extra macrochaetae: Biological Overview | Evolutionary Homologs | Regulation | Developmental Biology | Effects of Mutation | References

Gene name - extra macrochaetae

Synonyms -

Cytological map position - 61D 1-2

Function - transcription factor

Keyword(s) - transcriptional repressor

Symbol - emc

FlyBase ID:FBgn0000575

Genetic map position - 3-[0.0]

Classification - non-basic HLH

Cellular location - nuclear

NCBI links: Precomputed BLAST | Entrez Gene

Gene activation is a wonder. It sets off an explosive division of cells, like so many magical brooms in Disney's film, "Fantasia." What is to prevent this mass of ever-dividing cells from continuing their unrestrained growth? Fortunately, gene activation is only one function of transcription factors. Another task, one that is just as important, is gene inactivation. EMC is responsible for this "negative" growth function.

extramacrochaetae encodes a transcription factor of the HLH family, but unlike other members of this family, Extramacrochaetae lacks the basic region that is involved in interaction with DNA. EMC functions as a regulator of sensory organ precursor formation by forming inactive heterodimers with proteins coded for by proneural genes. EMC also regulates formation of other organs like the midgut, suggesting a general role in regulating morphogenesis (Ellis 1994).

An example of the disruptive effects of emc mutation becomes apparent when examining the resultant nervous system. Early maturational processes appear normal, that is, up through the formation of sensory mother cells, emc mutations show no visible effects. Just prior to germ band retraction however, the spatial distribution of neuroblasts and their descendents (ganglion mother cells) become disorganized. Fasciclin II staining reveals disrupted axonal patterns. Anomalies are found in the peripheral nervous system where a disruption of neuronal groups and axonal routing has occurred.

The function of emc is required during wing morphogenesis. Mitotic recombination clones of both null and gain-of-function alleles of emc, indicate that during wing morphogenesis, emc participates in cell proliferation within the intervein regions (vein patterning), as well as in vein differentiation (de Celis, 1995). The study of relationships between emc and different genes involved in wing development reveal strong genetic interactions with genes of the Ras signaling pathway (torpedo, vein, veinlet and Gap), and with several other genes (blistered, plexus and net) in both adult wing phenotypes and cell behaviour in genetic mosaics. These interactions are also analyzed as variations of emc expression patterns in mutant backgrounds for these genes. In addition, cell proliferation behaviour of emc mutant cells varies depending on the mutant background. The results show that genes of the Ras signaling pathway are co-operatively involved in the activity of emc during cell proliferation, and later antagonistically during cell differentiation, repressing EMC expression (Baonza, 1999).

Evidence that emc acts co-operatively with genes of the Ras pathway consists of studies of wing size in flies with multiple mutations. top1 homozygous mutant wings, mutant for the gene coding for the Epidermal growth factor receptor, are 14%-20% smaller than wild type, whereas top;emc double mutant wings are 36%-42% smaller. Surprising, the interaction between loss of function (LOF) alleles of emc and hypomorphic alleles of top and vein (vn) produces the same effect on reduction of wing size as the interaction between gain of function (GOF) hypermorphic emc and mutations in these genes. Thus, the vn wings are 15% smaller than the control wings, and in combination with the LOF and GOF alleles of emc the wings appear 27%-35% and 21%-29% smaller than wild type wings, respectively, suggesting that GOF alleles may have a LOF component (Baonza, 1999).

Evidence that emc acts antagonistically to Ras pathway genes during vein differentiation consists of observations of vein differentiation in genetic mosaics. LOF alleles of member genes of the Ras pathway exhibit the absence of veins, and conversely, mutations that cause an increase in the activity of that pathway result in the appearance of ectopic veins. Mutant vein phenotypes of LOF alleles of genes of the Ras pathway are suppressed in interactions with the LOF alleles of emc and enhanced with the GOF allele of emc. Reciprocally, the extra veins mutant phenotype of the GOF alleles for genes of the Ras pathway, is increased in interaction with LOF alleles of emc and reduced with the GOF allele of emc, indicating an antagonistic relationship between emc and genes of the Ras pathway. LOF alleles of emc rescue the lack of vein differention in emc;ve;vn triple mutant clones (ve is veinlet, coding for the protein better known as Rhomboid). Contrarily, double mutant clones of emc and alleles of members of the Ras pathway, which correspond to a hyperactivation of this pathway (Gap1 or heat shock rhomboid), differentiate ectopic veins everywhere in the wing vein (Baonza, 1999).

