Amino acid replacement: Q89term.
Nucleotide substitution: C?T.
C1889511T
C?T
Q89term | trr-PC; Q89term | trr-PD
Q89term
Eggs derived from trr1 germline clones form eggs that do not enter embryogenesis because they do not initiate embryo mitotic divisions. The eggs do not support male pronucleus formation (and Protamine B is not removed). Meiosis is invariably completed but seems unsuccessful (shown by abnormal polar body rosettes).
Homozygous trr1 clones in the eye lead to notching of the anterior boundary of the eye presumably caused by incomplete morphogenetic furrow progression, and there are defects in ommatidial organisation leading to a rough eye phenotype.
Hemizygous males derived from trr1/+ females (lack of zygotic trr+ activity combined with a 50% reduction in maternal trr+ activity) show embryonic lethality. When trr1 is introduced paternally rather than maternally, the percentage of hemizygous embryos that fail to hatch decreases, and some dead first instar larvae are seen, indicating that trr+ activity is required both maternally and zygotically during embryogenesis. trr1 does not affect the position effect variegation of the w gene caused by In(1)wm4.
trr1 is an enhancer of lethal phenotype of EcRB1-ΔC655.F645A.UAS, Scer\GAL4GMR.PF
trr1 has eye disc morphogenetic furrow | somatic clone phenotype, suppressible by EcRM554fs/EcR[+]
trr1 has eye | somatic clone phenotype, suppressible by EcRM554fs/EcR[+]
The lethality seen in EcRB1-ΔC655.F645A.Scer\UAS, Scer\GAL4GMR.PF animals is enhanced by the addition of trr1/+. The furrow stop phenotype (in the eye) is noticeably suppressed by the addition of EcRM554fs/+.