Transposable element inserted into an intron.
P-element insertion in the transcription unit.
microchaeta & abdominal segment 6 | ectopic
mitosis & nuclear chromosome
Approximately 12% of Trl13C homozygous flies hatch.
Heterozygotes have an average of about 10 sex combs, compared to about 11 in wild-type. 11% of animals have bristles on segment abdominal segment 6 (wild-type have none).
Homozygous Trl13C mutant flies have reduced viability and this lethality is enhanced in Trl13C/TrlR67 heterozygotes, with only a few percent of the mutant flies surviving to the adult stage.
Approximately 80% of homozygous Trl13C mutant males show a transformation of the sixth abdominal segment towards the fifth.
Homozygous Trl13C mutant females produce a reduced number of eggs compared to wild type.
Fewer than 20% of the embryos produced by homozygous Trl13C mutant mothers survive to the larval stages, even when fertilised by wild type males. A large proportion of embryos have severe defects in nuclear division during the syncitial blastoderm stage.
Approximately 80% of Trl13C/TrlR67 mutant males show a transformation of the sixth abdominal segment towards the fifth.
Fewer than 20% of the embryos produced by homozygous Trl13C/TrlR67 mutant mothers survive to the larval stages, even when fertilised by wild type males.
Lethality occurs at hatching.
Heterozygotes show the formation of "granular" chromatin during interphase and mitosis and high proportions of cells (which are arrested at the G2/M boundary) have hypercondensed chromatin. Cells with abnormal chromosome segregation are also seen. Heterozygous females have egg chambers with an abnormal number of trophocytes and defects in chromatin condensation.
A small percentage of homozygous Trl13C females survive to the adult stage and produce at least some eggs. Embryos can be divided into three classes. Class I arrest prior to cellularization. Class II arrest between stages 11 and 15. Class III survive gastrulation though later display segmentation defects and die by the first larval instar stage. The proportions of embryos falling into these three classes varies. Transheterozygotes with Trl62 exhibit a similar range of phenotypes. In eggs from Trl13C homozygous mothers, the nuclear cycles become asynchronous during the syncytial blastoderm stage. Chromosome segregation during anaphase is abnormal, and chromosome fragmentation is evident.
Homozygous female escapers can be obtained.
Reduced viability and a rough eye phenotype. Homozygous adult males show homeotic transformation of the sixth sternite into the fifth as shown by the presence of a few bristles on the sixth sternite, this phenotype is stronger in hemizygotes but they die just before hatching. In(1)wm4h males also heterozygous for Trl13C have almost white eyes, indicating a more frequent inactivation of the w gene. Heterozygotes with Trl62 eclose late, are poorly viable and exhibit the same phenotypes as Trl13C homozygotes.
Trl2.3/Trl13C has partially lethal | female phenotype, non-enhanceable by mle1/mle[+]
Trl62/Trl13C has partially lethal | female phenotype, non-enhanceable by msl-11/msl-1[+]
Trl2.3/Trl13C has partially lethal | female phenotype, non-enhanceable by msl-2[+]/msl-21
Trl2.3/Trl13C has partially lethal | female phenotype, non-suppressible by msl-2[+]/msl-21
Trl62/Trl13C has partially lethal | female phenotype, non-suppressible by mle1/mle[+]
Trl62/Trl13C has partially lethal | female phenotype, non-suppressible by msl-11/msl-1[+]
Trl13C, msl-2Hsp83.PK has partially lethal phenotype
Trl62/Trl13C, msl-2Hsp83.PK has partially lethal phenotype
Trl2.3/Trl13C, msl-2Hsp83.PK has partially lethal phenotype
Trl13C, Ubx130 has haltere phenotype, enhanceable by Df(3L)Aprt-21
Trl13C has sex comb phenotype, enhanceable by Df(3L)Aprt-21
Trl13C has abdominal segment 6 phenotype, enhanceable by Df(3L)Aprt-21
Trl13C has microchaeta & abdominal segment 6 | ectopic phenotype, enhanceable by Df(3L)Aprt-21
Trl13C is an enhancer of mesothoracic leg phenotype of Pc15
Trl13C is an enhancer of mesothoracic leg phenotype of Pc3
Trl[+]/Trl13C is a non-enhancer of phenotype of lolalk02512
Trl[+]/Trl13C is a non-suppressor of phenotype of lolalk02512
Df(3L)Aprt-21, Trl13C, Ubx130 has wing | ectopic phenotype
Adding at least one copy of the TrlHsp83.GAGA-519 or Hsp83GAGA581 transgenes allows the recovery of a much higher frequency of homozygous Trl13C escapers that are also heterozygous for lolalk02512 (up to approximately 80% when four copies of the transgene are added).
