The longitudinal connectives collapse in sim⁵ single and sim⁵; Df(3L)H99 double mutant embryos.

Embryonic ventral muscles are shifted ventrally and some span the midline due to mislocalisation of ventral muscle precursor cells. Dorsolateral embryonic muscles appear normal.

In stage 12/3 homozygous embryos, pioneering growth cones are collapsed at the midline. At stage 14 the longitudinal tracts also collapse at the midline. From stage 11 until stage 13 only a small cluster of VUM neurons are present that never migrate to the ventral nerve cord. By stage 14 no VUM neurons are present at the ventral midline. Only one third of the wild-type MP1 neurons are present at the dorsal midline and by stage 14 they are fused at the midline. No en⁺ neurons are present at the midline at stage 12.

Strong CNS phenotype. All or nearly all of the ventral epidermal cells are absent in mutant embryos.

Midline cells fail to undergo a characteristic synchronised cell division, they do not migrate into the nerve cell precursor layer but remain along the ventral epidermis and they retain the nonpolarised, rounded shape of blastoderm neuroectodermal cells.

CNS defect: specific alterations in the pattern of precursors that give rise to the 2 MP1 progeny, ventral unpaired median neurons and the specialized ectodermal cells, the midline ectodermal cells (MEC).