AbdB, iab-7, Mcp, Fab-7, iab-6
Gene model reviewed during 6.02
Double stop-codon suppression (UGA, UAG) postulated; FBrf0216884.
Gene model reviewed during 5.44
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 6.04
7.8, 4.7, 4.3, 3.7, 3.3 (northern blot)
The ABD-BI protein corresponds to ABD-BII with a large N-terminal extension; the two proteins contain the same homeodomain. There are two strong transcriptional activation domains in the common part of the two proteins. The ABD-BI-specific exon contains additional transcriptional activation potential, although it is a weaker transcriptional activator than the ABD-BII, apparently due to inhibitory sequences in the ABD-BI-specific exon.
ABD-BI corresponds to ABD-BII with a large N-terminal extension; the two proteins contain the same homeodomain. There are two strong transcriptional activation domains in the common part of the two proteins. The ABD-BI-specific exon contains additional transcriptional activation potential, although it is a weaker transcriptional activator than the ABD-BII, apparently due to inhibitory sequences in the ABD-BI-specific exon.
Antibodies that recognize both the 272aa and 493aa Abd-B proteins were made as well as an antibody specific to the 493aa form of the protein.
The antibody reported in
this paper recognizes both the Abd-B-m and Abd-B-r proteins.
The expression pattern is a composite pattern for the ABD-BI and ABD-BII proteins.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Abd-B using the Feature Mapper tool.
Comment: reported as posterior spiracle specific anlage
Comment: pattern is specific to transcript Abd-B-RB
Comment: pattern is specific to transcripts Abd-B-RA, Abd-B-RC, Abd-B-RD, Abd-B-RE
Comment: restricted to most posterior 4 nuclei of A8 in dorsal vessel
abd-A is expressed in the NB5-6A lineage starting at embryonic stage 11 in segments A7-A9.
Abd-B protein is detected in embryonic nuclear extracts.
At embryonic stage 15, Abd-B protein is expressed in two lateral anterior clusters of 6-7 cells in the genital disc, where it colocalizes with hdc, but is absent from the posterior cluster of hdc-expressing cells.
The Abd-B protein is expressed in a subset of the nuclei of larval fat body cells with an anterior boundary of A4 and a posterior limit of A8. Specific labeling of polytene chromosome bands by Abd-B antisera can be mapped from nuclei accumulating this protein.
Protein is detected in the posterior most section of the embryonic dorsal vessel in 3 pairs of cardioblasts.
The 272aa Abd-B protein is present in parasegment 14. Mutants affecting "r" function have greatly reduced levels of protein in parasegment 14.
The level of protein is highest in parasegment 13 at stage 12 and is high in parasegments 11-13 at later stages.
The Abd-B protein is first detected in stage 10 embryos in the anterior region of parasegment 15, parasegment 14 and the posterior region of parasegment 13. By stage 11, the anterior boundary of Abd-B expression is expanded into parasegment 11, and expression is detected mainly in the visceral mesoderm of parasegments 11-13. By stage 13 of embryogenesis, the anterior boarder of expression is extended into parasegment 10 of the ectoderm.
Abd-B protein is expressed in the embryo starting in stage 8. It is detected in the ectoderm and mesoderm of parasegments 13-15 and in the mesoderm of parasegments 11 and 12. It is strongly expressed in the CNS at germband retraction. CNS staining is strongest in parasegment 14 and diminishes in parasegments 12 and 13. It is also expressed in Malpighian tubules, in visceral mesoderm, in cells surrounding the posterior spiracles, and in the proctodeal primordium. In Pc embryos, Abd-B protein can be detected in the ectoderm and neuromeres of all segments.
Abd-B protein is expressed in the embryo starting in stage 8. It is detected in the ectoderm and mesoderm of parasegments 13-15 and in the mesoderm of parasegments 11 and 12. It is strongly expressed in the CNS at germband retraction. CNS staining is strongest in parasegment 14 and diminishes in parasegments 12 and 13. It is also expressed in Malpighian tubules, in the visceral mesoderm, in cells surrounding the posterior spiracles, and in the proctodeal primordium. In Pc embryos, Abd-B protein can be detected in the ectoderm and neuromeres of all segments. No labeling is observed in Abd-B-@ embryos.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Abd-B in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Source for merge of: Abd-B CG10291
Abd-B is required for the allocation of cells to the male and female genital disc primordia.
Abd-B is necessary and sufficient for specification of the male-specific somatic gonadal precursor cells.
