Portion of the Rho1 coding region is removed.
embryonic/first instar larval cuticle & embryonic head
Heterozygosity for Rho1rev220 leads to a low frequency of defects in leg morphogenesis.
Most Rho1rev220 mutant embryos lack head cuticle; with the remaining cuticle differing in size among different embryos. Approximately 17.5% of embryos have severe head defects. In 51.5% of the embryos the head is missing, with the entire embryo occupying less than 0.6 of the field at x20 magnification.
Rho1rev220 mutants are nearly normal during early dorsal closure, with defects becoming apparent during late dorsal closure. This phenotype is variable, in more severely affected mutants, both the leading-edge actin cable and cell shape changes are less uniform. In less severely affected mutants, when the leading edges meet at the dorsal midline the two epithelial sheets do not line up or intercalate normally.
Approximayely 97.6% of Rho1rev220 mutants exhibit some kind of head defect or head hole. Less than 1% of Rho1rev220 mutants are phenotypically wild-type.
In heterozygous mutants, an occasional loss of the RP3 neuron is seen.
Mutant embryos die with anterior dorsal hole, and bowed body shape. Head involution fails. The procephalon remains on the exterior giving rise to the anterior dorsal hole in the cuticle. Dorsal midline is puckered, though dorsal closure does occur. Cells on the dorsal midline are inappropriately shaped, pinched or stretched. Homozygous mutant embryos derived from mothers with reduced maternal Rho1 function show both the maternal segmentation phenotype and the zygotic morphogenetic phenotype.
Rho1rev220 has lethal | embryonic stage | maternal effect | dominant phenotype, enhanceable by capu1
Rho1rev220 has lethal | embryonic stage | maternal effect | dominant phenotype, enhanceable by capu2
Rho1rev220 has abnormal cell shape phenotype, suppressible by Scer\GAL4Act5C.PU/p120ctnUAS.cFa
Rho1rev220/Rho1[+] is a non-suppressor of abnormal neuroanatomy | heat sensitive phenotype of Nl1N-ts1
Rho1rev220 has leg phenotype, enhanceable by Df(1)YO17/+
Rho1rev220 has embryonic/first instar larval cuticle phenotype, enhanceable by p120ctn308
Rho1rev220 has phenotype, enhanceable by cta4
Rho1rev220 has phenotype, enhanceable by cta5
Rho1rev220 has embryonic/first instar larval cuticle & embryonic head phenotype, non-enhanceable by p120ctn308
Rho1rev220 has phenotype, non-enhanceable by chic01320
Rho1rev220 has phenotype, non-enhanceable by hepr75
Rho1rev220 has phenotype, non-enhanceable by pucE69
Rho1rev220 has phenotype, non-enhanceable by wgNZ
Rho1rev220 has phenotype, non-enhanceable by EgfrE1
Rho1rev220 has phenotype, non-enhanceable by Egfrf2
Rho1rev220 has phenotype, non-enhanceable by RhoGEF2unspecified
Rho1rev220 has phenotype, non-enhanceable by aop1
Rho1rev220 has phenotype, non-enhanceable by arm3
Rho1rev220 has phenotype, non-enhanceable by bsk1
Rho1rev220 has embryonic/first instar larval cuticle & embryonic head phenotype, suppressible by Scer\GAL4Act5C.PU/p120ctnUAS.cFa
Rho1rev220 has embryonic head phenotype, suppressible by Scer\GAL4Act5C.PU/p120ctnUAS.cFa
Rho1rev220 has embryo | dorsal closure stage phenotype, suppressible by Scer\GAL4Act5C.PU/p120ctnUAS.cFa
Rho1rev220 has embryonic/first instar larval cuticle & embryonic head phenotype, non-suppressible by p120ctn308
Rho1rev220 has phenotype, non-suppressible by chic01320
Rho1rev220 has phenotype, non-suppressible by hepr75
Rho1rev220 has phenotype, non-suppressible by pucE69
Rho1rev220 has phenotype, non-suppressible by wgNZ
Rho1rev220 has phenotype, non-suppressible by EgfrE1
Rho1rev220 has phenotype, non-suppressible by Egfrf2
Rho1rev220 has phenotype, non-suppressible by RhoGEF2unspecified
Rho1rev220 has phenotype, non-suppressible by aop1
Rho1rev220 has phenotype, non-suppressible by arm3
Rho1rev220 has phenotype, non-suppressible by bsk1
Rho1rev220 is an enhancer of embryonic/first instar larval cuticle phenotype of shgg119
Rho1rev220 is an enhancer of embryonic ventral epidermis phenotype of shgg119
Rho1rev220 is a suppressor of embryonic/first instar larval cuticle phenotype of shg2
