage of functional divergence after gene duplication of a common ancestor (Klingseisen, 2009).

Expression of Eve in the precursors of the pericardial cells and DA1 muscle founders depends on the activation of several signalling pathways in a group of mesodermal pre-clusters expressing lethal of scute. Wingless (Wg) and Dpp signalling define a dorsal domain of mesoderm cells that are competent to activate transcription of eve in response to localised activation of Ras1. This localised Ras1 activation is largely dependent on Htl signalling. During this specification process, Pyr is expressed in segmental dorsal ectodermal patches in close proximity to the sites in the mesoderm where the dorsal Eve-positive clusters form. Whereas the effect on Eve expression is fully penetrant, the generation of other dorsal mesodermal precursors, e.g. those expressing Lb, is only mildly affected in pyr mutant embryos. Interestingly, it was observed that overexpression of Pyr results in strong activation of MAPK and ectopic Eve expression in the absence of normal dorsolateral migration. These results indicate that Pyr expression causes cells to become more sensitive to Dpp and Wg signalling and thus represents a limiting factor of the signalling network that triggers specification of Eve-positive dorsal mesoderm (Klingseisen, 2009).

Interactive Fly, Drosophila even-skipped: Biological Overview | Evolutionary Homologs | Transcriptional regulation | Post-transcriptional regulation | Targets of activity | Protein interactions | Effects of Mutation | References

Home page: The Interactive Fly © 1997 Thomas B. Brody, Ph.D.

The Interactive Fly resides on the
Society for Developmental Biology's Web server.