Homozygous embryos show a significant increase in primordial germ cell number compared to controls.

Mutants show no defects in targeting of the DL1 glomerulus in the antennal lobe.

Most homozygotes die as small second instar larvae 2-7 days after hatching. These larvae never grow larger than the size they are as young second instars, they become increasingly lethargic and compromised in their movement and prior to death they stop moving entirely (their only sign of life is responsiveness to touch and contractions of the dorsal vessel). In addition, the bodies of the larvae appear to collapse and flatten over time. The organisation and morphology of the body wall musculature of mutant first instar larvae appears normal, but in mutant second instar larvae the body wall musculature is severely disrupted. The muscle function of newly hatched homozygous larvae is essentially normal; body wall contraction rates are unaffected, and dorsal vessel contraction rates and behaviour are almost indistinguishable from wild type. However, only 15% of newly hatched mutant larvae score positive for solid food ingestion within 30 minutes (in contrast to 100% of wild-type controls). All mutant larvae score positive for solid food ingestion by 7 hours after being exposed to food. Mutant larval excretion rates are normal. Newly hatched mutant larvae ingest liquid food at the same rate as wild-type controls. Mutant first instar larvae that are fed on sucrose show the same foraging behaviour and longevity as wild-type larvae fed on sucrose, arresting development as first instars and continuing to crawl incessantly and at normal rates long after age matched mutant larvae fed on solid food have become immobilised and died. The body wall contraction rates of mutant first instar larvae fed on sucrose are maintained at nearly wild-type levels. Homozygous embryos derived from homozygous germline clones (lacking both maternal and zygotic mir-1 function) have an identical phenotype to homozygous embryos (lacking zygotic mir-1 function), and do not show any defects in the differentiation or development of the embryonic mesoderm or muscle system.