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General Information
Symbol
Dmel\Myb2
Species
D. melanogaster
Name
FlyBase ID
FBal0023860
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

G15856575A

Reported nucleotide change:

G?A

Amino acid change:

R177K | Myb-PA; R177K | Myb-PB; R177K | Myb-PD; R177K | Myb-PE

Reported amino acid change:

R177K

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: R177K. Nucleotide substitution: G?A. Mutation is within the second of three imperfect tandem repeats that comprise the DNA binding domain.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Mutant animals are inviable at 28oC but viable at 24-25oC, 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 28oC. Homozygotes maintained at 18oC 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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

Myb1/Myb2 has lethal phenotype, enhanceable by nej3

Myb2 has lethal phenotype, enhanceable by nej3

Suppressed by
Statement
Reference

Myb2 has visible | recessive phenotype, suppressible | partially by stghs.PE2

Myb2 has visible | recessive phenotype, suppressible | partially by Cdk1hs.PS

Other
Phenotype Manifest In
Suppressed by
Statement
Reference

Myb2 has wing hair phenotype, suppressible | partially by stghs.PE2

Myb2 has wing hair phenotype, suppressible | partially by Cdk1hs.PS

Additional Comments
Genetic Interactions
Statement
Reference

When nej3 is added to Myb1 animals at 24oC a dramatic reduction in viability is seen as well as a significantly delayed emergence of surviving animals. When nej3 is added to Myb1/Myb2 animals an even more marked effect is seen on viability and emergence. When nej3 is added to Myb1 animals at 18oC no effect is seen on viability or any delay in development seen.

Myb2 pupae carrying stghs.PE2 or cdc2hs.PS raised at 25oC exhibit partial suppression of the Myb2 wing phenotype, increasing the number of hairs by 30-35% and correcting the orientation of the hairs. These results support the conclusion that Myb2 wing cells arrest at the G2/M transition.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (7)