Amino acid replacement: M153I. M153I falls in the first RNA-binding domain.
G12271966H
M153I | bru1-PA; M359I | bru1-PB; M153I | bru1-PE; M153I | bru1-PF; M359I | bru1-PG; M122I | bru1-PH; M122I | bru1-PI; M122I | bru1-PJ; M122I | bru1-PK
M153I
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
The indirect flight muscle (IFM) fibers of day 1 aretPD/aretQB mutant adults begin to thin and rupture close to their thoracic attachment sites. Additionally, the sarcomeres appear too short and are sometimes lost. Myofibrils are variable in diameter and often hollow, in contrast to dense, regular myofibrils in wild type. A few days after eclosion, generally all IFM fibers are ruptured and the myofibrils entirely lose their sarcomeric organisation. The tubular leg muscles do not display any obvious phenotypes.
Oogenesis proceeds as far as stage 7 before the egg chambers degenerate in aretPD/Df(2L)esc-P2-0 females. aretPA/aretPD females have a weak ovarian phenotype; many egg chambers produce mature oocytes that can be fertilised and progress through much of embryonic development. Only 3% of embryos derived from these females hatch. Oogenesis arrests at stage 6/7 in aretPD/aretQB females, although an oocyte is specified.
Oogenesis proceeds normally until approximately stage 9, when the egg chambers deteriorate, in hemizygous females. aretPA/aretPD females complete oogenesis and lay eggs, some of which hatch into viable larvae. However, the majority of embryos derived from these females have complex cuticle defects involving partial or complete fusion of adjacent segments.
Almost normal numbers of egg chambers that degenerate early.
Homozygous females usually have almost normal numbers of early stages of egg chambers in their ovaries which degenerated before yolk uptake occurs.
Df(2L)esc-P2-0/bru1PD has ovary phenotype, enhanceable by S[+]/S1
bru1QB/bru1PD has ovary phenotype, enhanceable by Lk6EP886/Scer\GAL4VP16.mat.αTub67C
bru1QB/bru1PD has ovary phenotype, suppressible by Df(3R)M-Kx1/+
bru1QB/bru1PD has ovary phenotype, suppressible by eIF4E1S251D
Delta9P, bru1QB/bru1PD has egg chamber phenotype
Delta9P, bru1QB/bru1PD has stalk follicle cell phenotype
Oogenesis arrests at the germarial stage in S1 aretPD/Df(2L)esc-P2-0 females. The ovarioles fail to bud off into individual egg chambers
and instead, multiple undifferentiated germ cells appear in the severely
truncated ovarioles.
Oogenesis arrests at stage 6/7 in S1 aretPA/aretPD females.
Oogenesis arrests at about stage 3 in S1 aretPD/aretQB
females and no oocyte is specified.
The oogenesis defects of S1 aretPD/Df(2L)esc-P2-0 females
are partially suppressed by one copy of Df(3R)M-Kx1; egg chambers
bud off from the germarium, although they are abnormal - each egg chamber
has more than the normal number of 16 germ cells and no oocyte is specified.
Df(3R)Dl-BX12 dominantly alters the ovary phenotype of S1 aretPD/Df(2L)esc-P2-0
females; the germarium is greatly expanded to produce a large volume
of germ cells surrounded by a layer of follicle cells.
The oogenesis arrest phenotype of S1 aretPD/Df(2L)esc-P2-0
females is suppressed by Df(3R)mbc-R1/+.
Df(3R)M-Kx1 dominantly suppresses the ovary phenotype of aretPD/aretQB
females; the arrest in oogenesis occurs later in the double mutants
than in the single mutant females.
Expression of Lk6EP886 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16
enhances the ovary phenotype of aretPD/aretQB females (oogenesis
arrests at 3), while in the absence of an Scer\GAL4 driver, Lk6EP886
suppresses the ovary phenotype of aretPD/aretQB females (oogenesis
arrests at stage 9).
The hatch rate of embryos derived from aretPA/aretPD females
is increased from 3% to 14% in the presence of Lk6EP886/+.
aretPD/aretQB eIF-4ES251D ; Lk6EP886/+ females arrest
oogenesis at the same stage (stage 9) as aretPD/aretQB ; Lk6EP886/+
females.
eIF-4ES251D suppresses the aretPD/aretQB ovary phenotype,
delaying arrest of oogenesis until stage 9.
Most egg chambers have more than 16 germline cells in aretQB/aretPD
; Dl9P/+ ovaries. Three classes of abnormal egg chambers are seen,
which are present in roughly equal numbers. In the first class, a
large number of germline cells of roughly equal size are enveloped
by a single epithelium of follicle cells. The remaining two classes
arise from partial fusion of separate cysts; no stalk cells can be
detected and the follicle cell layers of different egg chambers remain
in contact with each other. In the "anterior/posterior fusion" class,
a well-defined linear organisation within individual ovarioles is maintained,
and adjacent egg chambers are fused with each other at their anterior
and posterior boundaries. In the "random fusion" class, egg chambers
are positioned irregularly and can be closely apposed to multiple different
egg chambers on lateral as well as on anterior and posterior surfaces.
In both the partial fusion classes, each egg chamber contains an oocyte.
In the anterior/posterior fusion class the oocyte is present at the
posterior of the cyst and in the random fusion class the oocyte is
either lateral or posterior relative to the overall polarity of the
ovariole.