Abd-B divides the primordium of the posterior spiracle into two cell populations that develop using distinct morphogenetic mechanisms into the spiracular chamber and the stigmatophore.
P-element insertions containing the Mcp-element and mediating pairing sensitive silencing of w expression are subject to long distance silencing interactions with other similar inserts. This occurs in cis or in trans. This effect is strongest between nearest neighbours, and weakens as the distance between the partners increase. Addition of more than two elements does not interfere with the silencing effect. The long distance regulatory activity of the Mcp element can be enhanced by placing it in a mini-w transgene which is flanked by scs and scs'.
Whenever a Hox gene functions as a repressor in the dpp enhancer it prevails over others that function as activators.
Genetic evidence demonstrates that lin is required for the function of the Abd-B protein, but not for the function of other Hox genes. In mutant embryos Abd-B protein expression is normal but incapable of promoting its normal functions: formation of the posterior spiracle and specification of the eighth abdominal denticle belt.
Abd-B is required for a subset of somatic gonadal precursors (SGPs) to maintain their identity and to maintain their association with germ cells.
Mutants are isolated in an EMS mutagenesis screen to identify zygotic mutations affecting germ cell migration at discrete points during embryogenesis: mutants exhibit germ cell migration defects.
The IAB5 enhancer element (which interacts with the Abd-B promoter in vivo) preferentially activates TATA-containing promoters when challenged with linked TATA-less promoters.
Abd-B MCP725 element is a silencer that functions throughout proliferation of the imaginal discs. MCP725-mediated silencing requires the Pc and Pcl proteins (it is likely that other members of the PcG also interact with the MCP725 silencer).
The Fab-7 region can be subdivided into a chromatin domain boundary and a Polycomb-response element.
Abd-B is one of a class of genes with TATA-less promoters that have a subset of the conserved DPE sequence.
Ectopic expression of Ubx, abd-A and Abd-B cause similar transformations in the appendages (antenna and wing) but different transformations in the main body axis. abd-A, and to some extent Abd-B, can form haltere-like tissue in the absence of Ubx.
The expression pattern of a number of genes in the larval genital discs, including Abd-B, has been studied to determine the segment-parasegment organisation of the genital discs.
Abd-B function is required for and plays a distinct role in the development of gonadal precursors. abd-A and Abd-B act together to specify a posterior subpopulation of gonadal precursors. Proper regional identities of the gonadal precursors are required for the arrest of migration at the correct position.
Abd-B expression is controlled by gap gene activation of iab regulatory regions at the blastoderm stage, monitored by the distribution of iab transcripts along the embryo anterior posterior axis. Overall orientation not stated: abd-A- iab-4? CG10349? anon-89Ec? Abd-B-
The iab6 and iab7 elements can regulate Abd-B in trans. This regulation is insensitive to rearrangements that disrupt transvection effects at the nearby Ubx locus. A transposed Abd-B transcription unit and promoter on the Y chromosome can be activated by iab elements on the third chromosome. Breaks causing abd-A mutations on rearrangement chromosomes that break in the iab7 region induce the iab elements to switch their target promoter from Abd-B to abd-A.
The iab-5, iab-6 and iab-7 regulatory regions of Abd-B can promote fifth and sixth abdominal segment identities in the absence of an Abd-B gene in cis, by acting on the Abd-B gene in trans. The interaction is proximity-dependent and is an example of transvection. This transvection is independent of local synapsis, and is remarkably difficult to disrupt by heterozygosity for chromosome rearrangements. This suggests that the iab-5,6,7 region can locate and interact with Abd-B over considerable distances. The ability of iab-5,6,7 to act in trans requires the presence of a relatively small region located between distal iab-7 and Abd-B. The iab-5,6,7 region transvection is independent of the allelic state of z.
The organisation of the tail region of the embryo is documented from studies of cuticular markers enabling a more direct comparison between homologous structures on the embryo and larval cuticle.
The role of Fab-7 as a boundary element may be restricted to particular tissues in which the homeotic genes are active.
Heat shock induced expression of mouse Hox genes in Drosophila embryos deficient for homeotic genes demonstrates that functional hierarchy is a universal property of the homeobox genes. Correlations exist between the expression patterns of the mouse Hox genes along the antero-posterior body axis of mice and the extent of their effect along the antero-posterior body axis of flies.
Abd-B protein homeodomain regions binds preferentially to a sequence within an unusual core, which differs from the binding sequence of Antp, Ubx and Dfd. N-terminal amino acid differences are responsible for the sequence specificity difference between Abd-B and Ubx.
