<i>pnr</i> cooperate with <i>fred</i> to regulate SOP cell fate both positively and negatively in the medial notum of <i>Drosophila</i>.

According to the "Prepattern Hypothesis", the development of dorsal sensory organ precursors (SOP) in <i>Drosophila melanogaster</i> depends on the sequential regulation of prepattern genes, proneural genes, and neurogenic genes. In most cases, ectopic SOP formation caused by dysfunction of a single regulatory gene either exhibits spatial discontinuity or is restricted to proneural clusters. However, knockdown of the <i>fred</i> gene induces a novel phenotype of ectopic SOP that are spatially continuous and not confined to proneural cluster regions. This study reveals that <i>fred</i> knockdown-induced ectopic SOP formation is independent of proneural clusters, suggesting that nearly all wing imaginal disc cells possess neurogenic potential. Furthermore, we demonstrate that the prepattern gene <i>pannier</i> (<i>pnr</i>) cooperates with <i>fred</i> to regulate SOP cell fate through two distinct mechanisms: (1) <i>pnr</i> and <i>fred</i> are essential for endogenous SOP formation in the medial notum, while (2) they synergistically suppress SOP initiation outside proneural clusters. These findings challenge the canonical assertion in the "Prepattern Hypothesis" that SOP formation strictly relies on proneural cluster formation, thereby providing a critical extension to the hypothesis.