Local transposition of the P{PZ} element in CG4614602637, resulting in a P{PZ} element in the first exon of CG46146, 163bp downstream of the start codon.
Homozygotes are viable and develop normally without any visible phenotype in the eye.
PRAS40P17/+ partially suppresses the small eye phenotype caused by expression of PRAS40UAS.cCa under the control of Scer\GAL4ey.PU.
The P{PZ}PRAS40P17 chromosome was originally isolated as a lethal mutation that interacted genetically with an allele of L, enhancing the Lsi/+ eye phenotype (FBrf0151277). However, the lethality is a second site mutation and is separable from the P{PZ}PRAS40P17 insertion. A P{PZ}PRAS40P17 chromosome in which the second site lethal has been removed is homozygous viable, does not show any visible eye phenotype and does not modify the eye phenotype of L2.
Precise excision of the P{PZ} element reverts the mutant phenotype.