Amino acid replacement: P140L. The identified nucleotide substitutions are probably strain-specific polymorphisms. Nucleotide substitution: G52A. Nucleotide substitution: A216T. Nucleotide substitution: T253C. Nucleotide substitution: C317T. Nucleotide substitution: T329C. Nucleotide substitution: A542G.
C20262243T
P140L | PCNA-PA; P140L | PCNA-PB
P140L
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change. Other polymorphisms present in strain but are unlikely to be cause of mutant phenotype.
follicle cell | oogenesis (with PCNA2735)
nurse cell | oogenesis (with PCNA2735)
Exposure of PCNAB1 mutant larvae to DDVP for 48 hours results in a significant increase in the migration of DNA in midgut cells at 1.5 and 15ng/ml concentrations of DDVP as compared to controls.
mus209B1/mus2092735 mutants have a similar frequency of single-strand annealing repair (SSA) compared to controls in a P{wIw.FRT} hemizygous assay to study DNA double-stranded break repair when assayed at 32oC or 38oC.
Homozygotes are viable at 22oC, but die as pupae at 29oC. Homozygous females (raised at the permissive temperature) do not produce eggs. Homozygous ovaries are small and poorly developed. They are partitioned into ovarioles, but these are rudimentary and devoid of late stage egg chambers, containing only stem cells and early stage egg chambers. Germline clonal analysis demonstrates that the defective mus209 protein in mus209B1 very poorly sustains development of the female germ line. Mosaic females containing homozygous germ line clones produce only a small number of viable progeny. mus209B1/mus2092735 females are partially fertile. Ovaries from these females develop further than either of their homozygous mutant counterparts, but still show developmental defects. These can include defects in follicle cell proliferation or migration and egg chambers that contain approximately double the normal number of nurse cells. Some egg chambers appear normal. The syncytial embryos derived from these females show a range of defects. 10-20% appear wild type. Others show varying degrees of abnormality in distribution of the nuclei. Embryos with highly irregular nuclei often appeared to be arrested in cell cycle progression, while in others aberrant nuclear division leads to nuclear "fallout" from the cortex. The overall level of recombination on chromosome 2 is reduced in mus209B1/mus2092735 females compared to wild type, but only marginally so. The proportion of distal exchange events is reduced, while the proportion of centromere-proximal exchanges is actually increased.
Mutant pharate adult males show a crm-like phenotype, with an ectopic sex comb tooth being present in the second tarsal segment of prothoracic legs in approximately one third of mutant males.
Newly hatched larvae at 22oC are very sensitive to killing by methyl methanesulfonate and ionising radiation. Heterozygotes with mus2092735 are lethal at 29oC.
Larval survival hypersensitive to exposure to methyl methanesulfonate and gamma rays, but not to N-acetyl-2-aminofluorene, benzoapyrene, or nitrogen mustard.
PCNAB1, crm7 has mesothoracic leg phenotype
PCNAB1, crm7 has metathoracic leg phenotype
PCNAB1, crm7 has prothoracic leg phenotype
mus209B1 and mus2092735 partially complement each other for the female sterility and DNA double strand break repair defect seen in each homozygote.
mus209B1 fully complements mus209D-1368 and mus2092735. Homozygous mutant phenotype can be rescued by constructs mus209+t5 and mus209+t7.
mus209B1 flies cannot repair site-specific DNA double-strand breaks at the snw locus induced by P\TΔ2-3. This has dominant lethal effects.