P-element induced male recombination using P{GSV6}GS16964 as the progenitor has resulted in the deletion of the entire caps gene without disrupting any other genes apart from one tRNA gene.
~52 kp deletion resulting from P-element induced male recombination using P{GSV6}GS16964 as the progenitor removes the entire caps gene. Deleton boundaries from published sequence.
Large eye clones of capsDel1 mutants exhibit defects in the medulla and R8 axon guidance. However, there are no defects in R8 axon bundling nor undershooting of the M3 target layer. capsDel1 R8 axons extend over their target layer M3 and terminate at M4 or M5 at very low frequency. In contrast, capsC28fs mutant R7 axons do not show any targeting phenotype.
capsDel1 has abnormal neuroanatomy phenotype, non-enhanceable by trn28.4
capsDel1, trn28.4 has abnormal neuroanatomy | somatic clone phenotype
capsDel1 has photoreceptor cell R8 phenotype, non-enhanceable by trn28.4
capsDel1, trn28.4 has antennal lobe projection neuron of ALl1 lineage | somatic clone phenotype
capsDel1, trn28.4 has embryonic/larval salivary gland phenotype
capsDel1, trn28.4 has eye disc | cell non-autonomous phenotype
capsDel1, trn28.4 has eye disc morphogenetic furrow | cell non-autonomous phenotype
capsDel1, trn28.4 has ommatidium | cell non-autonomous phenotype
Lateral neuroblast clones in the antennal lobe that are doubly homozygous for capsDel1 and trn28.4 show two types of dendrite targeting defects; loss of innervation in glomeruli that are normally targets of lateral projection neurons and gain of innervation in glomeruli that are normally not the targets of lateral projection neurons. Loss of innervation of the VA7m, VC1 and VC2 glomeruli is frequently seen in the double mutant embryos.
trn28.4 capsDel1 double mutant clones in the eye disc show subtle but consistent defects. At the clone border, there is a consistent reduction in the apical constriction of cells. This phenotype is fully penetrant, but appears more pronounced when the clone boundary is perpendicular to the morphogenetic furrow. Within the morphogenetic furrow, cells at the clone boundary are also taller than their neighbours, as their apical surfaces are elevated, disrupting the furrow. The phenotypes of relaxation of apical constriction and increase in apical-basal height of cells are non-autonomous as they are seen in both mutant and wild-type cells at the clone boundary. The range of the phenotype is only 2-3 rows of cells beyond the clone border.
trn28.4 capsDel1 double mutant clones in the third instar eye disc result in a perturbation in ommatidial spacing. This is only apparent at the boundaries between mutant and wild-type cells, where ommatidia close to these boundaries are often clearly displaced from their normal positions with no obvious change to their individual morphology. The total number of ommatidia is not affected. This phenotype is non-autonomous, with both mutant and wild-type ommatidia showing mis-positioning. At pupal stages of development, spacing defects are still seen in eye discs with trn28.4 capsDel1 double mutant clones, and fusion of neighbouring ommatidia that are abnormally close to each other is seen in about 5% of ommatidia adjacent to clone boundaries. Very occasional defects are seen in the number of cone cells.
trn28.4 capsDel1 double mutant clones in the wing do not perturb or cross the dorsal-ventral boundary.
