Obvious but variable defects in cellularisation are seen in embryos derived from nuf¹ females. Furrow invagination is very slow or aborted in approximately half of the embryos.

In nuf¹-derived nuclear cycle 12 embryos, actin cap formation occurs normally. As the embryos progress into prophase, the actin caps are dismantled and the actin re-organises into furrows encompassing each prophase nucleus and its developing spindle. In nuf¹-derived embryos, the hexagonal furrow network is riddled with gaps, present at prophase during the initial stages of furrow formation. Similar defects are observed during cellularisation at nuclear cycle 14.

nuf^Cy3-23/nuf¹ females lay abundant eggs none of which hatch (and most die unpigmented).

During nuclear cycle 12 non-sister telophase nuclei dividing in parallel with each other fuse in the following interphase. During the cortical divisions embryos form normal interphase actin caps, but incomplete metaphase and cellularisation furrows. Breaks in the metaphase furrow correlate with the region nearest the metaphase plate and furthest from the centrosomes. nuf^Germ.10 increases the hatch rate of embryos from homozygous females from 0% to 33-38%.

Embryos from homozygous mothers successfully complete nuclear migration, but undergo abnormal cortical nuclear divisions prior to cellularization. Affected embryos cellularize with fewer surface nuclei and a corresponding increase in interior nuclei. The distribution of surface nuclei during cellularization is irregular. Affected embryos develop distinct defects in the cortical cytoskeleton.