abdA, iab-2, iab-4, Hab, iab4
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.48
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\abd-A using the Feature Mapper tool.
abd-A is expressed in the NB5-6A lineage starting at embryonic stage 11 in segments A2-A9.
abd-A is expressed in the parts of the developing female reproductive system that correspond to the internal genitalia. In third instar larvae, abd-A protein expression is localized to the female genital disc, in the region corresponding to abdominal segment 8.
The abd-A protein is expressed in a subset of the nuclei of larval fat body cells with an anterior boundary of around A2 and a posterior limit near A7. Specific labeling of polytene chromosome bands by abd-A antisera can be mapped from nuclei accumulating this protein.
Protein is detected in the posterior of the embryonic dorsal vessel exactly overlapping the region that becomes the heart. The protein is strongly expressed in cardioblasts and pericardial cells of abdominal segments A6 and A7. Lower levels expression are observed A5 and A8. Protein is also detected in the 4 posterior pairs of the 7 pairs of alary muscles.
abd-A protein is localized to cardial and pericardial cells of the heart from abdominal segment 5 through abdominal segment 8.
abd-A expression is observed in all of the cardioblasts in the heart region except in the most posterior cardioblasts in segment A8 or the two pairs of anterior-most cardioblasts in segment A5. It includes the two pairs of svp-expressing cells in A5 and the two last pairs of svp-expressing cells in A7. abd-A is also expressed in a subpopulstion of pericaridal cells in segments A5-A7.
A reduced level of abd-A expression is observed in parasegments 8-13, particularly in nuclei located in a dorsolateral position of the epidermis.
A reduced level of abd-A expression is observed in parasegments 8-13, particularly in nuclei located in a dorsolateral position of the epidermis. Ectopic abd-A expression is observed in some cells of the lateral epidermis of parasegment 6 and more rarely in parasegment 6 of the ventral nerve cord.
No major change in the pattern of abd-A expression was observed. Animals that are also homozygous for su(Hw)2 present ectopic abd-A expression in some cells of the lateral epidermis of parasegments 4-6 and in the ventral nerve cord.
Ectopic abd-A expression is observed in the ventral nerve cord in parasegment 6.
Df(3R)P-10 which removes the iab2 regulatory region and part of the abd-A transcription unit causes a gradient of expression of abd-A protein in the epidermis and a less evident gradient in the nerve cord. Staining is barely detectable in parasegment 7 and increases gradually posteriorly. In Abd-Biab9-Uab1 mutant embryos, there is a general reduction in abd-A levels and ectopic abd-A expression in the first abdominal segment and in parasegments 14 and 15. In embryo homozygous for Abd-Biab9-Uab1, Abd-Biab8-rv96 and sometimes Abd-Biab9-tuh-3, nuclei posterior to parasegment 13 stain for abd-A. The ectopic expression is in the posterior region of abdominal segment 8 and in some cells of the posterior region of abdominal segment 9.
abd-A protein is first detected in 4 hour embryos and persists through embryonic and early larval development. abd-A protein is expressed in parasegments 7-13 (PS7-13) which correspond to abdominal segements 2-7 (A2-7). Expression of abd-A is complementary to that of Ubx and highest levels are in the anterior of each parasegment. Throughout development abd-A is localized to the nuclei of expressing cells. At the beginning of germ band retraction, abd-A protein is detected in the mesoderm flanking the embryonic gut, surrounding the spiricle pits, the neuroblasts near the embryonic midline and in the developing tracheal tubes. Later in development expression is detected along the ventral nerve cord, and staining is more pronounced toward the posterior of the embryo. High levels of abd-A are detected along the anterior furrow of the gut sac and along the visceral mesoderm of the gut. Following dorsal closure, abd-A protein is detected in the pericardial cells and the lateral muscle fibers around the heart, as well as in the gonadal precursor and chordotonal organs.
abd-A product is observed in the normal domain in embryos, but the amount of antigen in A3-A7 appears slightly reduced with respect to wild type.
The anterior limit of abd-A protein is strictly parasegmental at parasegment 7. The posterior limit is less well defined. The expression is modulated within metameres with the strongest expression in the posterior compartments. In the anterior compartments there is a gradient which diminishes towards the posterior. abd-A protein is also present in the mesoderm but is out of register by one parasegment with respect to ectoderm expression and extends from parasegment 8-12. abd-A expression is observed in the ectoderm, the tracheal tree, the ventral nerve cord, the visceral mesoderm and the amnioserosa. Embryos homozygous for Df(3R)Ubx109 or Df(3R)P9 have no abd-A antigen. Ectopic expression of abd-A protein is observed in parasegments 13-15 (or subsets thereof) in several Abd-B mutants.