Genetic interactions have also shown synergistic mutant effects on venation between emc, plexus (px whose molecular nature is unknown) and net, which codes for a bHLH transcription factor. The net gene is required for intervein fate in wings. Furthermore, emc expression, which is absent in normal veins, also disappears in pupal extra veins caused by px and net. Given the molecular nature of net, the co-operative behavior wth emc could reflect direct molecular interactions. Similarly, genetic interactions and changes in expression pattern of emc are found with blistered (bs) mutants. blistered, coding for the Serum response factor of Drosophila, is expressed in the future intervein issue of the wing imaginal disc, in a complementary pattern to Ras pathway genes. In wing differentiation, bs plays a dual role in wing development. Two fully active copies of bs are required to ensure that the formation of wing veins is limited to vein territories. In addition Bs protein is essential for proper terminal differentiation of intervein cells. bs causes strong phenotypic interactions with mutants of the Ras pathway. Thus, it is proposed that emc, bs, px, net and the Ras signaling pathway set of genes are intimately related in vein/intervein patterning and differentiation. The Ras signaling pathway is thought to be involved in maintaining low levels of emc expression during vein pattern differentiation in cells that will differentiate as veins. This is consistent with observations of the expression pattern of emc. Emc protein and mRNA are found at highest levels in intervein regions (Baonza, 1999).

Some phenotypes caused by extramacrochaetae in the wing are similar to those observed when Notch signaling is compromised. Furthermore, maximal levels of extramacrochaetae expression in the wing disc are restricted to places where Notch activity is higher, suggesting that extramacrochaetae could mediate some aspects of Notch signaling during wing development. The relationships between extramacrochaetae and Notch in wing development have been studied, with emphasis on the processes of vein formation and cell proliferation. Strong genetic interaction between extramacrochaetae and different components of the Notch signaling pathway have been observed, suggesting a functional relationship between them. The higher level of extramacrochaetae expression coincides with the domain of expression of Notch and its downstream gene Enhancer of split-m beta. The expression of extramacrochaetae at the dorso/ventral boundary and in boundary cells between veins and interveins depends on Notch activity. It is proposed that at least during vein differentiation and wing margin formation, extramacrochaetae is regulated by Notch and collaborates with other Notch-downstream genes such as Enhancer of split-m beta (Baonza, 2000).

Notch mutant cells show reduced viability, whereas activation of Notch signaling causes strong mitotic activity in the wing disc, independent of the activation of vestigial and wingless. These observations suggest that Notch, in addition to its function in the establishment of the D/V boundary is also directly involved in the control of cell proliferation. In this function of Notch the genes of the E(spl) complex are not required. emc is also involved in regulating cell proliferation during wing disc development, because emc mutant cells do not proliferate at all, and clones of cells of strong emc hypomorphic alleles reduce cell proliferation in intervein territories. Mutant cells for both emc and Notch have extremely poor viability, indicating that emc and Notch cooperate to promote cell proliferation. However, this interaction does not rely on Notch controlling emc transcription, because the basal level of Emc expression in the wing pouch is not affected in Notch mutant cells. Thus, it is proposed that during imaginal cell proliferation emc and Notch signaling act in parallel, possibly on the same set of downstream genes, to promote cell proliferation (Baonza, 2000).

The activity of Notch is necessary for the formation and maintenance of the D/V boundary. Thus, loss of Notch prevents the formation of the wing margin and, conversely, ectopic Notch activity results in the formation of novel margin structures and wing outgrowths. During the third instar, Notch expression is maximal in the dorsal and ventral cells that form the D/V boundary. These cells also correspond to the places where E(spl)m beta, a Notch-downstream gene, is expressed, indicating high levels of Notch signaling there. The expression of emc at the D/V boundary is maximal in the same cells where Notch and E(spl)m beta genes are expressed, suggesting that Notch signaling could regulate emc expression. In fact, the expression of emc at the D/V border is eliminated in cells lacking Notch activity, whereas clones of cells expressing an activated form of N express ectopically high levels of Emc. Increased levels of Emc expression are also induced by the Notch ligands Dl and Ser in the dorsal and ventral compartments, respectively (Baonza, 2000).

