BIOLOGICAL OVERVIEW

Pair-rule and segment polarity genes are responsible for determining the uniformity of different segments, in contrast to homeodomain proteins that are responsible for establishing the diversity between segments. Abdominal-B acts in three germ cell layers to fulfill this latter function.

Abdominal-B is the last in linkage order and the most posterior acting of the linked homeodomain proteins of the bithorax. Abdominal-B is unique among the homeotics in that it is transcribed in two forms; a regulatory (r) protein and a morphogenic (m) protein. Regulatory transcripts of Abdominal-B act as repressors, suppressing embryonic ventral epidermal structures in the 8th and 9th segments of the abdomen. Thus ABD-B r and m proteins are critically involved in establishing cell fate in the tail segments of the fly.

Expression is driven by two promoters. The m form is transcribed in parasegments 10-13, corresponding to adult abdominal segments 5-8, while the regulatory protein is transcribed in parasegment 14, corresponding to adult abdominal segment 9. This division of labor does not appear until stage 13, relatively late in development. Earlier, in stage 10, both forms are transcribed in epidermis. In stage 11, both forms are found in epidermis and mesoderm. By stage 12 central nervous system (ventral cord) expression is evident for both forms. In stage 13 m expression becomes restricted to segments 11-13 for all tissues, while r expression becomes restricted to segment 14 for all tissues (De Lorenzi, 1990b). The r protein's designation as regulatory stems from its unique role in segment 14. There it suppresses myogenesis. It is believed that it also represses transcription of the m form.

The distinction between r and m functions was based on the discovery of three classes of regulatory mutations affecting Abdominal-B (Casanova, 1986). One class affects expression in five parasegments (10-14), a second affects expression in only four (parasegments 10-13) and a third class affects expression in just parasegment 14. The regulatory transcript of ABD-B is thought to suppress the proximal morphogenetic (m) function (Casanova, 1986). The smaller r protein differs from its m counterpart in its lack of an M repeat region. This is a particular amino acid segment that lies upstream of the homeobox. The M repeat is rich in glutamines, a classical transcription activation motif (De Lorenzi, 1988).

The lines gene of Drosophila is required for specific functions of the Abdominal-B HOX protein

Genetic evidence shows that lines, a Drosophila segment polarity gene that has yet to be cloned, is required for the function of the Abdominal-B protein. In lines mutant embryos Abdominal-B protein expression is normal but is incapable of promoting its normal function: formation of the posterior spiracles and specification of an eighth abdominal denticle belt. The tail and A8 segment of lin embryos are highly abnormal. The A8 denticle belt is replaced by naked cuticle that occasionally forms a few denticles less pigmented than the normal ventral denticles. This abnormal A8 cuticle does not resemble the cuticle of any region of the wild-type or of the lin mutant embryo. The absence of anal pads and the abnormal hindgut suggests abnormal development of abdominal segment 11, however, other aspects of the tail development are normal, such as the formation of an anal tuft. In lin embryos the sensory organs are formed at roughly correct positions but have an abnormal shape (Castelli-Gair, 1998).

The Abd-B gene directs the formation of the posterior spiracles by controlling downstream target genes. The defects associated with lines mutation arise because in lines mutant embryos the Abdominal-B protein cannot activate its direct target empty spiracles (ems) or other downstream genes, such as cut(ct) and spalt(sal), while it can still function as a repressor of Ultrabithorax and abdominal-A. empty spiracles is one gene required for the formation of posterior spiracles. ems expression in the posterior spiracles is regulated by Abd-B. In lin embryos the transcription of ems is not activated in the posterior spiracles, showing that lin is required for Abd-B to activate its direct downstream target. The other putative Abd-B downstream targets cut and spalt are also required for the normal development of the posterior spiracles. The activation of ct and sal in the anlage of the posterior spiracles requires Abd-B function but their activation remains independent of one another and of ems, suggesting that all three genes are independently controlled by Abd-B. In lin mutants neither ct nor sal are activated in the anlage of the posterior spiracles. These results show that in lin mutant embryos, Abd-B is incapable of activating some of its targets. The requirement of lines for Abd-B function is not a specific property of the A8 segment. In wild-type embryos, ectopic Abd-B expression using the GAL4 targeting system results in the formation of ectopic posterior spiracles in segments anterior to A8. In contrast, ectopic Abd-B expression in lin mutants does not form ectopic posterior spiracles showing that no matter where the Abd-B protein is expressed in the embryo it requires lines to be fully functional (Castelli-Gair, 1998).

