1kb deletion in the promoter region.
mirre48/mirr1825 mutants survive at a low frequency to first instar larval stages.
In stage 16 mirre48/mirr1825 mutants the vdaB neuron is lost with 34% frequency, and this is preceded by SOP1a loss. However, all other ventral cluster MD neurons, as well as v'ada, are never lost.
In mirre48/mirr1825 mutant vdaB neuronal clones, the dendritic field coverage is significantly reduced to 84% of wild-type, and branches fail to fully fill the body wall. This is not associated with a change in dendritic self-avoidance. However, it is correlated with a similar reduction of dendritic branching to 86% of wild-type.
mirre48/mirr1825 mutant vdaB neuronal clones fall to send axon terminal branches across the midline. In 19% of clones, both branches fail to cross the midline, and in a further 37% only the posterior branch crosses.
The majority of eggs derived from egg chambers containing complete homozygous follicle cell clones lack dorsal appendages.
Defects in encapsulation of the 16-cell cyst and separation from the germarium are seen in egg chambers of mirr6D1/mirre48 females. A reduction or loss of dorsal structures is seen in egg chambers; in stage 14 egg chambers the operculum has only 30 +/- 2.6 cell imprints (compared to the wild type number of 43 +/- 5.2). Dorsal appendages may be missing.
Homozygous clones in the eye affect ommatidial polarity.
Clones of cells homozygous for mirre48 in the notum induced during the first or second larval instar show malformations. Notum is transformed to wing hinge, with sclerites and tegula-like cuticle with characteristic sensory structures.
Homozygous clones in the eye can result in the formation of an ectopic equator. The formation of the ectopic equator is restricted to the segments of clonal borders that are located within the anterior third of the eye. Homozygous clones in the dorsal part of the eye are significantly rounder than wild-type clones, while no significant difference in clone shapes is seen between homozygous and wild-type clones in the ventral part of the eye.
Adult transheterozygotes with mirrB1-12 exhibit outheld wings, the alulae are completely missing and bristle defects.
Clonal analysis reveals loss of mirr function in the ventral half of the eye has no effect. Dorsal clones also have no effect on ommatidial polarity or chirality within the clone. Ectopic equators are formed at the equatorial borders of dorsal anterior clones. Ommatidia just outside the clone adopt ventral polarity and chirality. Ventral patterning extends for one to two ommatidial widths. Clones along the equator divert the equator to follow the new border of mirr expression for a short distance before resuming the posterior-anterior eye rather than continuing to follow the edge of the clone. Embryonic cuticles are smaller than wild type with sparse denticles, anterior denticles are often missing, denticle rows 2 and 3 are often fused together.
mirre48 has abnormal planar polarity | recessive | somatic clone phenotype, suppressible by fng13
mirre48 has eye equator | ectopic phenotype, suppressible by fng13
mirre48 fng13 double mutant clones in the dorsal part of the eye are still rounder than wild-type dorsal clones. One to three ommatidia of ventral polarity are often generated at the polar boundaries of homozygous fng13 clones in the dorsal region of the eye, producing an ectopic "mini-equator". There is a dramatic increase in the number of ommatidia with polarity changes at this mini-equator if the clone is also homozygous for mirre48.