Characterisation of Mcp mutation maps the sequences required for Mcp function to a DNA segment of about 0.4kb. The sequence and chromatin organisation of Fab-7 and Mcp have been compared.
Ubx and abd-A have equivalent functions in promoting the formation of particular muscle precursors in the abdominal segments, while Abd-B suppresses these same myogenic cells in the posterior region of the abdomen. Either Ubx or abd-A can override the inhibitory effect of Abd-B, when expressed in the same mesodermal cells. Homeotic cues specific to both the mesoderm and ectoderm cooperate to specify the pattern of muscle attachment sites.
Inactivation of Abd-B is not accompanied by substantial change in the accessibility of the chromatin fibre.
trx exerts its effects by positively regulating homeotic gene expression, but Ubx, Antp, abd-A, Abd-B, Scr and Dfd have different tissue-specific, parasegment-specific and promoter-specific reductions in expression in a trx mutant background.
The 3' flanking region of Abd-B includes three silencer regulatory regions, IAB5, MCP and Fab-7, whose function is dependent on segmentation gene products. hb may have a role in early anterior Abd-B repression and is required to promoter silencing, and Kr is necessary to define the anterior limit of Abd-B expression and to promote silencing in the middle region of the embryo. The kni repressor may be responsible for the graded expression of Abd-B protein within the embryonic Abd-B domain.
Sperm transfer defect.
The 3' regulatory region of Abd-B may be based on reiterated cell type specific elements controlled by adjacent position-sensitive activating elements. The gradient of Abd-B expression normally observed in the posterior abdomen appears to be achieved by varying the number of reiterated elements that are active in each segment.
An insulating boundary element in the 'Fab7' region is characterized by an unusual chromatin structure.
Boundary elements in the bithorax complex, such as Fab-7 organize the parasegment specific cis-regulatory sub-regions into a series of autonomous domains, insulating each domain from the regulatory influences of the adjacent ones.
Fab-7 and Mcp region chromatin structure contain distinct chromatin structures that display similarities to the scs and scs' structures of the Hsp70A locus, and are constitutive. Deletion analysis demonstrates that the DNA segment required for Fab-7 function contains 3 nuclease hypersensitive regions and that for Mcp function contains 1 major hypersensitive region and 3 minor nuclease hypersensitive regions.
Different homeotic genes have specific local effects on Dfd expression.
The gene products of Abd-B and Ubx compete for the specification of segmental identities in a dose-dependent fashion, supporting a quantitative competition model rather than strict functional hierarchy for their cross-regulatory interactions.
Abd-B is a member of the bithorax complex. The bithorax complex is a gene cluster that functions to assign unique identities to body segments in the abdomen and posterior thorax. Most, perhaps all, the bithorax complex functions are expressed within parasegments, metameric units composed of the posterior compartment of one segment and the anterior compartment of another. Complementation studies indicate that the bithorax complex is organized into three large functionally integrated regions, known as the Ultrabithorax (Ubx), abdominal-A (abd-A), and Abdominal-B (Abd-B) domains. The Abd-B domain functions primarily to assign identities to parasegments 10 to 14.
Heterozygotes for null alleles show weak anteriorly-directed transformations of A5, A6 and A7. In the male, this results in the presence of a tiny extra tergite in A7 and a loss of pigmentation on the A5 tergite. Heterozygotes are partially to completely sterile in both sexes, but are fertile if a duplication for the BXC (such as Dp(3;3)P5 or Dp(3;1)P68) is present. Hemizygotes and homozygotes are lethal; embryos lack posterior spiracles and filzkorper, have the ventral setal bands of A6, A7 and A8 transformed toward A5 or A4 and develop rudimentary chitinized plates in posterior A8. iab5 alleles are recessive: Hemizygotes show strong transformation of A5 toward A4, resulting in a loss of black pigment in the A5 tergite of the male. In addition, A6 may be weakly transformed toward A4. When homozygous, Abd-Biab5-301 causes a weak transformation of A3 toward A4 as well as a transformation of A5 to A4. iab6 alleles are recessive: Hemizygotes show strong transformations of both A5 and A6 toward A4. Males show a loss of pigment on the A5 and A6 tergites and show the development of bristles on the A6 sternite. Some alleles cause weak transformations of A4 toward A5. iab7 alleles are recessive: Hemizygotes show strong transformations of A5, A6 and A7 toward A4. In males, the A5 and A6 tergites show a loss of pigmentation and