Mutant late stage embryos have a large gap separating the anterior deutocerebral brain region from the neuromeres of the posterior suboesophageal ganglion, due to cell loss in the tritocerebral/deutocerebral region of the brain. This cell loss is associated with patterning defects; the longitudinal connectives that normally run from the protocerebrum to the suboesophageal ganglion are missing or strongly reduced and the tritocerebral commissure is completely absent. Glial cells appear to be present in the residual tritocerebral/deutocerebral region, but they are severely misplaced.

Stage 11 mutant embryos show a reduction in the number of lab-expressing neuroblasts, primarily affecting ventral neuroblasts of the tritocerebrum and adjacent part of the deutocerebrum. Invagination of the foregut appear to be affected in these embryos.

Stage 12 mutant embryos show a significant increase in the number of apoptotic cells in the tritocerebral lab-expressing domain compared to wild-type embryos.

vnd⁶ affects formation of some brain neuroblasts (as assayed by expression of molecular markers). The frequencies at which the following neuroblasts are present at stage 9 in the mutant embryos are indicated in parentheses; Pcv6 (55%), Pcv3 (78%), Pcv1 (50%), Ppv2 (60%), Dv6 (70%), Dv3 (90%), Dv2 (27%), Pcv7 (90%), Dd1 (90%). The following brain neuroblasts are present 100% of the time in stage 9 mutant embryos; Pad4, Pcd4, Pcd8, Pcd19, Pcd15, Pcd9, Pcv9, Pcd21, Pcd17, Pcd6, Pcd2, Ppd3, Dd6, Dd3, Dd8, Dd7. The frequencies at which the following neuroblasts are present at stage 11 in the mutant embryos are indicated in parentheses; Pcv6 (55%), Pcv8 (20%), Pcv5 (15%), Pcv3 (18%), Pcv2 (27%), Pcv1 (55%), Pcv7 (90%), Pcv4 (20%), Pav1 (90%), Pad1 (90%), Ppv1 (15%), Ppv2 (35%), Ppv3 (10%), Dv5 (15%), Dv1 (25%), Dv3 (82%), Dv6 (80%), Dv7 (9%), Dv2 (23%), Dv4 (35%), Dv8 (30%), Tv1 (5%), Tv2 (25%), Tv3 (15%), Tv4 (5%), Tv5 (30%), Td1 (5%), Td2 (75%), Td3 (90%), Dd2 (95%), Dd1 (91%). The following brain neuroblasts are present 100% of the time in stage 11 mutant embryos; Pad7, Pad4, Pad3, Pad15, Pcd4, Pcd5, Pcv9, Pcd6, Pcd2, Pcd3, Pcd1, Ppd1, Ppd2, Ppd5, Ppd8, Dd3, Dd4, Dd6, Dd7, Dd8, Dd5, Td5, Td4, Td6, Td7, Td8, Dd10, Dd11, Dd9, dd12, Dd13.

Mutant stage 11 embryos show increased cell death in the ventral procephalic neuroectoderm of the developing deutocerebrum and protocerebrum, but not in the developing tritocerebrum, compared to wild-type embryos.

Mutant stage 12 embryos show an increase in the number of glial cells in the deutocerebrum and tritocerebrum compared to wild-type embryos, but the number of glial cells in the protocerebrum is unchanged.

In vnd⁶ embryos, the longitudinal fascicles are abnormally close, while the commissures are fused and irregular. The number of motor neurons is reduced. The Central Nervous System (CNS) of vnd⁶ is collapsed, i.e., although the longitudinal connectives are generally formed in vnd⁶ mutants, they lie too close to the midline. The commissures are poorly formed and fused. SP1 forms late in vnd⁶ embryos and is abnormally localised too close to the ventral midline. In vnd⁶ mutant embryos the VUM axons exit the CNS posterolaterally. RP2 is either mislocated or duplicated in vnd⁶ mutants. RP2 pathfinding is also abnormal. The RP2 axon exits the CNS very near its cell body, in contrast to the wild-type situation where the axon projects anterolaterally to fasciculate with aCC. RP2 behaves like aCC in vnd⁶ mutants, in terms of the direction in which its axon extends and its fasciculation with the VUM axons laterally. In vnd⁶ mutant embryos, eve-expression is lost in aCC, pCC, u, and CQ neurons, while the RP2 neurons can be duplicated and/or mislocated. In stage 13 vnd⁶ mutant embryos there is a drastic reduction in the number of sim-expressing nuclei, and those nuclei that do stain are very small relative to those seen in wild-type embryos. Thus, midline glia numbers are reduced late in development in vnd⁶ embryos. In vnd⁶ mutant embryos, the VUM fascicles express Fas2. In addition, as seen with futsch, RP2 pathfinding is disrupted (RP2 axons extend posterolaterally rather than anterolaterally as seen in wild-type).

Ventral muscle founder cells are not specified in vnd⁶ embryos. Reproducible muscle deletions are seen in the ventral regions of the embryo; the ventral acute, most ventral longitudinal and the ventral transverse muscles are usually present, but the ventral oblique and ventral longitudinal 4 muscles fail to form.

Some ventral neuroblasts, including MP2 fail to form in homozygous embryos. The RP2/RP2sib neurons are duplicated.

Medial S1 neuroblasts of rows B and D (NB7-1 and MP2) do not form. All lateral neuroblasts form normally. At a low frequency, neuroblasts from the medial and intermediate columns of rows A and C (NB2-2, NB3-2, NB5-2, NB5-3) do not arise.

Hypoplasia of the CNS. The ventral cord is thinner than that of wild type and is imperfectly condensed. Hemizygous embryos lack 20--25% of the neuroblasts, neuroblasts in the intermediate and medial rows are affected. Cell death occurs earlier than in the achaete-scute complex^- embryos.

Hemizygous embryos die as pharate larvae with well-formed mouth hooks and air in the tracheal trunks. The ventral nervous system is disorganised.