Drosophila melanogaster’s distinctive morphology includes wings on the second thoracic segment (T2) and halteres on the third (T3). The molecular mechanisms that specify these structures are tightly controlled by homeotic (Hox) genes, particularly the Ultrabithorax (Ubx) gene, which suppresses wing development and promotes haltere formation on T3.

The Homeotic Gene Ultrabithorax (Ubx) and Its Function

Ubx encodes a transcription factor that regulates gene expression patterns during development to specify segmental identity. In particular, Ubx represses wing-specific genes in T3 imaginal discs, redirecting the developmental fate from wing to haltere. Its precise spatial and temporal expression is critical for normal body plan formation.

Molecular Basis of Wing to Haltere Transformation

Experimental mutations causing ectopic expression of Ubx in the second thoracic segment lead to conversion of wings into haltere-like structures. This transformation arises because Ubx represses key wing developmental genes such as Vestigial (vg) and modulates signaling pathways including Wingless (Wg), ultimately suppressing wing morphogenesis programs.

Classification as a Homeotic Mutation

Such transformations where one body part is replaced by another characteristic of a different segment are hallmark features of homeotic mutations. This confirms the functional significance of homeotic genes like Ubx in defining segment identity and morphological fate.

Analysis of Provided Statements

• Statement A: Ultrabithorax gene ectopically expressed in second thoracic segment — true.

• Statement B: Antennapedia gene ectopically expressed in second thoracic segment — false; Antennapedia mutations affect head to thoracic identity transitions, not wing to haltere.

• Statement C: A homeotic mutation — true, as wing-to-haltere transformations are classic homeotic phenotypes.

• Statement D: A mutation in a gap gene — false; gap genes regulate early segmentation and deletion, not homeotic transformations.

Correct Combination

The combination (4) A and C most aptly explains the molecular basis given the phenotype:

• Ectopic expression of Ultrabithorax in T2 leads to homeotic transformation of wings into halteres.