Mutant animals are inviable at 25^oC but viable at 18⁰C, though defects in the wing and abdomen are seen. There is a decrease in the density of hairs and a mild disturbance of tissue polarity, as judged by hair orientation and the presence of occasional small clusters of hairs protruding from a single position. The abdomens of mutant animals also display defects, including missing and misoriented bristles, and patches of undifferentiated cuticle, with occasional defects in segmentation. When developing wings are examined 30h after puparium formation, cell and nuclear sizes and shapes are more variable and generally larger than controls. A few cells with bi-lobed nuclei are seen. The size, shape and orientation of prehairs is also less uniform, and two prehairs extending from a single cell are occasionally observed. Mutant wing tissue also has a higher mitotic index than wild-type.

When mutants are grown at the permissive temperature (18^oC) abdominal cuticular defects are seen, including missing and unpigmented cuticle. 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 and less uniform in orientation. By contrast, the remaining abdominal bristles are wild-type in size, although they are often misoriented. In homozygous Myb¹ mutants abdominal development is delayed. Most defective mitoses in abdominal histoblasts that are Myb¹/Df(1)sd72a display an aberrant number of centrosomes with abnormal spindles and nuclear morphology.

Adults grown at the permissive temperature exhibit wing defects: wing veins are thicker and differ slightly in relative positions, wings have half the number of hairs as wild type and the mutant hairs are larger than normal. Hairs are less regularly spaced, less uniform in orientation and occasionally grouped in small clusters. Bristles on mutant wings are also larger and less uniform in orientation. Staining of pupal wings reveals the mutant wings have fewer cells due to a defect in cellular proliferation during the final stages of wing development. Wing cells enter their final S phase but do not undergo a final division, leaving them with a 4C content of DNA. Each wing cell is larger than wild type and produces a hair. 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 a biphasic reduction in viability at both 18 and 25^oC; the first period of low viability occurs during embryogenesis, and the second period occurs during pupal development. The main difference in viability between the two temperatures occurs during the pupal period. Embryos die throughout embryogenesis at both temperatures, and many appear to be fully formed larvae that do not hatch. Pupae also die at different developmental stages, with many appearing to be almost fully formed, pharate adults. First, second or early third instar larvae incubated at 25^oC develop into infertile adults. Both hatching and eclosion are delayed compared to wild-type. Flies raised at 18^oC have a number of cuticle defects, including reduced numbers of hairs on the wing and disruption of the orientation of hairs and bristles on the wing. Some bristles and hairs on the abdomen are missing, while the orientation of other hairs and bristles are abnormal. The abdomen also has patches of undifferentiated cuticle. Flight ability is impaired. Homozygotes maintained at 18^oC are fertile. Prepupae and very eary prepupae incubated at 25^oC produce adults with more severe cuticle defects than animals raised at 18^oC. 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.

Viable and fertile at 18^oC. Stages most sensitive to temperature for viability are middle to late 3rd instar larva and possibly very early prepupa. At 25^oC a maternal effect is exerted on embryonic viability. At 18^oC wing veins are thicker and differ from wild type in positioning. Wings have fewer hairs, which are larger than normal. Wing bristles are longer and less uniform in orientation than wild type. Abdomens show patches of undifferentiated and unpigmented tissue. Flight ability is impaired though affected flies are not flightless.

Myb¹/Myb² has lethal phenotype, enhanceable by nej³

Myb¹ has lethal phenotype, enhanceable by nej³

Myb¹ has increased cell size | pupal stage phenotype, enhanceable by nej³

Myb¹ has abnormal cell shape | pupal stage phenotype, enhanceable by nej³

Myb¹, nej³ has abnormal developmental rate phenotype

Myb¹/Myb², nej³ has abnormal developmental rate phenotype

Myb¹ has wing hair | precursor phenotype, enhanceable by nej³

Myb¹ has abdomen phenotype, enhanceable by nej³

Myb¹ has adult cuticle phenotype, enhanceable by nej³

Myb¹ has adult abdominal segment phenotype, enhanceable by nej³

Myb¹ has nuclear chromosome phenotype, enhanceable by nej³

Myb¹ has wing & cell phenotype, enhanceable by nej³

Myb¹ has wing & nucleus phenotype, enhanceable by nej³

Myb¹ has wing hair | precursor | increased number phenotype, enhanceable by nej³