Eyes from newly eclosed flies homozygous for the mutant chromosome Patj[synhypo], which consists of Df(3L)MY10 carrying the rescue fragments α-SpecUbi-p63E.PP, dltUbi-p63E.PP and Cdc37+t9.5 (which rescues Cdc37 and the N'terminal of Patj), show malformation or loss of photoreceptor rhabdomeres at low frequency. Eyes from 7 day old mutants reveal severe disruption in the proximal region toward the basement membrane of the retina. Rhabdomeres show a graded phenotype, abnormally shaped or missing in the proximal half of the eye but relatively well organised in the distal region towards the surface of the eye.
Flies homozygous for the mutant chromosome Patj[synnull], which carries the genomic rescue fragment Cdc37+t9.5.Δdpatj (lacking the coding region of Patj), in combination with α-SpecUbi-p63E.PP and dltUbi-p63E.PP recombined onto a Df(3L)MY10 mutant chromosome, die during second instar larval development. Flies heterozygous for Patj[synnull] in combination with Df(3L)MY10 are also second instar larval lethal. Patj[synnull] mutant clones show severe disruptions in rhabdomere development and partial or complete loss of photoreceptor in ommatidia.
Df(3L)MY10 flies with rescue transgenes for Cdc37, α-Spec and dlt but not for Patj (Cdc37+t9.5, α-SpecUbi-p63E.PP and dltUbi-p63E.PP) have typical planar cell polarity defects in the eye, including misrotated ommatidia and R3/R3 symmetrical clusters.
Df(3L)MY10 mutant flies in which the genes α-Spec and Cdc37 are complemented by the transgenes α-SpecUbi-p63E.PP and Cdc37+t9.5 have small eye discs that often lack the antennal part, similar to dltA1 mutants. Complementation of α-Spec, Cdc37 and dlt in a Df(3L)MY10 background generates viable, fertile female flies.
Homozygous clones of cells (in which Cdc37 function has been rescued with Cdc37+t9.5) induced before the follicular epithelium (FE) forms do not form an FE, resulting in follicles with gaps in the FE.