A reduced level of abd-A antigen is detected in abd-AP10 mutant embryos. The diminution is not uniform resulting in a gradient of antigen from almost none in A2 to higher levels in A6 and A7 segments.
abd-A protein is first detected at the germ band retraction stage in the visceral mesoderm of the midgut and in the ectoderm of parasegments 8-12.
abd-A protein is expressed in parasegments 7 through 13 in a segmentally repeated pattern. A gradient of the antigen is observed, with higher levels at the anterior border of the parasegments and lower levels toward the posterior. This gradient is not detected by in situ hybridization, and therefore, may be post-translationally regulated. Prominant expression is detected in the ventral nervous system.
GBrowse - Visual display of RNA-Seq signalsView Dmel\abd-A in GBrowse 2
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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 identity of: abd-A CG10325
The iab-8 ncRNA (and not Abd-B) represses the expression of the abd-A gene in the posterior central nervous system. This repression is accomplished by two redundant mechanisms: firstly via the mir-iab-8 miRNA produced from the iab-8 transcript and secondly by a mechanism that acts only "in cis". The most likely explanation for second mechanism is that iab-8 transcription interferes with the abd-A promoter, which lies just downstream of the iab-8 poly(A) site.
RNAi generated by PCR using primers directed to this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
A burst of abd-A expression in the postembryonic neuroblasts specifies the time at which apoptosis occurs, determining the number of progeny generated by each neuroblast.
"Uab" (Ultraabdominal) alleles show ectopic transcription of the "iab-2" regulatory region, which normally controls the differentiation of cells in the second abdominal segment (PS7). The ectopic transcripts are abundant in the cells of the first abdominal segment (PS6). It is not clear what site or function is affected by the ectopic transcripts.
the spatially restricted expression and activity of abd-A appears to determines heart identity in cells of the posterior portion of the dorsal vessel.
abd-A is required to confer a heart identity on cardiomyocytes in the developing embryo.
Subcellular localisation of exd is regulated by the BX-C genes and each BX-C gene can prevent or reduce nuclear translocation of exd to different extents. Ubx and abd-A require exd activity for their maintenance and functions.
Whenever a Hox gene functions as a repressor in the dpp enhancer it prevails over others that function as activators.
Mutants have been isolated in an EMS mutagenesis screen to identify zygotic mutations affecting germ cell migration at discrete points during embryogenesis.
The Pc protein is not distributed homogeneously on the regulatory regions of the repressed Ubx and abd-A genes, but is highly enriched at discrete sequence elements, many of which coincide with previously mapped Pc response elements (PREs).
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. Although exd product affects wing development the presence of exd fails to modify the wing to haltere transformation caused by ectopic expression of either Ubx or abd-A.
The expression pattern of a number of genes in the larval genital discs, including abd-A, has been studied to determine the segment-parasegment organisation of the genital discs.
Despite the absence of a syncytium in C.floridanum embryos monoclonal antibodies to en, Ubx and abd-A demonstrate their cognate proteins are expressed in a conserved pattern in the post-gastrulation stages of development. The expression of the eve cognate protein is not completely conserved and lacks a pair rule phase to its expression.
abd-A function is required for and plays a distinct role in the development of gonadal precursors. abd-A activity alone specifies the anterior gonadal precursor fate, 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. During late stages of gonadogenesis abd-A is required in a population of cells within parasegments 10 and 11 that partially ensheath the coalescing gonad.
abd-A 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-
Pc associates with multiple sites in the bithorax complex and these sites all contain maintenance element.
Ectopic expression of abd-A is able to rescue the early stages of gonad formation. Ectopic expression leads to the formation of ectopic gonadal tissue in the anterior segments. These cells behave like normal gonads, in that they condense with one another, but only in the abdominal segments are they colonised by pole cells.
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 iab5 element may trans-interact with abd-A similarly to the iab trans-regulation of Abd-B, and unlike the transvection effects at Ubx.
The transcription unit that produces the noncoding iab-4 transcript has been identified.
A 1.7kb fragment of the iab-2 regulatory region activates abd-A expression in parasegment 7. The products of Kr, hb and gt act at this enhancer. The 1.7kb fragment also causes pairing-dependent activation of a miniwhite marker in a P element.
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.
Initial distribution of abd-A product is approximately uniform within parasegments 7 to 13. Subsequent elaboration of the expression pattern results in differentiation between, as well as within, parasegments. Establishment of the original abd-A expression domain is independent of any pair-rule or segment polarity genes but most are required for the subsequent elaboration of the expression within its domain.
