Translocation breakpoint maps near the 3' end of the ftz transcription unit. Encoded protein is truncated: C-terminal 100 amino acids of normal protein are replaced by 10 novel amino acids (NLYVYTCLCS). The region of homology with the other homeotic genes Antp and Ubx is largely but not completely intact.
Breakpoint maps to a 3.2kb HindIII fragment that hybridizes to the 1.8kb ftz transcription unit.
Heterozygotes often have patchy transformations of posterior haltere to posterior wing and, rarely, of the first abdominal segment to a more posterior segment. Homozygotes die as mature embryos with defects in even-numbered parasegments.
Variable transformation of posterior haltere to posterior wing. Occasional patchy transformation of A1 tergite to a more posterior segment ( it is not known whether this is to A2, A3 or A4). No segmental transformations seen in the embryo. About 13% of adults heterozygous for ftzRpl show defects in abdominal segmentation, with these occurring almost exclusively in A4. Embryos hemizygous for ftzRpl show setal belt defects, occurring almost exclusively in odd-numbered segments. Similar odd-segment defects occur with lower penetrance in homozygous ftzRpl embryos. ftzRpl is homozygous lethal.
Hemizygous embryos have partial gaps and/or fusions in some denticle belts while others appear normal. This phenotype is similar to that of the temperature sensitive ftz5 at 28oC. Heterozygotes show a dominant post-bithorax-like phenotype where the metathoracic haltere is partially transformed into a mesothoracic wing.
dominant
ftzRpl has nervous system phenotype, enhanceable by hbD1
ftzRpl and hbD1 in a transheterozygous combination result in 100% penetrance of the transformation of posterior halteres to wings. Segmentation defects approximate to the expectations of simple additivity of the two mutants but the cuticular element defects and nervous system defects are more severe.
Duncan.