The effect of lin on Abd-B can be explained at the molecular level if lin is required for protein posttranscriptional modification or as a transcriptional cofactor of Abd-B. There is some evidence that the Abd-B protein is posttranslationally modified. If Lin were mediating this process, it would imply that such posttranscriptional modification is functional in vivo. Alternatively if Lines is a transcriptional cofactor of Abd-B, Lines would be interacting with Abd-B in a similar way to that proposed for Extradenticle with Ubx and Abd-A, or Ftz-F1 with Ftz. It is interesting that Exd does not have any effect on Abd-B protein binding or function, and that lin is specific for Abd-B but not for the other Hox genes tested. This suggests that different HOX proteins use different cofactors that contribute to the DNA binding specificity of the HOX proteins (Castelli-Gair, 1998).

The Hox gene Abdominal-B antagonizes appendage development in the genital disc of Drosophila

Abdominal-B is required to specify the posterior abdomen and the genitalia. Homologs of Abdominal-B in other species are also needed to determine the posterior part of the body. The function of Abdominal-B in the formation of Drosophila genitalia has been studied, and the absence of Abdominal-B in the genital disc of Drosophila has been shown to transform male and female genitalia into leg or, less frequently, into antenna. These transformations are accompanied by the ectopic expression of genes such as Distal-less or dachshund, which are normally required in these appendages. The extent of wild-type and ectopic Distal-less expression depends on the antagonistic activities of the Abdominal-B gene (as a repressor), and of the decapentaplegic and wingless genes (as activators). Absence of Abdominal-B also changes the expression of Homothorax, a Hox gene co-factor. These results suggest that Abdominal-B forms genitalia by modifying an underlying positional information and repressing appendage development. It is proposed that the genital primordia should be subdivided into two regions, one of them competent to be transformed into an appendage in the absence of Abdominal-B (Estrada, 2001).

Abd-B clones were induced, and they transform posterior abdominal segments into more anterior ones but are normal in the analia. Rare clones transform to distal antennae (second and/or third antennal segment and arista). Transformations to legs or antennae are cell autonomous. The formation of legs requires the activity of genes such as homothorax (hth), dac and Dll, which specify the proximal, medial and distal parts of the leg, respectively. Dll expression in wild-type discs is regulated by the combined activities of wingless and dpp in the genital primordia, and is confined to two groups of cells in male and female discs, the female domains being smaller and expressing lower levels of Dll protein. Since Abd-B is transcribed in the entire genital primordia of the two sexes, some cells co-express Abd-B and Dll. In the male disc, hth is not expressed in the Dll-expressing cells and is also excluded from a large group of cells surrounding them. Levels of antibody signal vary within the disc, and are higher in the female repressed primordium. In females, the hth domain of expression occupies the whole primordium. Lower levels of Hth are detected in a region encompassing the Dll-expressing cells, whereas higher levels are observed in the male repressed primordium. In both sexes, hth expression is absent from the anal primordium. dac is expressed differently in male and female genital primordia: in male discs, Dac protein is detected in two broad lateral bands, while in female discs it is found in the central region, almost coincident with the wg-expressing region. Therefore, the expression patterns of hth, dac and Dll differ substantially from those observed in legs (Estrada, 2001).

It is known that expression of Dll is not required to make male genitalia and that it has only a minor role in the formation of the female one. To ascertain the role of hth in the genitalia, hth minus clones were induced during the third larval period and they were examined in the adult structures. In the female genitalia, hth minus clones cause extra growths with additional vaginal teeth. In males, these clones show occasionally some abnormalities in the clasper teeth. hth clones in the analia are wild type. Possible interactions between Dll and hth in the genital disc were sought. In these experiments, unless stated, the results apply both to male and female genital primordia. Dll minus clones in the Dll domain of the male disc have no hth expression. Similarly, in hth minus clones Dll is not ectopically expressed. Dll was also expressed ectopically and the effect on hth expression was examined. Dll-expressing cells close to the wild-type Dll domain repress hth expression, although not all the cells do so. By contrast, clones far from the Dll domain do not affect hth expression (Estrada, 2001).

