Female sterile mutant that causes maternal effect lethality that generally ends in metaphase arrest during mitotic cycles 5 or 6, or earlier, in the preblastoderm embryo.

Fertilised eggs fail to develop past the first few mitotic cycles and undergo meiotic or mitotic arrest. Females undergo yolk deficient syndrome: reduction in egg production, small eggs and defects in egg chorion, chorionic filaments and/or vitelline membrane. Heterozygous females with mama^lto5 are sterile. Adults are obese.

Eggs laid show meiotic and mitotic arrest at metaphase.

RK2. Adult fat body hypertrophies as cells become distored by enormous oil globules. Adult corpus allatum of mated females hypertrophies. Eggs laid by females exhibit meiotic and mitotic abnormalities and never develop beyond early cleavage stages.

Adult fat body phenotype like adp⁶⁰; lipid accumulated at expense of glycogen in fat body; yolk deposition in ovaries retarded; carbohydrate levels low in 8-day-old adults (FBrf0023614). Corpus allatum hypertrophies in mated females to same degree as in adp⁶⁰. Females completely sterile; sterility autonomous. Eggs laid by homozygotes show meiotic or mitotic abnormalities, or both, never develop beyond early cleavage stages; chorion, chorionic filaments and vitelline membrane defective in some. Males 78% fertile. Heterozygotes fertile, but females become sterile with age. Viability generally good but longevity reduced; homozygotes with selective advantage under starvation; heterozygotes superior under desiccation. Average water content of well-fed adults reduced; percentage of lipids, as a function of dry body weight, almost double that of wild type. Iodine numbers show greater degree of saturation of mutant lipid extracts than of wild type. RK3.