56% of mutant embryos show brain defects; the brain has a deletion in the deutocerebral and tritocerebral brain anlagen, which leads to a prominent gap devoid of neuronal cells between the remaining protocerebral brain hemispheres and the subesophageal neuromeres.
66% of mutant embryos have an "open-head" phenotype in which the anterodorsal head ectoderm is defective. Head involution is perturbed and brain hemispheres protrude out of the embryo at the gap in the dorsal head.
The tracheal placodes are slightly smaller than normal in mutant embryos. The visceral branches of the tracheal system generally fail to form. Occasionally, the ganglionic or dorsal branches appear truncated.
In an ems2 mutant the ems staining interneurons in the ventral nerve cord do not extend axons across the midline and turn rostrally during stages 13-14 as seen in wild-type.
The stigmatophore protrudes normally but the spiracular chamber is defective in that it lacks a filzkorper and is not connected to the trachea. The stigma in developing embryos fails to slide posteriorly, a phenotype similar to that seen in Abd-BM1 mutants. The spiracle cells that are in contact with the trachea fail to invaginate, perhaps causing the failure of posterior sliding of the developing stigmatophore.
Neuromeres b2 and 3 are absent or reduced in all embryos.
Fail to develop filzkorper and the remaining spiracular structures are intact.
Embryos have no Dll expression in the antennae primordium, it is expressed in other limb primordium. Intercalary and antennal segments and a portion of the pre-antennal region defined by the en head spot are absent in ems mutant embryos.
Absence of head structures.