The regulation of emc expression at the D/V boundary by Notch is not mediated by E(spl)m beta, since clones of E(spl)m beta-expressing cells do not affect the expression of emc. Elimination of E(spl)m beta or emc does not affect the formation of the wing margin, indicating that these Notch targets are not required for Notch activity in the formation of this structure. However, emc and E(spl) are required during the formation of the sensory organs characteristic of the wing margin. Thus, ectopic expression of emc [or E(spl)] throughout the wing pouch eliminates most of the sensory elements of the anterior wing margin. It is likely that this function of emc and E(spl) relies on the repression of the activity and expression of the Achaete and Scute proteins (Baonza, 2000).

The expression of several genes such as vein (ve) and blistered is restricted to either vein or intervein regions during imaginal development, indicating that at this stage the veins are being specified. A key component of vein specification is the activity of the Egfr signaling pathway, although it is not known which genes localize Egfr activation to vein territories. Both emc and Notch are required at this early stage to position vein territories and to define their extent, respectively, and it is likely that Notch and emc interact during the definition of vein territories in third instar wing discs. This interaction could be based in the regulation by Notch and Emc of similar target genes controlling the appearance and extent of vein-competent territories. However, the results suggest that in this initial establishment of vein territories the expression of emc and the activity of Notch are independent of each other, because the heterogeneity in emc expression related to developing veins observed in third instar discs is not modified in Notch mutant backgrounds. Furthermore, some characteristic phenotypes of emc clones, such as the appearance of ectopic veins of normal thickness, are never observed in Notch clones, indicating that emc and Notch are affecting independent processes during the initiation of vein development (Baonza, 2000).

After puparium formation the activity of Notch is continuously required to maintain the correct width of the vein, and at this stage Notch activation occurs in two stripes of cells adjacent to each vein. The accumulation of E(spl)m beta in these cells, as a consequence of Dl-mediated Notch activation, contributes to the restriction of ve expression to the vein, and prevents the differentiation as vein of the flanking pro-vein cells. Interestingly, the elimination of Notch or Dl activity results in the formation of thicker veins than elimination of E(spl)m beta, suggesting that additional elements are activated in response to Notch and participate in the repression of vein differentiation (Baonza, 2000).

Several arguments suggest that emc is one of these components that mediate Notch signaling during the pupal development of veins. (1) The expression of emc in pupal wings is maximal in the same cells that express E(spl)m beta, suggesting that Notch activity is responsible for the preferential accumulation of emc expression. This expression is modified when Notch activity is compromised; in such circumstances emc is detected in the novel flanking cells associated with the thickened Notch mutant veins. (2) Clones of emc mutant cells occasionally cause vein thickening, and this phenotype is greatly exaggerated in Notch and Dl mutant backgrounds, suggesting that in a situation of insufficient Notch activity, the levels of emc are critical to repress vein formation. The analysis of emc clones in l(1)N ts heterozygotes indicates that during the pupal stage cells are particularly sensitive to reduction in emc and Notch activities. In addition, clones of Dl-expressing cells induced during pupal development cause ectopic expression of emc, indicating that during this stage the activity of Notch is enough to increase the levels of emc. These results do not discard an earlier requirement for both genes in vein determination, but show that during pupal development emc and Notch do interact in the definition of vein thickness (Baonza, 2000).

The molecular basis of this interaction is unclear; so far there is no emc-target gene identified affecting vein formation. By analogy to the function of emc in antagonizing the activity of proneural proteins, it is postulated that Emc modulates the function of some protein involved in promoting vein formation. Interestingly, when both emc and E(spl)m beta are overexpressed, an enhancement of the E(spl)m beta overexpression phenotype of loss of veins is observed, suggesting that the combination of high levels of both emc and E(spl)m beta results in more effective repression of vein differentiation. Thus, it is proposed that Notch signaling, in addition to activating the expression of E(spl)m beta, induces high levels of emc expression in flanking cells, and that the combination of emc and E(spl)m beta is more efficient in suppressing vein formation than E(spl)m beta alone. Emc and E(spl) do not physically interact with each other, and therefore it is unlikely that emc contributes to E(spl)mb activity. Therefore it is suggested that Emc and E(spl)mbeta contribute to the regulation of the activity and expression of a vein-promoting protein and gene, respectively, thus explaining the observed synergy between Notch signaling and emc function in vein formation (Baonza, 2000).

