mib2¹ homozygous late stage 16 embryos display severe loss and detachment of somatic muscles, as compared to mib2¹ heterozygous controls; mib2¹ homozygous and mib2^S0768/mib2¹ transheterozygous late stage 16 embryos present a bloated midgut phenotype, and an irregular arrangement of longitudinal visceral muscle fibers, as compared to mib2¹ heterozygous controls.

Homozygous embryos show progressive degeneration of muscles. All muscles are initially present in stage 15 homozygous embryos and make correct contact with tendons. However, when contractions start (during stage 16), muscles begin to detach and form myospheres. Unfused myoblasts are still present in homozygous embryos at stage 16, when fusion is completed in wild-type embryos. The muscles are smaller than normal, for example, the number of eve-expressing nuclei incorporated into the DA1 muscle is reduced compared to wild- type. Some muscles are missing in stage 16 embryos (the lack of muscles is usually associated with the presence of myospheres). Approximately one-third of mutant embryos die before hatching, while the remaining reach the first larval instar. Most muscles are missing in homozygous first instar larvae, and they die soon after hatching. Most muscles are affected, but some are more resistant to detachment than others.

Homozygous stage 16 embryos lack gut constrictions.

The fine structure of the dorsal oblique (DO) muscles (which persist in the mutant embryos) is affected in stage 17 mutant embryos. Some DO muscles maintain a certain alignment of Z bands in sarcomeres, but other DO muscles lack any sign of regularity of the Z bands. Muscle contraction only occurs in muscles that main Z banding regularity, although contractions are erratic in frequency and extension. Fractures of Z bands are seen in mutant larval muscles.

Embryos derived from homozygous female germline clones have essentially the same phenotype as homozygous zygotic mutant embryos, indicating no major contribution of maternally derived mib2.

mib2¹/Df(2L)TW130 embryos derived from homozygous mib2¹ female germline clones have a well developed somatic musculature at stage 15, although a small number of detached muscles can be seen. However, by stage 16, the muscle pattern is highly deranged, with a massive number of detached muscles. Many of the detached muscles undergo degeneration, such that at stage 17, normal somatic muscles are absent and the size of the rounded, detached muscles is dramatically decreased. The midgut muscles do not disintegrate in these embryos. Homozygous mib2¹ embryos that lack only zygotic mib2 function show similar somatic muscle and gut defects as those derived from germline clones, although the defects are delayed and less severe. Heterozygous embryos that are derived from homozygous mib2¹ female germline clones have a normal somatic muscle pattern.

Homozygous stage 16 embryos show strong apoptotic signals in the detached and shrinking somatic muscle syncytia.

Hemizygous l(2)37Be¹/Df(2L)TW130 animals do not survive to the third larval instar stage.

mib2¹ has increased cell death | recessive | embryonic stage 16 phenotype, suppressible | partially by Df(3L)H99/Df(3L)H99

mib2¹ has increased cell death | recessive | embryonic stage 16 phenotype, suppressible | partially by Scer\GAL4^tey-5053A/BacA\p35^UAS.cHa

mib2¹ has embryonic/larval somatic muscle cell | embryonic stage 16 phenotype, suppressible | partially by Df(3L)H99/Df(3L)H99

mib2¹ has embryonic/larval somatic muscle cell | embryonic stage 16 phenotype, suppressible | partially by Scer\GAL4^tey-5053A/BacA\p35^UAS.cHa

mib2¹ has embryonic/larval somatic muscle cell | embryonic stage 16 phenotype, non-suppressible by Scer\GAL4^{kirre-rP298-G4}/mib1^UAS.cWa

mib2¹ has embryonic/larval somatic muscle cell | embryonic stage 16 phenotype, non-suppressible by Scer\GAL4^{kirre-rP298-G4}/neur^UAS.cPa

mib2¹ is a non-suppressor of eye phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

mib2¹/mib2[+] is a non-suppressor of visceral muscle fiber phenotype of tn^MJO-348

mib2¹/mib2[+] is a non-suppressor of filamentous actin phenotype of tn^MJO-348