LanB1^1B1/LanB1^28a third instar larvae show overgrowth of the neuromuscular junction.

Migration of midgut endodermal cells in LanB1^1B1 mutant embryos is delayed such that anterior and posterior endodermal cells do not contact each other at embryonic stage 13 when the normal wild-type cells would have already met. Also, unlike in wild-type stage 13 embryos, macrophages in LanB1^1B1 mutants fail to migrate along the ventral nerve cord. By embryonic stage 15, multilayered clumping of the endoderm is observed, and formation of midgut constrictions and elongation is not seen in mutants. Homozygous LanB1^1B1 mutant embryos show gaps in the dorsal tracheal tubes, and the visceral branch fails to migrate normally. Similarly, the salivary glands of mutant embryos fail to migrate properly, remaining at the point of contact with the visceral mesoderm. Homozygous mutants fail to form the multilayered architecture of the proventriculus. The Malpighian tubules are abnormally short and of irregular thickness. This failure in tube elongation is not a consequence of stellate cells failing to incorporate in the tubules.

In 11.1% of LanB1^1B1 mutants, the VL1 muscle is detached from tendon cells. Gaps are evident between the muscle and epithelial cells of the midgut, which are normally closely associated. Similarly, the visceral circular muscles fail to stretch along the dorsoventral axis, and a misarrangement of the longitudinal visceral muscles along the dorsoventral axis are observed.

Adult wings with large homozygous LanB1^1B1 clones show a wing blister phenotype.