| PubMed Abstract |
During development of the adult Drosophila visual system, axons of the eight photoreceptors in each ommatidium fasciculate
together and project as a single bundle towards the optic lobes of the brain. Within the brain, individual photoreceptor axons
from each bundle then seek specific targets in distinct layers of the optic lobes. The axons of photoreceptors R1-R6 terminate
in the lamina, while R7 and R8 axons pass through the lamina to terminate in separate layers of the medulla. To identify genes
required for photoreceptor axon guidance, including those with essential functions during early development, we have devised
a strategy for the simple and efficient generation of genetic mosaics in which mutant photoreceptor axons innervate a predominantly
wild-type brain. In a large-scale saturation mutagenesis performed using this system, we recovered new alleles of the gene
encoding the receptor tyrosine phosphatase PTP69D. PTP69D has previously been shown to function in the correct targeting of
motor axons in the embryo and R1-R6 axons in the visual system. Here, we show that PTP69D is also required for correct targeting
of R7 axons. Whereas mutant R1-R6 axons occasionally extend beyond their normal targets in the lamina, mutant R7 axons often
fail to reach their targets in the medulla, stopping instead at the same level as the R8 axon. These targeting errors are
difficult to reconcile with models in which PTP69D plays an instructive role in photoreceptor axon targeting, as previously
proposed. Rather, we suggest that PTP69D plays a permissive role, perhaps reducing the adhesion of R1-R6 and R7 growth cones
to the pioneer R8 axon so that they can respond independently to their specific targeting cues.
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