lolalk02512 ; Trl13C heterozygous flies are viable and do not show any visible phenotype. Approximately 4% of lolalk02512/+; Trl13C/Trl13C flies hatch. Adding at least one copy of the Hsp83GAGA519 or Hsp83GAGA581 transgenes allows the recovery of a much higher frequency of homozygous Trl13C escapers that are also heterozygous for lolalk02512 (up to approximately 80% when four copies of the transgene are added). lolalk02512/+; Trl13C/Ubx130 flies display a higher frequency (18%) of strong haltere-to-wing transformations compared to Trl13C/Ubx130 siblings (6.3%). This increased transformation is often accompanied by a notal transformation.
Trl13C/+, lolalk02512/+ animals show no enhancement or suppression of the lolalk02512 phenotype.
56% of Ubx130, Trl13C double heterozygotes have halteres that quite heterogeneous in size and larger than Ubx130 alone. 78% of Ubx130, Df(3L)Aprt-21, Trl13C triple heterozygotes have halteres that quite heterogeneous in size and larger than Ubx130 alone, also exhibiting a stronger phenotype than any two of the alleles used. The haltere becomes a wing -like structure with wing veins and hairs on the wing margin. Trl13C Df(3L)Aprt-21 double heterozygotes have an average of about 7 sex combs. 67% of animals have bristles on segment abdominal segment 6.
Mutant strongly suppresses the CycEJP rough eye phenotype.
Trl13C suppresses the pairing-dependent silencing of wenh.iab-7PRE.260 seen in flies homozygous for P{iab-7PRE-wenh.260}1.
Mutant heterozygotes show no enhancement or suppression of the eye phenotype see in P{UAS-lacZ.Abd-B.5F24}.
Trl13C, wFab-7.24F6 mutants show a 2 fold reduction in eye pigment levels compared to Trl+ siblings: PcG-mediated silencing.
Trl13C is partially rescued by TrlHsp83.PG
TrlR67/Trl13C is partially rescued by TrlHsp83.GAGA-581
TrlR67/Trl13C is partially rescued by TrlHsp83.GAGA-519
Trl13C is partially rescued by TrlHsp83.GAGA-519
Trl13C is not rescued by TrlHsp83.GAGA-581
Expression of TrlHsp83.GAGA-519 partially rescues the lethality seen in Trl13C/TrlR67 mutants, with a survival rate of between 10 and 20% depending on the insertion line.
Expression of TrlHsp83.GAGA-581 partially rescues the lethality seen in Trl13C/TrlR67 mutants, with a survival rate of between 25 and 60% depending on the insertion line.
Expression of a single copy of TrlHsp83.GAGA-519 partially rescues the abdominal segment transformation seen in Trl13C mutant males.
Expression of a single copy of TrlHsp83.GAGA-581 does not rescue the abdominal segment transformation seen in Trl13C mutant males.
Expression of a single copy of TrlHsp83.GAGA-519 partially rescues the reduction in egg production seen in Trl13C mutant females.
Expression of a single copy of TrlHsp83.GAGA-581 does not rescue the reduction in egg production seen in Trl13C mutant females.
Expression of TrlHsp83.GAGA-519 partially rescues the lethality seen in embryos produced by homozygous Trl13C mutant mothers.
Expression of TrlHsp83.GAGA-581 does not rescue the lethality seen in embryos produced by homozygous Trl13C mutant mothers.
Expression of a single copy of TrlHsp83.GAGA.T:Ecol\lacZ rescues the zygotic lethality in Trl13C/TrlR67 mutants. However the A6 to A5 abdominal transformation or the maternal-effect lethality are rescued.
Separable from: a putative second-site mutation on the right arm of the chromosome that is responsible for the homeotic transformations seen in flies carrying the original '13C' chromosome.
Ubx expression is reduced. Trl13C in a heterozygous condition promotes heterochromatinization. Precise excision of the P-element results in complete reversion of the homeotic transformation phenotype and enhancer of position effect variegation phenotype.
Attempts to make germ-line clones with this allele failed.
All mutant phenotypes are reverted by excision of the P{bluetail} element.