Abstract
The Drosophila l(2)35Ba/nocA gene is involved in the development of the adult ocelli and the embryonic head. Mutations in this gene lead to at least two distinct phenotypes. Several larva lethal l(2)35Ba alleles cause both hypertrophy and mislocation of the embryonic supraesophageal ganglion (brain) to the dorsal surface of the embryo. A second class of mutant alleles (nocA) is homozygous viable, but the surviving adults either lack or have greatly reduced ocelli and associated bristles. The l(2)35Ba/nocA gene encodes an approximately 3.0-kb transcript doublet; all l(2)35Ba alleles which have been physically mapped delete or disrupt the transcribed region, whereas all of the viable nocA alleles are caused by gross chromosomal aberrations with breakpoints near the 3'-flanking region of the gene. Several nocA breakpoint alleles downregulate the level of l(2)35Ba/nocA transcripts in adults, and their defective ocellar phenotype also fails to be complemented by the lethal alleles, implying that l(2)35Ba and nocA are different phenotypic manifestations of mutations in the same gene. In the l(2)35Ba mutant embryos, cells from the procephalic lobe which normally migrate over and overlie the supraesophageal ganglion during head involution can become incorporated into the supraesophageal ganglion; many of these misplaced cells, which normally form the frontal sac, also adopt a neuronal fate. Sequence analysis of two full-length l(2)35Ba/nocA cDNAs with distinct polyadenylation sites shows that they encode the same deduced protein of 537 amino acids with a serine- and threonine-rich N-terminal region, two putative zinc finger motifs near the carboxyl terminus, and several alanine-rich domains. Consistent with the observed embryonic phenotype, l(2)35Ba/nocA shows a complex embryonic expression pattern which includes the procephalic lobe.