To characterize the transformation of genitalia into leg or antennal tissues, Abd-B minus clones were examined. Abd-B minus clones in the genital primordia tend to segregate from the rest of the tissue, round up and have smooth borders, suggesting they have acquired different affinities. By contrast, clones in the analia have indented borders and do not segregate. Abd-B minus clones in the genital primordium close to the normal Dll domain show ectopic, cell-autonomous Dll expression, whereas those far apart do not show such expression. dac is also activated cell autonomously in many Abd-B minus clones. As expected, Dll target genes, such as Bar, also become activated in these clones (Estrada, 2001).

Abd-B minus clones exhibit differential effects on hth, depending on their position: those close to the Dll domain show no hth expression, whereas those located away from the Dll domain show a slight increase in hth signal. Clones in intermediate positions do not significantly change hth levels. This distribution, however, is clearer in females, since in males there is a wide region with no hth expression. The repression of hth observed in some Abd-B minus clones may be mediated by the ectopic Dll (Estrada, 2001).

In the genital disc, the transcription of Dll depends, as in the leg disc, on dpp and wg signals. Abd-B represses Dll expression. Moreover, increasing Abd-B levels in the Dll domain suppresses Dll transcription. The antagonistic activities of dpp/wg and Abd-B in determining the Dll distribution was analyzed. Mutations in PKA ectopically activate wg and dpp expression. PKA minus clones in the genital primordia activate Dll, although only in some places. This activation is not mediated by changes in Abd-B levels. Similarly, although Dll is derepressed in many late Abd-B minus clones, derepression of either dpp or wg was not observed. It is concluded that there is an antagonism between the activation of Dll by dpp/wg signaling and its repression by Abd-B. This is not mediated by changes in the expression of either dpp, wg or Abd-B (Estrada, 2001).

To characterize this antagonism further, Abd-B minus clones that were made were also unable to transduce the dpp signal. This signal requires the presence of the type II receptor encoded by the gene punt. In put;Abd-B double mutant clones, Dll is not activated, indicating that, in the absence of Abd-B, Dpp (and possibly Wg) are still required to activate Dll. Abd-B minus clones far from the wild-type Dll domain fail to activate Dll ectopically, suggesting that activation of Dll in the absence of Abd-B depends on the range of diffusion of Dpp and Wg, as in the leg disc and in the anal primordium (Estrada, 2001).

Dll is required for the development of legs and antennae, and induces these structures when expressed ectopically in the wing or eye-antennal discs. However, although Dll is also expressed in the genital primordia this expression does not lead to the formation of any of these appendages. To test if Abd-B prevents Dll function Abd-B was eliminated in Dll-expressing cells; these cells formed leg tissue. However, it is possible that the high levels of Dll observed in these mutant cells account for the leg transformation. To test this, use was made of the GAL4/UAS system to increase Dll expression in the genital disc (dpp-GAL4/ UAS-Dll flies). Male and female genitalia of this genotype are abnormal, but not transformed into leg. To extend these observations, the ability of Dll to promote Bar transcription, a gene expressed in the leg disc and activated by Dll, was examined. Bar is not expressed in the female genital primordium and only in a few cells within the Dll domain in the male genital primordium; however, Abd-B minus clones show Bar expression in both sexes. When Dll is ectopically expressed in the genital disc, Bar expression is activated in some of the cells that express Dll. These results suggest that, in females, Dll levels are insufficient to activate Bar when Abd-B is present, but that increasing Dll expression or removing Abd-B activates Bar transcription. Abd-B, therefore, prevents some Dll activity in females. In males, although there is Bar transcription, leg tissue is not formed, probably because Abd-B modifies or prevents the activation of other Dll target genes. A similar case has been reported in the wing disc: ectopic Dll activates bric a brac, a gene downstream of Dll, both in the wing pouch and the body wall region of the wing disc; however, legs appear in the wing, but not in the notum (Estrada, 2001).