Rho1rev220 is a suppressor of embryonic/first instar larval cuticle phenotype of shgR69
Rho1rev220 is a suppressor of larval VL3/4 motor neuron phenotype of PlexBUAS.cHa, Scer\GAL4elav.PLu
Rho1rev220 is a suppressor of larval intersegmental nerve phenotype of PlexBUAS.cHa, Scer\GAL4elav.PLu
Rho1rev220/Rho1[+] is a non-suppressor of larval intersegmental nerve | heat sensitive phenotype of Nl1N-ts1
Rho1rev220/Rho1[+] is a non-suppressor of larval intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype of Nl1N-ts1
Rho1rev220/Rho1[+] is a non-suppressor of larval segmental nerve branch SNa of A1-7 | heat sensitive phenotype of Nl1N-ts1
Polr2Bwimp, Rho1rev220 has egg chamber phenotype
Polr2Bwimp, Rho1rev220 has nurse cell ring canal phenotype
Polr2Bwimp, Rho1rev220/Rho1[+] has egg chamber phenotype
Polr2Bwimp, Rho1rev220/Rho1[+] has nurse cell ring canal phenotype
Double Rho1rev220/+ Df(1)YO17/+ heterozygotes show more severe leg defects than either mutant alone.
Heterozygosity for Rho1rev220 fails to suppress the axonal defects found in Nl1N-ts1 mutants.
Most embryos double mutant for p120ctn308 and Rho1rev220 lack head cuticle, with the remaining cuticle differing significantly in size among different embryos.
p120ctn308 does not substantially modify the Rho1rev220 phenotype, nor is a novel double-mutant phenotype observed. The percentage of embryos with head holes is similar, for example 76.1% of Rho1rev220 mutants versus 74.6% of double mutants. However double mutants do have twice as many long cuticles as Rho1rev220 single mutants.
Rho1rev220 p120ctn308 double mutants exhibit the same range of phenotypes as Rho1rev220 single mutants during early and later stages of dorsal closure.
Overexpression of p120ctnScer\UAS.cFa under the control of Scer\GAL4Act5C in a Rho1rev220 background may result in slight suppression of the Rho1rev220 phenotype (although this may be due to differences in the genetic background).
Loss of Rho1rev220 enhances the shgg119 phenotype. Most double mutants have holes in their ventral epidermis that are not present in most shgg119 single mutants. As both Rho1rev220 and shgg119 affect head involution, the enhancement of this phenotype may simply reflect additive effects. However, because loss of Rho1rev220 does not affect integrity of the ventral epidermis, enhancement of this aspect of the phenotype is likely to reflect a genetic interaction.
Rho1rev220 enhances the weak shgg119 phenotype, leading to more severe embryonic defects. The percentage of phenotypically-wild-type embryos is reduced from approximately 7.6% in shgg119 embryos to approximately 0.5% in shgg119 Rho1rev220 mutants. The majority of shgg119 Rho1rev220 mutants (approximately 54%) exhibit ventral holes in the embryonic cuticle, compared to 21.7% in shgg119 mutants and 0.4% in Rho1rev220 mutants.
The shg2 embryonic cuticle phenotype is partially suppressed by Rho1rev220. Approximately 4.5% of shg2 mutants are phenotypically wild-type, while 5.9% of Rho1rev220 shg2 double mutants are wild-type. Approximately 39.9% of double mutants exhibit ventral holes in the cuticle compared to 11.4% in the single shg21 mutant, with 55% of shg2 mutants exhibiting fragmentary ventral cuticle, while only 46.3% of the double mutants exhibit this phenotype. In summary, over 80% of Rho1rev220 shg2 double mutants have ventral holes or fragmentary ventral cuticle. This illustrates the general suppression of the shg2 phenotype in a Rho1rev220 background.
Females with reduced Rho1 function (Rho1rev220/+; +/RpII140wimp) show disrupted actin cytoskeletal structure in the egg chambers, particularly in the outer ring canals and oocyte cortex. The inner ring canals appear relatively normal. Embryos derived from mothers with reduced Rho1 function die with moderate segmentation defects as seen by denticle belt fusions. Approximately 10% of the dead embryos have cuticular holes that are randomly placed, as opposed to being dorsal. Cell morphology is abnormal with cells showing irregular shapes. Gastrulation is not blocked.