lola^e76 homozygous stage 14 embryos show disrupted gonad formation, with disrupted germ cell migration; mutant stage 15/16 embryos show severe axonal growth and pathfinding defects at the ventral midline.

lola^e76/lola^46.38 and lola^e76/lola^22.05 transheterozygous embryos display a significant increase in defects in the fusion together and compaction of primordial germ cells and somatic gonadal precursor cells, as compared to controls.

Dendritic wiring defects are observed in all lineages of projection neuron (PN) MARCM clones as well as anterodorsal single cell clones that normally target the DL1 glomerulus.

In general, phenotypes of lola^e76 anterodorsal PNs (adPNs) and lateral PNs (lPNs) can be classified into two main categories: a loss of targeting to normal target glomeruli and a gain of targeting to off-target (ectopically targeted) glomeruli. However, the phenotypes are highly variable between brains and have variable penetrance. lola^e76 dendrites also appear more diffuse in general, and often 'wander' through the lobe, wrapping around, but not actually innervating, glomeruli. Additionally, lola^e76 dendrites are frequently not restricted to the antennal lobe and innervate regions of the suboesophageal ganglion. Additionally, ventral lola^e76 clones show a significant loss of targeting.

Nearly 80% of lola^e76 DL1 single cell clones show targeting defects, indicating that lola has cell-autonomous effects on dendritic targeting.

Axonal wiring defects are also observed in all lineages of projection neuron (PN) MARCM clones as well as anterodorsal single cell clones that normally target the DL1 glomerulus. Phenotypes are highly variable in penetrance and severity.

In lola^e76 adPNs and lPNs, the most common defect was ectopic branching outside of the region of the mushroom body (MB) or the lateral horn (LH). Some clones show a lack of innervation, where innervation of the MB failed to occur or branch extension in the LH was severely limited. Axons of vPNs are the most severely affected: nearly 100% of clones exhibit defects, including ectopic branching defects, misrouting defects and mis-targeting to the suboesophageal ganglion.

More than 50% of DL1 single cell clones show axon defects, indicating that lola acts cell-autonomously in axon targeting. These defects include ectopic branches and failure to extend branches into the mushroom body.

MARCM clones simultaneously mutant for lola^e76 and any one of lola^3.8.Scer\UAS, lola^4.7.Scer\UAS, lola^L.Scer\UAS, induced using Scer\GAL4^GH146, exhibit: i) cell loss and lack of dendritic extensions in adPN and lPN neuroblast clones; ii) a strong reduction of VA1lm and DA1 targeting in vPN clones, with the pan-AL neuron often showing little dendritic process elaboration and only rare innervation of much of the AL.

DL1 MARCM clones simultaneously mutant for lola^e76 and lola^4.7.Scer\UAS, induced using Scer\GAL4^GH146 either fail to innervate DL1 or have extensions into other regions of the AL. Axonal defects range from a failure to extend or elaborate branches in the LH to an increase in ectopic branching.

DL1 MARCM clones simultaneously mutant for lola^e76 and lola^L.Scer\UAS, induced using Scer\GAL4^GH146 innervate DL1 in addition to having extensive dendritic innervation in the rest of the AL. Axonal defects range from a failure to extend or elaborate branches in the LH to an increase in ectopic branching.

DL1 MARCM clones simultaneously mutant for lola^e76 and lola^3.8.Scer\UAS, induced using Scer\GAL4^GH146 are variable, with half appearing normal . Axonal defects range from a failure to extend or elaborate branches in the LH to an increase in ectopic branching.

Fas2-expressing axons are seen crossing the midline in mutant embryos, in contrast to wild type. ap-positive axons cross the midline in lola^c46/lola^e76 embryos, in contrast to wild type. These axons then stall when they reach the mediolateral position where the contralateral connective would be found in wild-type embryos. Axons of the pCC and MP1 neurons do not cross the midline in these embryos.

Mutants have CNS longitudinal interruptions, ISN stalling and failure of SNb innervation. In mutant embryos neuronal and muscle cell identities are normal, though with low penetrance ventral longitudinal muscles can be missing.

lola^e76 has embryonic/larval neuromuscular junction | embryonic stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/futsch^EP1419

lola^e76 has axon | embryonic stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/futsch^EP1419

lola^e76 has ventral midline of embryo | embryonic stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/futsch^EP1419