Sequence-specific transcription factor which is part of a developmental regulatory system that regulates segmental identity in the mesothorax. Provides cells with specific positional identities on the anterior-posterior axis.

(UniProt, P02833)

Null loss-of-function alleles result in embryonic lethality. Animals succumb at the end of embryogenesis and show homeotic transformations in the larval cuticle of the first, second, and third thoracic segments. Specifically the cuticle derived from parasegments 4 and 5 are transformed to a more anterior identity such that the posterior of the first thorax produces fragments of mouth hook material on its dorsal surface presumably owing to a new posterior labial identity, whereas the anterior of the second thorax resembles the first thorax. The anterior of the third thoracic segment is weakly transformed toward a T1-like identity. The posterior of T2 is presumably T1 like as there are no gnathal structures seen in this compartment. There are also partial loss-of-function mutations which allow survival into the larval, pupal, and adult stages. Those that allow adult survival produce animals in which the anterior of the dorsal mesothorax shows a transformation to prothorax. There are no other apparent defects associated with these lesions. Those "leaky" mutants which die in the pupal and larval stages show similar parasegmental transformations as the null alleles, except that only the parasegment 4 to 3 homeosis is generally apparent. Animals which survive to the pupal stage fail to evert their anterior spiracles resulting in a blunt appearance of the anterior pupa. This same phenotype is seen in genotypes which survive to the adult stage. These partial mutants in many cases are associated with chromosome rearrangements notably deletions which approach the locus from its distal end. Moreover these mutations have been shown to complement fully other seemingly null mutations. Subsequent molecular analyses have shown that these results are accounted for by the presence of two promotors, one, P1, distal to the other, P2. The partial mutants affect the ability of the P1 promotor to initiate transcription, while the complementing lesions inactivate P2. Null mutants affect the transcription unit and protein encoding portion of the gene which is common to both promotors (see below). X-ray induced somatic clones of Antp- cells demonstrate that the locus is required in the adult for the proper development of the dorsal pro and mesothorax, and legs. The former is reduced in size presumably reflecting an anteriorward transformation while the latter are transformed to antennae. Thus Antp+ function is required in the embryo and adult in parasegments 4 and 5 to prevent more anterior segmental identities, specifically those normally found in the anterior thorax and head. The Antp locus was initially recognized by virtue of several striking dominant gain-of-function alleles. Thirteen of these transform the antenna of the adult into a mesothoracic leg (Antp49, AntpB, AntpYu, AntpPw, AntpLC, AntpR, AntpWu, Antp50, AntpRM, Antp73b, AntpCB, Antp72j, and AntpNs). Three of these also have effects on the orbit of the eye and the vibrissal region of the ventral head (AntpRM, Antp72j, and AntpNs). There are also two dominant alleles (AntpCtx and AntpW) which transform portions of the head capsule (dorsal and posterior) and the eye to a dorsal mesothoracic identity. In some cases this includes the production of wing tissue in the eye. Finally, a unique dominant AntpHu produces bristles on the normally bald propleurae just ventral to the mesothoracic spiricle. This latter phenotype has been interpreted as the production of sternopleural bristles on the propleurae, and thus a T1 to T2 transformation. With the exception of AntpNs and Antp72j all these dominant lesions are associated with recessive lethality and gross chromosome rearrangements. All the breakpoints fall in the interval between the distal and proximal promotors. The dominant gain-of-function phenotype results from the misregulation of the P2 promotor by position affect or by the production of novel transcripts initiated in the newly juxtaposed sequences and spliced to the downstream Antp coding sequences. Both events result in the ectopic accumulation of the Antp protein product in the eye-antennal disc where the normal head repressive function of the gene causes the observed alteration. The recessive lethality associated with these lesions falls into the partially deficient category mentioned above. That is, these lesions show complementation with the P2 specific (Antp1 and Antp23) mutations and in general show only strong parasegment 4 -> parasegment 3 transformations. However, there is a gradient of this affect among the breakpoints. Those closest to P1 and furthest from P2 are the weakest, whereas those close to P2 show the strongest phenotype and earlier lethal phase. This same result is obtained with breakpoint mutations in the P2-to-P1 interval which are not associated with a dominant phenotype. Therefore this interval likely contains sequences necessary for the proper regulation of the P2 promoter. Three of the dominant gain-of-function lesions (AntpHu, Antp73b, and AntpNs) have been reverted. The revertants are either complete nulls, thus obviating the potential for ectopic expression, or are partial mutants; the latter mutants likely remove the potential for ectopic expression by altering the juxtaposed sequences required for abnormal P2 activity. Both in situ hybridization and immunostaining have been used to determine the spatio-temporal pattern of Antp expression. Both the protein and RNA are strongly accumulated in the ventral nerve cord and more weakly in the epidermis and mesoderm of the embryo. Protein and RNA are first detected during cellular blastoderm in a band of cells in the parasegment 4-6 anlagen. This initial spatial pattern is further elaborated at full germ-band extension. In the ectoderm Antp products are found starting in the region of the first thoracic segment (parasegments 3 and 4) and extending posteriorly to the level of the seventh abdominal segment. In the mesoderm, they are found in parasegments 4-6. During germ band shortening the gene products are accumulated in the CNS from parasegment 4 (posterior T1) through to the posterior end of the ventral nerve cord. In the integument transcripts and protein are mainly restricted to the parasegments 4-5 interval although some weak expression can be seen in parasegments 3. As embryogenesis proceeds, the posterior CNS expression diminishes but is still detectable at the end of embryogenesis. The major accumulation in the CNS at this time is in the neuromeres of parasegments 4 and 5. The mesodermal expression is found in the anterior midgut; quenching of Antp expression is found in the posterior portion of the anterior midgut and has been shown to be dependent on the expression of Ubx. In later stages Antp protein can be detected in the leg, dorsal prothoracic, and wing discs.

Males and heterozygous females show variable expression from small additional segment on the third antennal segment to a nearly complete leg including femur, tibia, and tarsus. Arista usually present. Homozygous females lethal but X0 males survive. Crosses involving either Apx males or females produce many inviable embryos.