Nucleotide substitution: G4471A.
Amino acid replacement: D886N. Nucleotide substitution: G4471A.
G11566648A
G4471A
D886N | RpII215-PA
D886N
Exhibits the Ubx effect: heterozygotes partially transform the capitellum of the haltere into the wing blade.
Heterozygotes have a partial transformation of haltere to wing (a Ubx-like phenotype). Flies carrying both RpII215Ubl and Ubx130 show a greater transformation of haltere to wing than flies carrying RpII215Ubl alone. Patches of hemizygous tissue (even in the halteres) appear morphologically normal in gynandromorphs. Mutant germ cells often differentiate into morphologically abnormal oocytes.
Ultrabithorax-like phenotype.
Homozygous and hemizygous lethal. Heterozygotes mimic Ubx in adding several hairs to and enlarging the
capitellum of the haltere; females homozygous for
RpII215Ubl, surviving by virtue of a duplication for
RpII215+, more severely affected with capitellum
approximately three times the size of that observed in
RpII215Ubl/+ and with two or more rows of bristles;
about 10% normal viability; poorly fertile in crosses
to wild type; sterile when crossed to RpII215Ubl
males with a duplication of RpII215+. Similarly
males with one mutant and one normal allele are more
extreme than females with one mutant and two normal
alleles. Acts as a dosage sensitive enhancer of Ubx,
transforming halteres into wing-like structures;
enhancement by RpII215Ubl/RpII215Ubl/+ >
RpII215Ubl/+ > RpII215Ubl/+/+. RpII215Ubl/+
interacts with heterozygotes for Ubxbx-3 and Ubxabx-1 but
not Ubxbx-1 to produce enlarged capitellum and with
Ubxbxd-100/+ to transform halteres into wing-like
structures; extra doses of Ubx+ counteract the
enhancing effects of RpII215Ubl. A second
interaction with Ubx/+ is the production of
miscadestral-like pigmentation. Ubx enhancement by
RpII215Ubl reduced in transheterozygotes with other
interacting alleles (Mortin, Kim and Huang, 1988). Furthermore in
RpII215Ubl/+//RpII215Ubl/0 gynandromorphs, the X0
tissue is without any RpII215Ubl phenotype,
displaying neither enlarged halteres nor enhancement
of Ubx expression, whereas the XX tissue exhibits both
enlarged halteres and Ubx enhancement (Mortin,
Perrimon and Bonner, 1985). RpII215Ubl/+ also display increased
frequencies of duplicated bristles in Dl/+ and in some
crosses causes Sb/+ flies to exhibit shortened and
broadened wings whose longitudinal veins fail to reach
the margin (Mortin, Kim and Huang, 1988). RpII215Ubl in
heterozygous combination with deficiencies for either
ct or sno is lethal and with lethal alleles of ct
produces a strong cut phenotype; produces a mutant
phenotype of allele specific severity in heterozygous
combination with deficiencies for or lethal alleles of
br, N, dm, slc, bi, oc, m, sd and sw; interacts with
heterozygotes for mutant alleles of oc, sno and sw,
but not the others; no interaction with dor, sn, ras,
or g deficiencies. Influence of the maternal genotype
apparent since patroclinous RpII215Ubl/Y and
RpII215Ubl/0 males from non-mutant mothers survive
at 20% the expected rate; they are phenotypically
normal but are sterile (Voelker et al.).
The recessive lethality of RpII215Ubl is not rescued by one copy of RpII140S1, RpII140S2, RpII140S5, RpII140S6, RpII140S8, RpII140S7, RpII140S11 or RpII140S12.
Causes the Ubx effect.
Gynandromorph analysis shows that the dominant Ubx-like phenotype, and the synergistic enhancement of Ubx by RpII215Ubl requires that both a wild-type RpII215 and a RpII215Ubl allele are present in the same cell.
Degree of transformation of the haltere when heterozygous: RpII215H1 < RpII2157 < RpII215K2 < RpII2154 < RpII215Ubl.
Reduces the "Cbx" mesothorax phenotype of some Cbx alleles of Ubx. The reduction of the Cbx phenotype follows the order: UbxCbx-Hm > UbxCbx-2RM = UbxCbx-2 = UbxCbx-M1 > UbxCbx-1RM = UbxCbx-1 = UbxCbx-3 = UbxCbx-Twt.