The P{SUPor-P} insertion is within the first intron of slik.
In mutant wings, the columnar epithelium is abnormally thin. Many cells lose their capacity to remain intergrated in the epithelium and are extruded basally to form a disorganised mass. Many apoptotic cells are seen below the epithelial layer. Some of the extruded cells are alive and appear mesenchymal, having lost their polarized epithelial character. These cells produce F-actin rich filopodia and appear to acquire motile behaviour.
Homozygous larvae show a growth defect phenotype. Mutants are delayed with respect to growth and developmental timing. After 5 days the largest mutant larvae grow to about one-third of the size of controls. Relatively few progress as far as third instar larvae. Some larvae have an abnormally long lifespan. More than 5% of mutant larvae remain alive for 15 days and some reach a relatively normal third-instar larval size. slik1/slikKG04837 animals are viable, 90% of expected flies survive. slikKG04837/slik1 flies how a 15% decrease in viability. Nearly 40% of the wings in the surviving flies have defects. Most show curvature of the wing blade surface or small isolated vesicles. However 30% of affected wings show a stronger phenotype characterised by accumulation of vesicles and reduction in wing size. These defects correlate with an increased level of apoptosis in wing discs.
SlikKG04837/Slik1 has partially lethal - majority die phenotype, enhanceable by Raf7
SlikKG04837/Slik1 has increased cell death phenotype, enhanceable by Raf7
SlikKG04837/Slik1 has wing phenotype, enhanceable by Raf7
When heterozygous phl7 is added to slik1/slikKG04837 animals about 40% of animals survive(as opposed to 90%) and the penetrance of the wing phenotype is increased from 11% to almost 100%. The number of apoptotic cells seen also increases.
