The epidermis of crb1 Kr1 double mutant embryos exhibit relatively normal distributions of cell polarity and junctional proteins. There is some suppression of the crb1 phenotype; a continuous, through reduced, cuticle sheet is formed.
KrmCD; Kr1/Kr1 enhances the reduction in later born neurons of the NB7-1 an NB2-3 lineages see in svp1/svp2 embryos so that U4 and U5 are almost completely eliminated, as are EW2 and EW3. This enhanced phenotype is partially suppressed if the embryos are also hb12/hb15.
The frequency of cuticular segmentation phenotypes in Kr1/+ first instar larvae is not significantly changed in animals with a egl3e/egl1 mutant mothers, however the identity of segments affected differs slightly: there are less defects in A1 and A2, and more defects in A3.
KrmCD, Kr1/+, caps05121/+ embryos show a SNb nerve phenotype, without affecting the ISN and SNa. In about 1/3 of cases the SNb stops along the ventral longitudinal muscles, ending with a large growth cone structure. In addition properly defasciculated RP axons fail to continue along their normal paths, a portion of them elongate and stall along their normal paths; a portion of them elongate and stall either in a position close to the transversal nerve or are directly connected to it. Kr1, caps05121 or Kr1, caps65.2 double homozygotes (that have been partially rescued by the addition of KrmCD) develop an even stronger phenotype; the SNb is absent in most of the double mutants analysed or do not extend beyond its second choice point close to muscle 28. In only a few cases the SNb stalls in the ventral muscle field. Fas2EB112/+, Kr1/+, double heterozygotes (that have been partially rescued by KrmCD) exhibit an axon guidance phenotype. The SNb enters the ventral muscle field normally in most cases but the nerve stops at the second choice point by forming a growth cone-like structure. No individual RP axons are observed.
Reduced maternal RpL36 activity increases the penetrance and severity of the segmental defects observed in larvae heterozygous for Kr or kni mutations. Heterozygous Kr or eve embryos derived from heterozygous l(2)41Ae34-4, Nipped-A1/+ females show increase in embryonic cuticular phenotypes.