Gene Dmel\bcd

Maternal-effect lethal mutations showing defective head and thorax development. Females homozygous for strong alleles produce embryos in which head and thorax are replaced by duplicated telson, including anal plates, tuft, spiracles, and filzkorper; however, no pole cells formed at the anterior end. Deletions and fusions of anterior abdominal segments and occasionally anterior abdominal segments in reversed polarity are also observed. Strong alleles amorphic based on phenotypic similarities of embryos produced by homozygous and hemizygous females. Weak alleles result in pattern defects in heads of embryos; lack only labral derivatives (median tooth, dorsal bridge); intermediate weak genotypes produce reduced head but retain normal thoracic development; intermediate strong produce further reduction of head, deletion of second and third and reduction of first thoracic dentical belts; thoracic segments fused. Partial rescue of embryonic phenotype effected by injection of cytoplasm (5% of volume) from the anterior ends of unfertilized wild-type eggs into the anterior pole of newly fertilized eggs of bcd mothers; injection into ectopic sites stimulates differentiation of anterior structures at site of injection; efficiency proportional to number of bcd+ alleles carried by cytoplasm donor. Phenocopies result from leakage of 5% of egg volume from anterior perforation of normal embryos. The distance of the head fold at gastrulation is proportional to the number of bcd+ alleles in the maternal genotype. bcd mRNA appears as a flattened disc plastered to the anterior extremity of early embryos; by the time of pole cell migration it has become localized to the clear cytoplasm at the periphery, forming a cap over the anterior end of the egg and is distributed in a steeply decreasing gradient such that 90% of the RNA is in the anterior 18% of egg length; by nuclear cycle 14 the RNA begins to disappear and becomes undetectable by midway through cellularization. bcd protein on the other hand forms a shallower gradient in which 57% of protein is in the anterior 18% of egg length, and the gradient doesn't reach baseline until the posterior 30% of egg length; the gradient forms from two to four hours after oviposition in both fertilized and unfertilized eggs, and except during mitosis is concentrated in nuclei; diffusion postulated to account for the establishment of the protein gradient following translation from anteriorly anchored RNA. Protein levels decrease during cellularization, although some nuclear staining persists until the end of germ-band elongation. bcd transcript first detectable in the ovaries of bcd females; forms a ring around the anterior margin of the developing oocyte in stages 5 and 6; in stages 9 and 10 nurse-cell accumulation observed to be localized toward the periphery of the cyst; by stage 12 the nurse cells have emptied their contents into the oocyte and the bcd transcript appears as an anterior cap (St. Johnston, Driever, Berleth, Richstein, and Nusslein-Volhard, 1989, Development Supplement: 13-19). No evidence of translation of bcd protein during oogenesis. Formation of the bcd gradient is regulated by three maternally active genes exu, sww, and stau; exu appears necessary for nurse cell accumulation; sww is required for anterior localization of bcd mRNA in the oocyte; and stau appears to be involved in RNA localization in the embryo. A defect in any of these functions results in little or no gradient of bcd activity. bcd in turn appears to control the activity of anterior gene activity; specifically the anterior pattern of hb expression is not observed and is replaced by a mirror-image posterior hb stripe in bcd- embryos (Tautz, 1988, Nature 332: 281-84; Schroder, Tautz, Seifertz, and Jackle, 1988, EMBO J. 7: 2881-87).