RhoGEF21.1 embryos display defects in cellularisation including an irregular, wavy cellularisation front. Despite this RhoGEF21.1 embryos that reach the end of cellularisation look normal. The irregularity of the cellularisation front recovers, particularly in the ventral cells, and both the increased cell depth and basal loss of myosin occur normally in these cells.
In mid-cellularisation embryos derived from RhoGEF21.1 germline clones, the furrow canals are considerably enlarged compared to wild-type and are filled with large cytoplasmic blebs. Interruptions in the regular F-actin array (a hexagonal array is normally evident in surface views) are seen in these embryos and a variable proportion of the forming cells contain multiple nuclei. Embryos derived from RhoGEF21.1 germline clones show normal membrane invagination and nuclear extension during cellularisation.
RhoGEF21.1/RhoGEF24.1 animals show 97% embryonic viability, 96% first larval instar viability and 0% adult viability. Large homozygous clones in the wing disc result in defects in folding of the disc; bifurcations of the folds are found at the boundary between mutant and wild-type tissue.
Homozygous clones contain on average the same number of cells as wild-type twin clones. The planar polarity of bristles in homozygous clones in the wing is normal.
The mitotic pattern in early embryos derived from females containing RhoGEF21.1 germline clones shows the same delay in the ventral domain as in wild-type embryos.
Embryos derived from homozygous female germline clones have normal dorso-ventral and anterior-posterior patterning, and normal mesoderm specification. Germband extension and posterior midgut invagination appear defective. The cells of the mesectoderm fail to intercalate at the ventral midline. Gastrulation is highly disorganised and ventral furrow formation never occurs. Inappropriate lateral folds are formed. Invagination of the anterior midgut is also defective.