The Hox gene Antennapedia is involved in leg development. Therefore, an examination was performed to see whether Antp is derepressed in Abd-B minus clones. Antp is not transcribed in the wild-type genital disc, but some Abd-B clones show Antp signal. The presence of the Antp product, however, is not required to transform the genitalia into a leg, since Antp:Abd-B double mutant clones still form ectopic legs. This result is consistent with the view that the role of Antp in leg specification is simply to repress hth expression. It seems that Dll alone is able to direct leg development, provided that Hox and hth genes are not transcribed. Under these conditions, leg tissue can be formed in several appendages: leg, wing, antennal and genital primordia (Estrada, 2001).

Ubx and abdominal A expression were examined in Abd-B minus clones. Ubx was not derepressed in these clones, whereas some clones presented weak ectopic abd-A expression, but only in some cells (Estrada, 2001).

Requirement of Abdominal-A and Abdominal-B in the developing genitalia of Drosophila breaks the posterior downregulation rule

The genitalia of Drosophila derive from the genital disc and require the activity of the Abdominal-B (Abd-B) Hox gene. This gene encodes two different proteins, Abd-B M and Abd-B R. The embryonic genital disc, like the larval genital disc, is formed by cells from the eighth (A8), ninth (A9) and tenth (A10) abdominal segments, which most likely express the Abd-B M, Abd-B R and Caudal products, respectively. Abd-B m is needed for the development of A8 derivatives such as the external and internal female genitalia, the latter also requiring abdominal-A (abd-A), whereas Abd-B r shapes male genitalia (A9 in males). Although Abd-B r represses Abd-B m in the embryo, in at least part of the male A9 such regulation does not occur. In the male A9, some Abd-B m^–r^– or Abd-B r^– clones activate Distal-less and transform part of the genitalia into leg or antenna. In the female A8, many Abd-B m^–r^– mutant clones produce similar effects, and also downregulate or eliminate abdominal-A expression. By contrast, although Abd-B m is the main or only Abd-B transcript present in the female A8, Abd-B m^– clones induced in this primordium do not alter Distal-less or abd-A expression, and transform the A8 segment into the A4. The relationship between Abd-B and abd-A in the female genital disc is opposite that of the embryonic epidermis, and contravenes the rule that posteriorly expressed Hox genes downregulate more anterior ones (Foronda, 2006).

Abd-B is a complex gene: the use of four different promoters and the existence of specific exons give rise to several transcripts that encode two different proteins. The A (m) transcript encodes the Abd-B M (or Abd-B I) protein, and the B, C (r) and gamma RNAs encode the Abd-B R (or Abd-B II) protein. The Abd-B M protein has 221 amino acids more than the Abd-B R product does in its N-terminal domain but both proteins share a common C-terminal region, which includes the homeodomain. In the embryonic epidermis, the Abd-B M transcript and protein are expressed in parasegments (PS) 10-13 (A5-A8 segments), whereas the Abd-B R transcript and protein are present in PS14-PS15 (A9-A10) initially, and in PS14 (A9) at late stages. The gamma RNA is transcribed in just a few cells of PS14 or PS15 (Foronda, 2006 and references therein).

The role of Abd-B M and Abd-B R products in genital development remains unclear. Abd-B m mutations transform the A5-A8 segments into the A4 segment, both in males and females; the female genitalia are lost whereas male genitalia remain intact. Significantly, the transformations obtained in either Abd-B m or Abd-B r mutants clearly differ from those observed when all Abd-B functions are eliminated: in some of the clones mutant for Abd-B (m and r), part of the male or female genitalia are transformed into leg or antenna. Therefore, the precise role of abd-A, Abd-B m and Abd-B r in genitalia development is not well defined (Foronda, 2006).

This study has analyzed homeotic expression and requirement in terminalia development. It is proposed that in the embryonic genital disc, as in the larval discs, Abd-B m, Abd-B r and cad are expressed in the A8, A9 and A10, respectively. It is also reported that abd-A, Abd-B m and Abd-B r are needed for development of the internal female genitalia, Abd-B m for the development of female external genitalia and Abd-B r for the development of male genitalia. Strikingly, abd-A and Abd-B bear unexpected relationships in mature genital discs. In the A8 of the female genital disc, Abd-B M maintains abd-A expression. In Abd-B m mutant clones, however, another Abd-B protein maintains abd-A expression but does not prevent abd-A function, since these clones transform the A8 segment into the A4. In the male A9, Abd-B r function does not repress the Abd-B m transcript, at least in part of the primordium, and some Abd-B r mutant clones transform male genitalia into leg or antenna. These relationships between Hox genes are different from those reported in the embryonic epidermis and contravene the rule that posteriorly expressed Hox genes repress those expressed more anteriorly (Foronda, 2006).

