To address whether Bib and Dl colocalize, embryos were simultaneously labeled with Bib and Dl antibodies. The Bib and Dl proteins did in fact colocalize in the plasma membrane and in the punctate cytoplasmic structures of prospective mesoderm cells, although the intensity of the two signals was not always similar. In third instar wing discs, Bib expression is found in the proneural clusters for wing margin bristles, sensory organs along the dorsal radius and SOs of the notum, where there is a known requirement for bib . Previous studies suggest that bib functions in a pathway separate from the one involving Notch and other known neurogenic genes, that is, bib shows no genetic interactions with other neurogenic genes. Loss of bib function approximately doubles the number of neuronal precursors and their progeny cells in the embryonic peripheral nervous system.
Mosaic studies reveal a hypertrophy of sensory bristles in bib mutant patches in adult flies.
The neurogenic genes of Drosophila control mesoderm development. The mesodermal defect does not appear to be a simple consequence of associated neural hypertrophy, suggesting that the neurogenic genes may function similarly and independently in establishing cell fates in both ectoderm and mesoderm. Altered patterns of beta 3-tubulin and myosin heavy chain gene expression in the mutants indicate a role for the neurogenic genes in development of most visceral and somatic muscles. All of the neurogenic mutants show abnormalities in many different organs derived from all three germ layers. Abnormalities in tissues derived from the mesoderm were observed in all six neurogenic mutations.