RhoGAP100F^w46 homozygous MARCM clones of R7 photoreceptor neurons at 40-60 percent through pupal development (P40-60) have significantly reduced lifespan of bulbous growth cone filopodia (bulbs) at axon terminals, with significantly more transient bulbs, significantly fewer stable bulbs and no change in the total number of bulbs, compared to controls, with no effect on other filopodia; unlike controls there are timepoints during P60 where no bulbs are present; at P70, significantly fewer synapses are present, compared to controls; axons begin to retract at P40, and there is a low level of retraction by P70, unlike controls, which do not retract.

Most axon terminals of homozygous R7 photoreceptor cell clones are reduced in size compared to wild type and many fail to contact the M6 layer of the medulla. Many of those terminals that do contact M6 project thin extensions either beyond or within it. These extensions vary in length and orientation, can branch and often terminate in small bouton-like varicosities. The mutant axon terminals are indistinguishable from wild type at 24 hours after puparium formation (APF), but at 55 hours APF the defect of R7 axons failing to contact M6 is maximal. The mutant R7 axons do not project extensions at 55 hours APF, but extensions are visible by 72 hours APF.

R7 axon terminals in RhoGAP100F^w46/RhoGAP100F^CD animals often fail to contact the M6 layer of the medulla. Some R7 axon terminals project thin extensions beyond M6.