A 4bp insertion is present at cDNA nucleotide 3940, which changes Cysteine 1307 to a stop codon.
AGTG
An insertion of 4bp (AGTG) within tefu codon C1307, which changes C1307 to a stop codon.
Homozygous mutant neuroblast cells display severe mitotic abnormalities that are characterised by the fusion of chromosomal arms. These arms seem to establish these attachments through their telomeres. Mitotic chromosomes display end-to-end fusion behaviour from early stages of mitosis since associations are observed as early as prophase. Most metaphase cells exhibit fusion between one or more chromosomes. These may be single or double chromosome attachments (SCAs or DCAs). These attachments persist during anaphase and cells may contain one or multiple DNA bridges, even after chromatin decondensation in telophase. Analysis of attachments indicate that intrachromosomal associations are less frequent than homologous or heterologous interactions. The most frequent interactions are observed between chromosomes 2 and 3. DCAs are far more frequent (86%) than SCAs (36% and linear attachments (82%) are more frequent than ring (14%) conformations. The long arm of the X chromosome is much more likely to undergo association (83%) than the short arm (21%). A wide range of chromosomal rearrangements are also observed, including the exchange of subtelomeric sequences from one chromosome to heterologous chromosomes, unusual-sized euchromatic arms, duplication of subtelomeric sequences and DNA breakage in subtelomeric regions. The mitotic index of neuroblasts in the these flies is considerably reduced compared to wild-type. Polyploid cells with highly rearranged chromosomes are observed, but at low freqencies. Mutant neuroblasts exhibit more apoptotic cells than wild-type and appear to have normal DNA damage checkpoint.
tefu1 has abnormal mitotic cell cycle phenotype, enhanceable by cavunspecified
tefu1 has abnormal mitotic cell cycle phenotype, enhanceable by mei-41D3
tefu1 has abnormal mitotic cell cycle phenotype, enhanceable by mus304D2
tefu1 has abnormal mitotic cell cycle phenotype, non-enhanceable by nbs1
tefu1 has increased cell death phenotype, suppressible by nbs1
tefu1 is an enhancer of abnormal mitotic cell cycle phenotype of cavunspecified
tefu1 is an enhancer of abnormal mitotic cell cycle phenotype of mus304D2
tefu1 is a non-enhancer of abnormal mitotic cell cycle phenotype of nbs1
tefu1 is a suppressor of increased cell death phenotype of nbs1
tefu1 cavunspecified mutant cells exhibit DNA breaks and telomere fusions in metaphase and anaphase, resulting in approximately 8 fusions/cell, compared to 0.02 in wild-type.
tefu1 mei-41D3 double mutant cells exhibit more DNA breaks and telomere fusions in metaphase and anaphase than in wild-type cells.
nbs1 tefu1 double mutants fail to exhibit high levels of apoptosis and fail to induce further apoptosis following irradiation, as in the nbs1 single mutant.
nbs1 tefu1 double mutant cells exhibit DNA breaks and telomere fusions in metaphase and anaphase.
nbs1 tefu1 double mutant cells exhibit similar fusion rates as tefu1 single mutants, indicating that these genes act in a common telomere protection pathway.
tefu1 mus304D2 double mutant cells exhibit more DNA breaks and telomere fusions in metaphase and anaphase than in wild-type cells.