In the third instar genital disc of Drosophila, Abd-B is expressed in the A8 and A9 segments, and cad in the A10. To study whether these expression domains are established early in development, Abd-B and cad transcription were examined in the embryonic genital disc. This disc is identified by the expression of genes like snail, escargot or headcase (hdc), and the hdc-lacZ B5 line, which reproduces the pattern of hdc RNA expression, was selected to mark the genital disc. At about stage 15, hdc is expressed in three clusters of cells, two anterior ones placed bilaterally, and a third one located in a more posterior and central position. The three clusters fuse later in development to form the genital disc. At stage 15, six to seven cells were counted at each of the two anterior groups, and two to three cells in the posterior one, making up a total of 14-17 cells. Double staining with anti-Abd-B and anti-ß-galactosidase antibodies (in hdc-lacZ embryos), or with GFP and anti-ß-galactosidase antibody (in cad-Gal4/UAS-GFP; hdc-lacZ/+ embryos), shows that Abd-B is expressed in the two anterior clusters and cad in the posterior one (Foronda, 2006).

To ascertain whether the two Abd-B products (Abd-B M and Abd-B R) are present in the genital disc primordium, the expression driven by an Abd-B m-Gal4 line was compared with the signal detected with an antibody that recognizes both Abd-B M and Abd-B R proteins. In UAS-myc-EGFP^F/+; Abd-B-Gal4^LDN/hdc-lacZ embryos, a GFP signal was seen in about two cells located laterally in each of the two anterior clusters; these cells most likely express Abd-B m, and, therefore, are also labelled with the anti-Abd-B antibody. There are also 8-10 Abd-B-expressing cells not labelled with GFP, and these, probably, correspond to those expressing the Abd-B R protein. Taken together, these results suggest that the embryonic genital primordium includes three groups of cells that probably express Abd-B m, Abd-B r and cad, respectively (Foronda, 2006).

Study of mutant phenotypes reveals that as in the embryonic cuticle, abd-A and Abd-B m are needed in the A8 whereas Abd-B r is required in the A9. The relationship between these homeotic products in the mature genital discs, however, clearly differs from what is observed in the embryonic epidermis. The embryonic genital disc has three distinct cell populations at stages 15/16: some anterior-lateral cells transcribe Abd-B m, anterior-central and middle cells express Abd-B r and posterior cells transcribe cad, although the expression of these products may overlap. Because the genital disc is formed by the fusion of cells coming from the A8, A9 and A10 segments, and by analogy to the expression of these genes in the mature genital discs, it is concluded that Abd-B m, Abd-B r and cad are probably expressed in the A8, A9 and A10 segments, respectively, of the embryonic genital disc (Foronda, 2006). Abd-B is not only expressed, but also required in the embryonic genital primordium. In the absence of Abd-B m, the number of hdc-expressing cells in the disc is reduced, most likely because these cells adopt now a more anterior fate, as occurs in the cuticle. When Abd-B r is absent, the genital primordium lacks some cells and is disorganized, and when both Abd-B products are absent, the primordium is reduced to a few, dispersed cells, some of which express Dll ectopically, suggesting a transformation into a leg primordium (Foronda, 2006).

The A8, A9 and A10 primordia of the mature genital discs bear anterior and posterior compartments, with expression of en and wg in each of these three primordia. Curiously, although three primordia in the embryonic disc can be defined, based on the expression of Abd-B m, Abd-B r and cad, neither en nor wg is expressed in the three separate domains at this stage. This may suggest, as was also recently proposed, that new bands of en and wg expression may be formed later in development, in precise concordance with the three primordia defined by the Abd-B m, Abd-B r and cad genes. It is noted that late en expression is also characteristic of the antennal primordium of the eye-antennal disc (Foronda, 2006).

abd-A is expressed in the whole internal female genitalia except for the parovaria, and this is consistent with experiments indicating that parovaria derive from the female A9 segment. abd-A has been shown to be required for gonad development, and in the abd-A^iab-3/Df mutant, combinations ovaries are also absent. However, the defects observed in the female internal genitalia are not simply due to an indirect effect of the lack of gonads, since iab-4 mutations prevent the formation of the ovaries but do not alter internal genitalia formation (Foronda, 2006).

