dia² homozygotes in which maternal Rho1 function is reduced (derived from Rho1^72O heterozygous females) nearly all die as embryos, with defects in head involution, ventral cuticle or the completion of dorsal closure.

Maternal heterozygosity for dia² enhances the dia² homozygous phenotype, resulting in ventral holes in the cuticle.

13% of the progeny of dia² Rho1^72O double heterozygous females die as embryos, largely with defects in head involution. These embryos show dramatic alterations in amnioserosal cell behaviour compared to wild type; during germband retraction, amnioserosal cells along all the germband of the mutant embryos form long persistant cell extensions extending over neighbouring epidermal cells. The protrusions are especially prominent caudally, but are also observed laterally and anteriorly. Long protrusions are occasionally seen from epidermal cells and amnioserosal cells also extend abnormal processes over one another as well as over epidermal cells. Dorsal closure in these embryos is otherwise normal, except that drop-out cells appear much earlier in dorsal closure than normal.

The progeny of dia² RhoGEF2⁰⁴²⁹¹ double heterozygous females have abnormal protrusions extending from amnioserosa cells over the adjacent epidermis during dorsal closure.

Heterozygosity for dia² enhances the Abl⁴ phenotype.

Dominantly suppresses the rough eye phenotype of the Rho1^GMR.PH and pbl^Scer\UAS.cPa expressed under the control of Scer\GAL4^GMR.PF, and dominantly enhances the eye phenotype of pbl^{ΔDH497-549.Scer\UAS} expressed under the control of Scer\GAL4^GMR.PF.