Sec239G mutant embryos display tracheal tube diameter abnormalities.
Homozygous, sec239G/sec23CK or sec239G/Df(3R)ED5187 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 disorganized: it has a reduced epicuticle layer that often contacts the envelope, and the chitin-protein organization of the procuticle layer is lost. The envelope layer is of normal appearance. 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, sec239G 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 properly formed but the tracheal lumen is much narrower compared to wild type. The larval tracheal cuticle dilates and the taenidial folds are sloppy: their size is variable and their spacing is irregular. The lumen of larval tracheae is not completely 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.