The results indicate that Abd-B m is required for the development of female external and internal genitalia, both derived from the female A8. The internal genitalia of Abd-B-Gal4^LDN/UAS-lacZ females (driving expression only where Abd-B m levels are high) were stained with X-gal except in two structures, the oviducts and parovaria. The absence of oviduct staining in Abd-B-Gal 4^LDN/UAS-lacZ females is probably due to the particular expression driven by this reporter, and does not imply an absence of Abd-B m transcription in these organs, for two reasons: (1) Abd-B m transcripts are present in the whole A8 segment of the female genital disc, and (2) oviduct development is affected in Abd-B m mutant females. Parovaria, by contrast, are not stained in Abd-B-Gal 4^LDN/UAS-lacZ or abd-A-lacZ females, and this agrees with their A9 provenance. This is supported by the observation that in some Abd-B m mutant females parovaria are the only structures that remain in the internal female genitalia (Foronda, 2006).

Abd-B M seems to be the main or only Abd-B product present in the female A8, so it was expected that elimination in this segment of just Abd-B M or of all Abd-B proteins would give similar results. This is not so. Some Abd-B^– clones transform part of the female genitalia into leg or antenna, whereas Abd-B m mutant clones convert the eighth tergite, and probably the female genitalia, into an anterior abdominal segment. The differences between Abd-B m^– and AbdB^– clones in the A8 of the female genital disc reveal the existence of unsuspected regulatory interactions between the abd-A and Abd-B genes: whereas Abd-B m^– clones do not affect abd-A, in AbdB^– clones abd-A expression is eliminated. This is a surprising result, because it is contrary to what is observed in the embryo, where Abd-B represses abd-A (Foronda, 2006).

Abd-B m^– clones induced in the female A8 do not alter abd-A expression but do not change Abd-B expression levels either. This is observed with mutations that do not make Abd-B M protein, so the Abd-B protein detected is not the Abd-B M product. Surprisingly, although some Abd-B r expression is detected in the female A8, uniform Abd-B r expression is not seen throughout this primordium and Abd-B r transcripts seem not to be derepressed in Abd-B^M5 mutant clones. No explanation is available for this conundrum. Perhaps the probe used, although it includes sequences complementary to all of the Abd-B r cDNA sequences that have been published, does not efficiently detect all of the non-Abd-B m transcripts (Foronda, 2006).

The differences in regulatory and functional interactions among gene products in the embryo and the genital discs are not limited to those of Abd-B and abd-A that have been discussed above. Three other possibilities should be considered. (1) There may be changes in phenotypic suppression: the transformation of the eighth tergite to the fourth one in Abd-B m^– clones is due to abd-A. Because in these clones Abd-B protein is still present, this suggests that abd-A may phenotypically suppress Abd-B, differently from what is generally observed in the embryo. (2) Abd-B r represses Abd-B m in the embryo, but some Abd-B r^– clones do not activate Abd-B m in the male disc. (3) abd-A represses Dll in the embryo, but not in the female genital disc, and ectopic Dll can repress abd-A instead. abd-A does not repress Dll in the leg discs either, and this resembles Ubx function, which represses Dll only early in development. By contrast, Abd-B represses Dll in the embryo, in the larval genital disc, and in the leg disc when ectopically expressed (Foronda, 2006).

Abd-B r expression is restricted to the A9 segment in male genital discs, but shows expression in the A9 and in some cells of the A8 in female genital discs. In spite of this, Abd-B r^– clones in the external female genitalia (A8) are phenotypically wild type. In the male A9, some Abd-B r mutant clones eliminate Abd-B, activate Dll and transform part of the genitalia into distal leg or antenna. This is similar to the result obtained in some Abd-B^– clones, and it implies that Abd-B m is not derepressed in these mutant clones. However, Abd-B m is perhaps derepressed in those Abd-B r mutant clones where Abd-B signal remains (Foronda, 2006).