A re-examination of the selection of the sensory organ precursor of the bristle sensilla of Drosophila melanogaster

The bristle sensillum of the imago of Drosophila is made of four cells that arise from a sensory organ precursor cell (SOP). This SOP is selected within proneural clusters (PNC) through a mechanism that involves Notch signalling. PNCs are defined through the expression domains of the proneural genes, whose activities enables cells to become SOPs. They encode tissue specific bHLH proteins that form functional heterodimers with the bHLH protein Daughterless (Da). In the prevailing lateral inhibition model for SOP selection, a transcriptional feedback loop that involves the Notch pathway amplifies small differences of proneural activity between cells of the PNC. As a result only one or two cells accumulate sufficient proneural activity to adopt the SOP fate. Most of the experiments that sustained the prevailing lateral inhibition model were performed a decade ago. This study re-examined the selection process using recently available reagents. The data suggest a different picture of SOP selection. They indicate that a band-like region of proneural activity exists. In this proneural band the activity of the Notch pathway is required in combination with Emc to define the PNCs. A sub-group in the PNCs was found from which a pre-selected SOP arises. The data indicate that most imaginal disc cells are able to adopt a proneural state from which they can progress to become SOPs. They further show that bristle formation can occur in the absence of the proneural genes if the function of emc is abolished. These results suggest that the tissue specific proneural proteins of Drosophila have a similar function as in the vertebrates, which is to determine the time of emergence and position of the SOP and to stabilise the proneural state (Troost, 2015).

This study has re-examined the development of the SOP of the MC (macrochaetae) using recently available reagents. Evidence was found that strongly suggests that the range of the Notch signal is restricted to the next cell: The elevated expression of Notch activity reporter Gbe+Su(H) around the SOP is observed only in adjacent cells. In addition, cells of PNCs that are not able to receive the Notch signal, but can send a strong signal to adjacent wildtype cells, cannot prevent a wildtype cell from adopting the SOP fate at a distance of two cell diameters away. Likewise, cells that are not able to send a signal cannot be prevented by wildtype SOPs from adopting the SOP fate more than one cell diameter away. These results suggest that the discovered filopodia of the SOP, which contact more remotely located cells do not extend the range of the inhibitory signal to these cells (Troost, 2015).

This study reveals the existence of a band of proneural activity. The PNCs are regions of elevated proneural activity in this band, rather than discrete clusters. In the band, the Notch pathway exerts an additional novel function, which defines the extent of the PNCs. In the absence of Notch function, most cells in the proneural band accumulate high levels of proneural activity that allows them to become SOPs. Thus, the pathway suppresses the proneural activity and the SOP fate in cells located between the PNCs in the proneural band. The short range of the Notch signal indicates that it is probably local mutual signalling among direct neighbours that generates the necessary Notch activity (mutual inhibition). The expression of Dl and Ser and the overall activity of Gbe+Su(H) (with exception of the halos) is unchanged in the absence of Ac and Sc. This suggests that the widespread activity of Notch in the notum that prevents most cells in the proneural band to become SOPs is not influenced by the proneural factors. It provides a baseline activity of Notch that suppresses the proneural activity in the band to prevent the formation of ectopic SOPs (Troost, 2015).

The presented results indicate that a subgroup within the PNCs exists, which is operationally defined via the requirement of the activity of Neur. The existence of a subgroup has previously been suggested on basis of experiments with a temperature sensitive allele of Notch. These data and the ones presented here, suggest that the cells of the subgroup require Notch activity that is stronger than the baseline activity to be inhibited from adopting the SOP fate. This increase in activity is generated by the nascent SOP through a Neur enhanced Dl signal: This study found that if only one cell in the subgroup is neur positive, it can prevent all other neur mutant members to adopt the SOP fate. Thus, initiating the expression of Neur first, is a critical step for a cell to adopt the SOP fate, since it allows a cell to strongly inhibit its neighbours. The inhibitory signal prevents the accumulation of sufficient proneural activity to also activate Neur in the neighbours. This inhibition is probably reflected in the observed halo of Gbe+Su(H) expression around SOPs. The findings are in good agreement with a previous study that showed that the level of Neur in a cell is a critical factor for the formation of the SOP of the microchaetae (mc) (Troost, 2015).

Loss of Notch activity results in expression of Neur and a dramatic increase in proneural activity in all cells of the PNC. Moreover, the nascent SOP, which contains the highest proneural activity, is the only cell that initiates Neur expression during normal development and expression of neur is abolished in ac sc mutant discs. These data indicate, that high proneural activity is required for the expression of Neur. Thus, the cell in the subgroup with the highest proneural activity is the cell that will express Neur first. The expression of Neur enables it to inhibit its neighbours from adopting the SOP fate by suppressing their proneural activity (Troost, 2015).

