94% of eggs laid by homozygous females have minor defects in the dorsal appendages. 85% of eggs have an altered operculum which is expanded posteriorly and ventrally. Every eggshell with an enlarged operculum is also missing the collar structure at the operculum edge and the boundary between operculum imprints and mainbody imprints is rotated ventrally.
Homozygous somatic clones in the ovaries produce defective eggs that are small and infertile, with short dorsal appendages that are variably rounded with branched split ends (approximately 5% of eggs laid by bunrI043 females 2-3 days following homozygous clone induction have this phenotype).
Semilethal; homozygous escapers have slightly small, rough eyes, the roughness is predominantly due to missing photoreceptors. In the heads of adult homozygotes the R7 and R8 axons often project anteriorly relative to their wild type position. This phenotype reflects the failure of the medulla to undergo its normal developmental rotation between 39 and 48 hours of pupal development. Homozygous escapers exhibit loss of parts of the wing margin.
Mutant phenotype is enhanced by S05671 or loss of one copy of hh (eye becomes smaller and rougher) and suppressed by aopyan-1 or loss of one copy of wg (restored to wild type). Double mutants of bunrI043 and the eye specific allele hhbar3 all die as pupae, although hhbar3 itself is viable. In double mutants of bunrI043 and the eye specific allele dppd-blk the frequency of survivors is decreased relative to the single bunrI043 mutant and the eye is extremely reduced due to differentiation of a very small number of ommatidia. The third instar larval eye imaginal disc exhibits a delay in neuronal differentiation relative to the morphogenetic furrow.
bunrI043 is rescued by buncDNA2.GMR
G. Rubin.
Complements: l(2)0181001810. Complements: Aats-thrk04910. Complements: aret01284.