Homozygous, gho¹/gho^IP, gho^IP/Df(2L)BSC688or gho^IP/Df(2L)Exel7010 animals exhibit the same defects. Mutant embryos produce a discontinuous or thin larval cuticle, tracheae do not become air-filled and are barely visible, and the head skeleton is less melanised (though has normal morphology). Ventral denticles and dorsal hairs are missing, though the surface is not smooth but wrinkly. There is reduced chitin in the epidermis and trachea. Animals die at the first instar larval stage within the egg case.

The cuticle of mutant larvae is very thin and fragmented. It lacks the epicuticle layer. The epidermal cells usually do not establish apical undulae.

The epidermis of mutant larvae eventually disintegrates and single cells leave the tissue. In contrast to wild type, gho^IP cells are cuboidal or round and their lateral membrane does not meander. Adherens junctions look loose and basolateral septate junctions are less complex compared to wild type. Occasionally, cell-cell contacts are lost.

In contrast to wild type, mutant epidermal cells lack a basement membrane and the basal plasma membrane is smooth rather than jagged. Muscles often detach from the apodemal cells.

In late stage 17 mutant embryos, the chitin cables of the dorsal trunk are largely disorganized and often absent. The tracheal lumen is much narrower compared to wild type, and the tracheal tubes have an irregular diameter. The larval tracheae have shallow taenidial folds and their lumen fails to be cleared of solid material.

The ER of mutant epidermal and tracheal cells consists of large spherical compartments instead of tubules as in wild type. Perinuclear ER is affected as well. These defects can be traced back to stage 15. Tracheal ER appears to be less affected than in the epidermis.

The organization and identity of the Golgi apparatus are compromised in mutant epidermal cells at embryonic stage 16.