One generated through mutual signalling, which is not regulated by Ac and Sc and is sufficient to inhibit all cells in the proneural band outside the neur subgroup to become SOPs. This signalling requires the ubiquitously expressed Mib1 and antagonises the activity of Ac, Sc and Da. However, there is residual activity of Notch in mib1 mutants sufficient to prevent most cells from adopting the SOP fate. This residual activity is generated either independently of E3 ligases or by another unknown E3-ligase. In any case this component contributes to the baseline activity of the Notch pathway in addition to Mib1. The second activity on top of the baseline activity in the neur subgroup is generated by a Neur mediated strong signal from the nascent SOP. This signal suppresses the proneural activity of the other members of the neur subgroup. It is dependent on proneural activity, which initiates the expression of Neur. Thus, lateral inhibition is probably operating after the emerging SOP reaches a threshold of proneural activity. It serves to prevent the formation of supernumerary SOPs in the neur group and assures that other cells can generate the necessary SOP in case the selected one is lost (Troost, 2015).

How is the neur subgroup defined? It was found that the PNCs are small in their beginning, comprising the number of cells typical for the subgroup. These cells probably also constitute the small groups of SOPs observed in early third instar discs mutant for Psn. It is likely that E(spl)m8-SM expression defines this subgroup since this study shows that it is expressed in a small group of cells from which the SOP arises. This construct contains only one E box, the binding sites for Ac and Sc, and response to high proneural activity. It is therefore believed that the cells of the early PNC are the neur group and possess the highest proneural activity (Troost, 2015).

During normal development, a cell with more proneural activity is already recognisable at the early phase of the PNCs. This suggests the existence of a pre-selection mechanism that assures that one cell in the neur-subgroup is advanced in its development. Evidence for such a mechanism has been also previously found during rescue experiments studying the function of the proneural genes Ac and Sc. This study has obtained additional experimental evidence for this pre-selecting mechanism: In neur clones one of the cells is advanced in its development towards the SOP fate. Moreover, clonal analysis of kuz and Psn mutants revealed that wildtype cells at positions in the PNC where the SOP arises cannot be prevented from adopting the SOP fate, even if a mutant SOP that cannot be inhibited (e.g., kuz mutant), is its neighbour. The mutant cells can generate a strong inhibitory Notch signal. This indicates that the pre-selecting mechanism renders the wildtype SOP immune to the signal. The nature of this mechanism is not clear, nor whether it is always the same cell in a cluster that is selected (Troost, 2015).

Recent work demonstrated that in the eye disc a regulatory loop between Da and Emc assures correct expression of both factors and results in their complementary expression. Consequently, loss of emc function results in an increase of expression of Da. The consequences of this up-regulation for the proneural state of the mutant cells have not been investigated in detail. A published study focused on the eye imaginal disc and revealed that a few of the mutant cells in clones could adopt the neural fate. The neural cells do not express Runt, a marker expressed in the normal neural cells. Thus, the loss of emc does not result in the complete determination of the neural fate. The state of the vast majority of the cells in clones remained unknown. This study observed up-regulation of proneural activity in emc clones already in early third instar wing imaginal discs, indicating that it is an immediate reaction to the loss of emc function. Some of these cells progress to become SOPs. The increase in proneural activity was also observed in emc clones of the leg disc. Thus, the cells of imaginal discs must be permanently inhibited from adopting a proneural state through the activity of Emc. It has to be pointed out that this situation is remarkably similar to that in the early vertebrate embryo, where all cells of the blastula adopt the proneural state unless they are inhibited through BMP signalling. The cells of the neural plate maintain the proneural state due to the presence of BMP antagonists (Troost, 2015).

In the eye disc and during oogenesis expression of Emc is regulated by the Notch pathway. This study failed to find evidence that supports a regulatory relationship between Emc and the pathway in the notum during SOP development, since the loss of Psn function did not affect the expression of EMC. However, it has been previously shown that the expression of Emc along the dorso-ventral boundary in the wing primordium depends on the activity of the Notch pathway. This correlates well with the finding that this domain is independent of the activity of Da. However, the genetic network of the wing is significantly different from that in the notum. For example Notch signalling induces the expression of Wg along the D/V boundary. However, its expression in the proximal wing and in the notum is independent of the activity of the Notch pathway. This appears to be true also for the different domains of expression of Emc (Troost, 2015).

