Despite the normal appearance of homozygous or hemizygous mre11^58S females, they lay embryos that do not hatch (>10,000 embryos counted), even when mated to wild-type males, indicating maternal effect lethality.

mre11^58S animals display mild telomere-capping defects, with 0.2 associations per mre11^58S nucleus, compared with the wild-type level of 0.04.

Early mre11^58S mutant embryos (those examined before cycle 7) appear to be mostly normal, with nuclei occasionally connected by chromosomal bridges (8%). As the embryos developed, more nuclei appear connected by bridges, and nuclei with abnormal DNA content become abundant. Sister nuclei separation failed in 69 out of 228 mitoses; likely, the result of unresolved chromosome bridges. Some of these polyploid nuclei apparently attempt to divide in the next mitosis, creating multiple-lobed nuclei. Mitotic bridges are observed in 38% of anaphases and telophases. Most late-stage mre11^58S embryos display large nuclei-free areas, and their interior is filled with abnormally large and highly condensed nuclei. These embryos rarely develop signs of gastrulation. Unresolved telomere associations are the most likely mechanism leading to chromosome bridging. Telomere associations are unequivocally identified in 95.3% of mre11^58S embryos. Covalent telomere fusions are abundant in mre11^58S mutant embryos.

Contrary to the severe capping defect in the embryos, mre11^58S postembryonic animals develop mild telomere dysfunction, and are viable.

mre11^58S has abnormal mitotic cell cycle phenotype, enhanceable by nbs^2K

mre11^58S is an enhancer of abnormal mitotic cell cycle phenotype of nbs^2K

mre11^58S, nbs^2K has lethal | pupal stage phenotype