Sec61α¹/Sec61α^k04917 animals show 46 +/- 6% embryonic lethality, with the majority of the animals dying during the early first larval instar.

Homozygous and Sec61α¹/Df(2L)BSC6 animals show 100% embryonic lethality. The dead embryos have no ventral denticle belts, differentiated head skeleton or any recognisable cuticle.

Peripheral nervous system development and salivary gland morphogenesis appear normal in mutant embryos. Patterning of the tracheal system is also unaffected, but the diameter of the tracheal tubes is smaller than normal. Approximately 50% of mutant embryos have at least one discontinuity indicating a failure in the fusion of tracheal metameres. The mutant embryos are alive and moving through the end of embryogenesis.

Mutant embryos show a 1-2 hour developmental delay and undergo dorsal closure when their heterozygous siblings have already completed the process. The dorsal-most epithelial cells of the epidermis (DME cells) in stage 14 mutant embryos elongate in the dorsal-ventral axis suggesting that the initiation of dorsal closure begins normally. However, the leading edge of the epidermis appears disorganised and the lateral epidermal cells fail to fully elongate in stage 15 mutant embryos. Although there is some zippering observed at the anterior and posterior ends of the epidermis in the mutant embryos, the majority of DME cells never come in close apposition and therefore cannot fuse. The amnioserosa starts to tear apart from the epidermis in stage 15 mutant embryos. Late stage 17 mutant embryos have no epidermis over the dorsal third of the embryo with the brain and gut extruded through the dorsal hole, indicating a completely penetrant defect in dorsal closure.

A four-chambered midgut is never seen in stage 16 mutant embryos. The most obvious defect is the lack of a second midgut constriction, although the guts may sometimes be more extremely affected.

Sec61α¹/Df(2L)BSC6 have normally involuted heads, despite the failure in dorsal closure.