This study found that the function of ac and sc is dispensable for bristle development in the absence of emc function. How is the SOP fate initiated in these emc ac sc triple mutant cells? It is believed that the activity of Da is sufficient for SOP development in this situation for the following reasons: 1) Da is expressed ubiquitously and is required for the formation of all external sense organs. 2) Strong over-expression of Da induces bristle formation in cells that lack the whole AS-C. In contrast, over-expression of Sc fails to induce SOP formation in the absence of Da. 3) Da can form homodimers that bind to the same DNA target sequences as Ac/Da and Sc/Da heterodimers in bend-shift assays. 4) Loss of emc activity increases the activity of Da. This study show that this increase is independent of the activity of Ac and Sc. 5) The results show that Da regulates the expression of sca independently of Ac and Sc. 6) It has been shown that the mammalian homologue of Da, E2A, acts without its class II partners during B-cell development. Thus, it is likely that in the absence of function of emc, ac and sc, Da forms active homo-dimers that initiate the required neural program (Troost, 2015).

While it is clear that the activity of Ac and Sc is required during normal development, the formation of normal bristles in their absence after concomitant loss of emc function raises the question about their function. The data suggest that an important function is the neutralisation of Emc through formation of heterodimers with it or with Da. This releases Da from inactive heterodimers with Emc. The neutralisation of Emc by Ac and Sc, which are expressed in precise spatial and temporal regulated patterns, allows the differentiation of neural precursors at the correct position and time. The recent finding that a Sc variant without its transactivation domain is fully active fits well to this view of the function of Ac and Sc. Thus, through their intricate and dynamic expression, Ac and Sc and other tissue specific proneural factors determine when and where a neural precursor cell develops. In this view the function of the tissue-specific proneural genes of Drosophila, is similar to that in mammals where their orthologs also promote differentiation of neural precursors in a proneural field, the neural plate, at correct positions and time (Troost, 2015).

Based on the current results, a working model is suggested for the selection of the SOP of the MC: The differential expression of Emc defines a proneural band in the notum with changing proneural activity. The PNCs in this band are determined and positioned through the cluster-like expression of Ac and Sc, which increases the proneural activity at these positions. A baseline of activity of the Notch pathway generated by mutual inhibition prevents cells between the PNCs to accumulate high levels of proneural activity. In addition, it prevents cells located in the PNC, but outside the neur group, to accumulate high proneural activity required for adopting the SOP fate (Troost, 2015).

In the PNCs, expression of Ac and Sc neutralise Emc. Consequently, the proneural activity increases dramatically, since the released Da can form homodimers and/or heterodimers with Ac or Sc. The cells of the initial small PNCs later constitute the neur subgroup. The cells of this subgroup have the highest level of proneural activity and experience this activity also for the longest time. Within this subgroup a cell is pre-selected to become the SOP by a so far unidentified mechanism. Hence, it is the first to reach the threshold level of proneural activity required to initiate the expression of Neur. The expression of Neur enables it to efficiently inhibit the other cells of the subgroup through lateral inhibition. As a consequence these cells never accumulate sufficient proneural activity to activate Neur expression and to become a SOP. The strong signal also further activates the expression of Brd proteins that inhibit the activation of Neur, which might be accidentally activated weakly in one of the neighbours. This activation contributes to the precision of determination process. Thus, a combination of mutual and lateral inhibition mediated by the Notch pathway operates in the PNC during the determination of the SOP. Only the lateral inhibition component depends on proneural activity through transcriptional activation of expression of Neur (Troost, 2015).

The model differs from the lateral inhibition model in the following points: No feedback loop between expression of Dl and proneural activity and, hence, no differential Dl expression is required. Instead the future SOP is pre-selected and advanced in its development. Subgroups within a proneural band defined through its requirement of Neur exist. In this subgroup the activation of the expression of Neur is critical for SOP development since it enables a cell to potently inhibit its neighbours. The pre-selection mechanism favours a cell at the right position to initiate the expression of Neur before the others of the Neur group and therefore secures its development as SOP. Moreover, the existence of mutual signalling explains the inhibition of cells in the proneural band outside the subgroup without the necessity of signalling of Dl over longer distances (Troost, 2015).


cDNA clone length - 2.3kb

Bases in 5' UTR - 258

Exons - 1 of 2.7 kb

Bases in 3' UTR - 1252 bases


Amino Acids - 199

Structural Domains

EMC is a helix-loop-helix transcription factor lacking the basic domain that usually activates transcription (Ellis 1990 and Garrell 1990)

extra macrochaetae: Evolutionary Homologs | Regulation | Developmental Biology | Effects of Mutation | References

date revised: 20 April 98

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