Mutant animals are inviable at 28^oC but viable at 24-25^oC, though defects in the wing and abdomen are seen.

When mutants are grown at the permissive temperature (24[o]C) abdominal cuticular defects are seen, including missing and unpigmented cuticle. When grown at 28[o]C the phenotypes are much stronger. Mutant animals have wings of the appropriate size, but contain approximately half the number of hairs as wild-type. Mutant hairs are considerably larger than wild-type and often misoriented. Bristles are never missing on mutant wings or elsewhere on the thorax and head, but the mutant bristles are less uniform in orientation. By contrast, the remaining abdominal bristles are wild-type in size, although they are often misoriented. In Myb²/Df(1)sd72a and homozygous Myb² mutants abdominal development is delayed. For example, Myb² homozygous abdomens are less developed at 42 hours APF than were controls at 30 hours APF. At 18 and 24 hours APF, mutants have approximately half the number of histoblast nuclei as wild-type, indicating cells are about one cell cycle behind. This delay is increased in Myb²/Df(1)sd72a animals or in homozygotes shifted to 28[o]C. At 18 and 24 hours APF, mutants have approximately 1/6 the number of abdominal histoblasts, suggesting a lag of two to three cycles. Also the spreading of histoblast cells to displace adjacent larval epidermis cells, and the subsequent flattening of the adult cells occurs more slowly in mutants.

Homozygous Myb², or Myb²/Df(1)sd72a mutant abdominal cells proliferate more slowly than wild-type, and also unlike wild-type cells continue to divide well beyond 41 hours APF - mitotic cells are detected through to at least 50 hours APF. In spite of their slower proliferation, at 24 hours APF, the mitotic index of Myb² cells is similar to that of wild-type cells. The Mitotic index of Myb²/Df(1)sd72a cells at 24 hours APF is significantly higher than wild-type or Myb² cells, and remains higher throughout the experimental time course. No significant difference in either the total percentage of cells in S phase or in the percentage of cells in late S between wild-type and mutant cells at 24 hours APF. However, there is a higher percentage of mutant cells in the early stages of mitosis, before metaphase, and a corresponding decrease in the percentage of cells in metaphase and anaphase. The 'pre-prophase' stage of mitosis, (rarely seen in wild-type cells) is much more common in mutant cells, suggesting that progression of mutant cells through the early stages of prophase is abnormally slow.

Mitotic defects are not detected in early divisions in the abdominal histoblasts of homozygous Myb², or Myb²/Df(1)sd72a animals, but become increasingly commonplace later. Defects occur in as many as 22% of Myb² homozygotes and 48% of Myb²/Df(1)sd72a mitotic histoblasts. Most defective mitoses display an aberrant number of centrosomes (usually 3 to 4) with abnormal spindles and nuclear morphology. One such defect in which two centrosomes are present at or near each pole during anaphase/telophase occur more frequently in Myb² than in Myb²/Df(1)sd72a. These spindles are seen less frequently in metaphase and early anaphase cells, suggesting this defect reflects precocious separation of the centriole pairs associated with each centrosome. Multipolar spindles and completely malformed spindles are seen when multiple centrosomes are present. Monopolar spindles are also occasionally seen. Chromosomal abnormalities are seen in mitotic cells with both normal or abnormal centrosomes. Metaphase cells with lagging chromosomes are observed more often than in wild-type. Another defect seen is a cell with more than one metaphase plate. During anaphase straggling strands of DNA are frequently observed. The abnormal mitoses seen in mutants give rise to unequal chromosome segregation and produce aneuploid and polyploid cells.

Adults grown at the permissive temperature exhibit defects in wing hair number and orientation. Quantitative microscopic analysis of mutant nuclei reveals the mutation causes endoreplication in a fraction of the arrested wing cells, the severity of which varies from one cell to another.

Homozygotes show reduced viability during embryogenesis at all temperatures, and during pupal development at 25 and 28^oC. Homozygotes maintained at 18^oC are fertile. Adult homozygotes transferred to the restrictive temperature are viable. The viability of embryos derived from homozygous females is greatly reduced when oogenesis occurs at the restrictive temperature.

Myb¹/Myb² has lethal phenotype, enhanceable by nej³

Myb² has lethal phenotype, enhanceable by nej³

Myb² has visible | recessive phenotype, suppressible by stg^hs.PE2

Myb² has visible | recessive phenotype, suppressible by Cdk1^hs.PS

Myb², nej³ has abnormal developmental rate phenotype

Myb¹/Myb², nej³ has abnormal developmental rate phenotype

Myb² has wing hair phenotype, suppressible by stg^hs.PE2

Myb² has wing hair phenotype, suppressible by Cdk1^hs.PS