an unpigmented A4-type tergite develops in A7. Both A6 and A7 show the development of sternites with bristles. Heterozygotes show a small A7 tergite in the male. Two gain-of-function alleles recorded. Abd-Biab7-Spth (split thorax) heterozygotes display a longitudinal furrow in the mesothorax; Abd-Biab7-SGA heterozygotes causes abdominal structures to develop in the back of the head. iab8 alleles are recessive: Hemizygous adult males show strong transformation of A5, A6, A7 toward A4. In addition, an A8 tergite develops which is half the size of a normal tergite. In these males, A5 and A6 tergites show a loss of pigmentation and an unpigmented A4-type tergite develops in A7. A6, A7 and A8 all develop sternites, the first two with bristles. iab9 alleles are recessive except for one allele: Adult homozygotes or hemizygotes show absent or defective genitalia and analia in both sexes. Adults homozygous or heterozygous for Abd-Biab9-65 show in addition a partial transformation of A6 toward A7. Embryos hemizygous for iab9 mutations show the development of a zone of naked cuticle and a rudimentary ninth abdominal setal belt posterior to the eighth abdominal setal belt. Posterior spiracles are absent in Abd-Biab9-65 and Abd-Biab9-48 hemizygotes and are defective in Abd-BUab-1, Abd-Biab9-tuh-3 and Abd-Biab8-rv107 hemizygotes. Abd-Biab9-65 and Abd-Biab9-48, but not the other iab9 mutations, cause transformations of the A8 setal belt (located in anterior A8) toward A7. Mcp homozygotes have the fourth (A4) and fifth (A5) abdominal segments transformed to a state intermediate between A5 and A6. Similar, but weaker, transformations occur in Mcp/+ heterozygotes. Abd-BMcp-1 can be scored in males by dark pigmentation of the A4 tergite and in females by an effect on the orientation of the lateral bristles of the A4 tergite. Abd-BSab-1/+ adults show patchy transformations of A3 and A4 to A5. Homozygote viable and more extreme than heterozygote. Abd-BMcp-1 Abd-BSab-1 homozygotes show transformations of A3, A4 and A5 to a state intermediate between A5 and A6.
Abd-B consists of two distinct elements: a morphogenetic (m) function in parasegments 10-13 and a regulatory (r) function in parasegment 14.
Abd-B r protein is present throughout development and m protein is detected after germ band extension.
Abd-B has two genetic elements m and r that are required in parasegments 10--13 and parasegment 14 respectively.
The iab5, iab6 and iab7 classes of Abd-B alleles fail to complement m mutations but complement r.
Homeotic gene activity programs primordia as either discs or histoblast nests by the early extended germ band stage.
The substitution of the Abd-B homeodomain for that of Dfd results in a protein that differs from the Dfd protein at only 30 residues so providing a different spectrum of regulatory targets. Heat shocked embryos carrying the chimeric gene exhibit ectopic expression of Abd-B in parasegments 9--12.
High levels of Abd-B product are required to down-regulate abd-A gene expression. Abd-B has two distinct functions, m and r. The m function is specific to parasegments 10, 11, 12 and 13, r function to 14 and 15.
Abd-B r protein expression demonstrates that r function is required for normal morphogenesis of the larval epidermis.
The iab region is transcribed showing distinct and spatially restricted patterns of hybridisation but no transcripts are localised to specific abdominal regions. Expression patterns at blastoderm follow an antero-posterior order and suggest an initial double parasegment subdivision for the activation of the bithorax complex. Hybridising probes of genomic DNA fragments to embryonic tissue sections did not find any previously unknown transcription units.
The position of the Abd-B expression domains in the visceral mesoderm have been defined with respect to parasegment boundaries.
In the absence of the bithorax complex genes, Pc- clones develop prothoracic patterns: Scr activity overrules Antp. Adding contributions of Ubx, abd-A and Abd-B results in thoracic or abdominal patterns.
A transcript (pH189) encoding a small homeoprotein that may provide Abd-B r element function has been identified.
Embryos lacking Abd-B develop into larvae in which abdominal segments 5-8 appear to develop like the normal 4th abdominal segment, indicating a transformation of parasegments 10-13 into parasegment 9. This phenotype is extended to several head segments as well as the thoracic and abdominal segments when the embryos are also mutant for esc. Embryos lacking both abd-A and Abd-B develop into first instar larvae in which all eight abdominal segments appear to be composites of the anterior compartment of A1 and the posterior compartment of T3. Embryos also mutant for esc show this same pattern in a head segment, the cryptic ninth abdominal segment and the three thoracic segments, as well as the other abdominal segments.