Although Abd-B r^– clones affect, almost exclusively, male genitalia development, Abd-B r hemizygous or trans-heterozygous flies lack genitalia and analia in both sexes. This probably reflects the absence of proper interactions between the different primordia needed for the growth of the genital disc. In Abd-B r mutant females, the internal genitalia are abnormal, and in some of these females, an absence of parovaria and the presence of three or four spermathecae is observed. This phenotype is consistent with a segment-autonomous transformation of A9 derivatives (parovaria) into A8 structures (spermathecae), similar to the embryonic cuticular transformation of A9 into A8 observed in Abd-B r mutations. A transformation of parovaria into spermathecae has been described in Polycomblike mutants, and may also indicate a transformation of A9 to A8 (Foronda, 2006).

These results illustrate that there are quite different Hox cross-regulatory interactions in the embryo and in the genital disc. The effects in the genital discs contradict the general rule that genes transcribed more posteriorly suppress or downregulate the expression of more anterior ones. This rule has, nevertheless, some exceptions in genes of the Antennapedia complex. Further, differences in Hox cross-regulation between the embryo and imaginal discs are not unprecedented: the proboscipedia (pb) Hox gene is positively regulated by Sex combs reduced in the embryo, but pb activates Sex combs reduced in the labial imaginal disc (Foronda, 2006).

It has been proposed that the primordia of female and male genitalia could be subdivided into an 'appendage-like' and a 'trunk-like' region). These two regions of the female A8 can now be defined more precisely. The 'appendage-like' region would be that expressing abd-A and low levels of Abd-B, and corresponds approximately to the presumptive internal female genitalia. This domain is roughly coincident with the region of expression of a reporter insertion in buttonhead, the gene that defines ventral appendage development, and this is also, approximately, the domain where Abd-B^– clones may activate Dll. If this subdivision is correct, the 'appendage' specification defined by buttonhead would be repressed in the wild type by Abd-B, which both limits Dll expression to a few cells of the A8 primordium and prevents Dll function. Abd-B^– clones in this region eliminate abd-A expression and promote leg or antenna development. This subdivision may also apply to the male disc, the penis apparatus presumptive region being the main 'appendage' domain. Similar to what is described in this study, the labial disc possesses a large 'appendage' region that is revealed by Dll derepression in pb mutations. This characteristic, and the changes in Hox gene cross-regulation between the embryo and the imaginal disc, are two features shared by pb/labial disc and Abd-B/genital disc (Foronda, 2006).

GENE STRUCTURE

Four classes of overlapping transcripts are generated from the Abd-B gene The transcription initiation sites for the class A (4.6 kb) and class B (3.4kb) transcripts show that they are generated from separate promoters. Both of these transcripts are present throughout the period during which the ABD-B subfunctions are required. A mutation that inactivates the morphogenetic function is associated with a 411bp deletion of the initiation site for the 4.6 kb RNA. Regulatory function mutations disrupt the transcription unit for the 3.4 kb RNA, but not the 4.6 kb RNA. A morphogenetic (m) function is assigned to the 4.6 kb RNA and a regulatory (r) function to the 3.4 kb RNA.

A 7.8 kb RNA expressed during embryogenesis may also contribute to the regulatory function. Sequence analysis of cDNAs indicates that the 4.6 kb RNA encodes the 55-kD morphogenetic protein, whereas the 3.4 kb RNA encodes a 30-kD regulatory protein. The m and r proteins share a carboxy-terminal sequence that includes the homeodomain, but the r protein lacks a glutamine-rich amino-terminal domain found in the m protein (Celniker,1989 and Zavortink, 1989).

Exons - four for class A transcript and five for class B transcript

Bases in 3' UTR - 1604

PROTEIN STRUCTURE

There are two variants to the ABD-B protein. One, a morphogenetic function can be assigned to the 55 KD protein and a second, regulatory function can be assigned to a 30 KD protein (Boulet, 1991).

Amino Acids

The class r 4.6 kb transcript encodes for a protein of 493 amino acids. The class m 3.4 kb transcript encodes for a protein of 270 amino acids (Zavortink, 1989).

See Four paralogous Hox clusters of mammals for homologies of Abd-B with mammalian Hox cluster genes.

date revised: 25 APR 97  

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