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.
Comparisons of early development to that in other insects have revealed conservation of some aspects of development, as well as differences that may explain variations in early patterning events.
Ectopic expression of dpp eliminates Scr and Antp expression, attenuating abd-A expression, inducing Ubx, dpp, wg and tsh expression in the visceral mesoderm and inducing lab expression in the apposing endoderm.
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.
Pattern of adult muscle precursors characteristic of embryonic thorax can be converted to abdominal pattern by ectopic mesodermal expression of abd-A, demonstrating an autonomous role for abd-A in mesodermal patterning.
The bithorax complex genes are regulated by the Pc group of genes, acting via 'Pc group response elements' (PREs), that can work even when removed from the normal the bithorax complex context.
Mcb region chromatin structure contains 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 Mcb function contains 1 major hypersensitive region and 3 minor nuclease hypersensitive regions.
Mutations of the iab4 allele group of abd-A transform epidermal structures of parasegment 9 and cause loss of gonads in adult flies. The gonadless phenotype of iab4 mutant can be rescued by nuclear transplantation with wild-type nuclei, marked with an Hsp70:lacZ transgene.
Different homeotic genes have specific local effects on Dfd expression.
Mutants of abd-A exhibit ectopic paired lateral dots in the abdominal segments of the larval CNS. Two copies of abd-A are required for the complete suppression of lateral dots in segments A2 through to A4 and in some but not all alleles other elements of the bithorax complex (iab-3 and iab-4) act in trans on the abd-A+ gene to increase its rate of transcription or processing in A3 and A4. This would result in higher level of lateral dot suppression in the corresponding segments.
abd-A 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-A domain functions primarily to assign identities to parasegments 7 to 13.
Null abd-A alleles are recessive lethal. Homozygous larvae show transformations of the ventral and dorsal setal belts of A2 through A8 toward A1. These transformations are complete in A2 through A4, but are incomplete more posteriorly. Partial Keilin's organs composed of monohairs occur variably on all segments from A1 through A7. In the adult cuticle, homozygous abd-A mitotic recombination clones are completely transformed to A1 in segments A2 through A4 and show characteristics of A1 to A4 in segments A5 to A7. Recessive mutations of abd-A belong to the 'infra-abdominal' iab2, iab3 and iab4 groups of E.B. Lewis; dominant mutations were described as 'Hyperabdominal', Hab. abd-AHab-1/+ has the third thoracic segment (T3) and first abdominal segment (A1) variably transformed toward the second abdominal segment (A2), occasionally resulting in the loss of one or both metathoracic legs and one or both halteres; an A2 type tergite and sternite appear on T3; but A1 is only weakly transformed toward A2. Strongly enhanced when mother is from stock of Df(3R)red-P93, l(3)tr1, Sb1/In(3L)P + In(3R)UbxP18, Me1 Ubx1. iab2 alleles are recessive: Adult homozygotes or hemizygotes show transformations of A2 toward A1. The known alleles cause only partial transformations. Wheeler's organs (A2 structures) are reduced or absent and A2 tergite bristles are reduced in size. These alleles do not affect the larval cuticle pattern. iab3 alleles are recessive: Hemizygote and homozygote have third, fourth, fifth and sixth abdominal segments (A3, A4, A5 and A6) transformed toward the second abdominal segment (A2). The Wheelers Organ (normally only on A2) is now partially to fully developed on A3 to A6, inclusive. Hemizygotes are viable and show a loss of gonads in both sexes. In homozygotes A1 is weakly transformed toward A2. iab4 alleles are recessive: Both the hemizygote and homozygote are viable and have a transformation of A4 toward A3 as well as a weak transformation of A5 toward A4 or A3. Gonads are absent in both sexes (or partially developed in some alleles). In some of the alleles, A2 transforms weakly to A3, especially in the homozygote.
Homeotic gene activity programs primordia as either discs or histoblast nests by the early extended germ band stage.
Spatially restricted expression of dpp in the visceral mesoderm is regulated by the homeotic genes Ubx and abd-A. abd-A represses dpp expression in the visceral mesoderm cells of the anterior midgut. abd-A function is required for expression of wg in the visceral mesoderm posterior to dpp expressing cells.
A regulatory element in the iab-2 region programs abd-A expression with a proper anterior limit in parasegment 7 and a regulatory element in the iab-3 region programs proper anterior limit in parasegment 8.
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-A 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.
Embryos lacking abd-A develop into larvae in which parasegments 7-10 appear cleanly transformed into parasegment 6 and parasegments 11-13 appear partially transformed into parasegment 6. 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.