Amino acid replacement: Q67term.
C11903406T
Q20term | MCPH1-PA; Q67term | MCPH1-PB; Q20term | MCPH1-PC; Q67term | MCPH1-PD
Q67term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Homozygous females are completely sterile; embryos derived from these females arrest in a metaphase-like state in cycles 1-8. The embryos have acentrosomal, barrel-shaped spindles. Chromatin bridging is often seen.
Embryos derived from MCPH1Z1861/MCPH1Z0978 females arrest with condensed chromosomes and unevenly spaced nuclei. Asynchronously dividing nuclei and centrosome duplication prior to chromosome segregation are often seen. Tubulin foci are often missing from one or both poles of mitotic spindles, which are typically shorter or more barrel-shaped than normal. Chromosomes are poorly aligned and are occasionally displaced from the metaphase plate. Spindles with centrosomal detachment at one or both poles (43.6%) and spindles with more than one centrosome per pole or ectopic centrosomes within the spindle (46.0%) are seen.
Chromatin bridging is seen in 68.3% of late anaphase-to-telophase figures in embryos derived from MCPH1Z1861/MCPH1Z0978 females. Spindle pole-to-pole distances are increased dramatically compared to wild-type figures.
Mutant larvae undergo normal G2 arrest in response to ionizing radiation (assayed by scoring mitotic cells in larval eye-antennal imaginal discs).
Mutant larvae undergo intra-S phase arrest similar to that of wild-type larvae in response to ionizing radiation (assayed by scoring mitotic cells in larval brains).
Mutant larvae show normal survival following low dose (10 Gray) irradiation exposure.
22% of MCPH1Z1861 and 11.5% ofMCPH1Z1861/Df(2R)BSC39 adult males have variable morphological defects in the mushroom bodies.
MCPH1Z1861/MCPH1[+] is an enhancer of lethal | embryonic stage phenotype of mei-41D5/mei-41RT1
MCPH1Z1861 has spindle | maternal effect phenotype, suppressible by lokp6
The mitotic defects seen in embryos derived from MCPH1Z1861 females are suppressed if the females are also mutant for lokp6; mitotic spindles are restored to near normality and the early developmental arrest is suppressed, such that most of the double mutant embryos complete syncytial divisions, cellularise and cease developing near gastrulation (most of the embryos initiate gastrulation but it is grossly aberrant). The double mutant embryos occasionally have abnormal DNA aggregates shared by more than one spindle and multipolar spindles.
