Polytene chromosomes normal.
Mutation is not visible cytologically. Southern blots reveal a breakpoint between coordinates -12.0 and -12.5.
The increase in lamellocyte number and melanotic capsule formation that are seen following wasp infestation in wild type are not seen in heterozygous S1 larvae.
Heterozygotes have a rough eye phenotype.
Heterozygotes do not have defects in the ovary.
Homozygous female germline clones do not develop beyond stage 1 of oogenesis.
Projection patterns of retinal axons in heterozygous larvae are indistinguishable from wild type.
In stage 12/3 homozygous embryos the commissures are thicker and narrower than wild type and by stage 14 they remain incompletely separated. In stage 12/5 embryos the wild type number of midline glia are present but appear tightly clustered and displayed dorsally. Reduction in cell number from stage 13 until 14. Reduction in the VUM cell number at stage 11, during stage 13 half the wild type number of neurons migrate ventrally, these are still present at stage 14. MP1 neurons appear wild-type at stage 13 but there is a reduction in number. In stage 14 embryos there is a reduced number of en+ neurons present at the midline.
Anterior and posterior commissure fuse. Initial development of the axon commissures appears normal but the axon tracts fail to separate at the time of midline glia migration. Midline glial cells appear and then die.
Heterozygotes have slightly reduced eyes with irregularly shaped facets and disarranged facet hairs.
DCTN1-p150Gl-1, S[+]/S1 has visible | dominant phenotype, non-suppressible by Dhc64C77/Su(Gl)77[+]
DCTN1-p150Gl-1, S[+]/S1 has visible | dominant phenotype, non-suppressible by Dhc64C[+]/Dhc64C8-1
S[+]/S1 is an enhancer of visible | dominant phenotype of DCTN1-p150Gl-1
DCTN1-p150Gl-1, S[+]/S1 has eye phenotype, enhanceable by Dhc64C[+]/Dhc64C1-1
S1 has ommatidium phenotype, enhanceable by ast1
S1 has ommatidium phenotype, enhanceable by ml1
DCTN1-p150Gl-1, S[+]/S1 has eye phenotype, non-suppressible by Dhc64C77/Su(Gl)77[+]
DCTN1-p150Gl-1, S[+]/S1 has eye phenotype, non-suppressible by Dhc64C[+]/Dhc64C8-1
DCTN1-p150Gl-1, S[+]/S1 has eye phenotype, non-suppressible by Dhc64C8-1/Dhc64C77
S[+]/S1 is an enhancer of eye phenotype of DCTN1-p150Gl-1
S[+]/S1 is an enhancer of ovary phenotype of Df(2L)esc-P2-0/bru1PD
ast1/S1 is a suppressor of phenotype of netunspecified
S1 is a suppressor of phenotype of netunspecified
ast1/S1 is a suppressor of phenotype of pxunspecified
S1 is a suppressor of phenotype of pxunspecified
Gll1 shows little or no dominant interaction with S1 in the eye.
Dhc64C1-1/+ enhances the rough eye phenotype of S1/+ flies, resulting in more disruption of the hexagonal packing of the ommatidia. and in a smaller eye.
The S1 mutation overcomes the suppression of the Gl1 rough eye phenotype by Dhc64C8-1 or Dhc64C77, so that triple heterozygotes have an enhanced rough eye phenotype compared to Gl1 single heterozygotes.
The enhanced rough eye phenotype of Gl1/+ S1/+ flies is not suppressed by Dhc64C77/Dhc64C8-1.
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/+.
The phenotype is dominantly enhanced by ast1 : double heterozygotes have extremely small, diamond-shaped eyes in which many of the facets are fused and the remainder are irregular in size and distribution. The phenotype is dominantly enhanced by E(S)1. Lethal in double heterozygous combination with ast2. S1 ast3 flies are late hatching, those flies which emerge have good viability and fertility, normal wing venation and extremely small eyes. S1/ast4 flies have smaller eyes than S1/+ flies and they also occasionally have gaps at the tips of the longitudinal wing veins. Partially suppresses the phenotype of netunspecified or pxunspecified homozygotes. S1/ast1 tends to completely suppress the phenotype of netunspecified or pxunspecified homozygotes. astrv3 produces a slightly rougher eye than that characteristic of S1/+ in combination with S1.
Bridges, 21st Feb. 1915.
Dominantly enhances the mutant eye phenotype of rux3.