The expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4da.PU results in hyper-constriction of epidermal leading edge cells during dorsal closure, as compared to controls.
Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4c381 results in uniform amnioserosal cell rounding.
Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4prd.RG1 in individual amnioserosa cells induces premature apical constriction in these cells.
Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4prd.RG1 results in deep segmental grooves in the embryo.
Stage 16 embryos overexpressing Ggal\MLCKct.Scer\UAS driven by Scer\GAL4ftz.ng display axon bundles that cross the midline inappropriately.
When Ggal\MLCKct.Scer\UAS is driven by Scer\GAL4ftz.ng, midline crossovers are seen in the pCC/MP2 pathway axons in 8.2% of embryos. An average of 1.4 crossovers are seen per embryo.
Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4elav.PLu causes specific defects in the formation of the pCC/MP2 pathway. Initial extension of the pCC axons at stage 12 appears normal. By stage 14, the common MP2 pathway and the separate MP1 pathway are formed normally, but some of the axons of the vMP2 pathway cross the midline. By stage 16, pCC/MP2 pathway axons are seen to cross the midline in several segments, while the remaining longitudinal connectives appear unaffected. Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng causes axons of the pCC/MP2 pathway to cross the midline incorrectly in 9-19% of embryos.
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by Abl4
Abl4/Abl[+], Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by Rho1V14.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by fraUAS.cKa, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy phenotype, enhanceable by robo[+]/robo11
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy phenotype, enhanceable by sli2/sli[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy phenotype, enhanceable by sqhE20.E21
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy phenotype, enhanceable by fraUAS.cKa, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Rho1V14.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy | embryonic stage 16 phenotype, suppressible by sqhT20A.S21A.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy | embryonic stage 16 phenotype, suppressible by Abl4/Abl[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa has abnormal neuroanatomy | embryonic stage 16 phenotype, suppressible by Abl4/Abl[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy phenotype, suppressible by fra3/fra[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy phenotype, suppressible | partially by fra4/fra[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy phenotype, suppressible | partially by sqhA20.A21.Tag:FLAG
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy phenotype, suppressible | partially by sqh1
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng is an enhancer of abnormal neuroanatomy | embryonic stage 16 phenotype of Rac1V12.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng is an enhancer of abnormal neuroanatomy | embryonic stage 16 phenotype of Rho1V14.UAS, Scer\GAL4ftz.ng, fraUAS.cKa
Ggal\MLCKct.UAS/Scer\GAL4ftz.ng is an enhancer of abnormal neuroanatomy phenotype of robo11
Ggal\MLCKct.UAS/Scer\GAL4ftz.ng is an enhancer of abnormal neuroanatomy phenotype of sli2
Ggal\MLCKct.UAS/Scer\GAL4elav.PLu is a suppressor of abnormal neuroanatomy phenotype of comm1
Ggal\MLCKct.UAS/Scer\GAL4ftz.ng is a suppressor of abnormal neuroanatomy phenotype of comm1
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa has commissure | embryonic stage 16 phenotype, enhanceable by Abl4
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa has larval ventral nerve cord commissure | embryonic stage 16 phenotype, enhanceable by Abl4
Abl4/Abl[+], Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has commissure | embryonic stage 16 phenotype, enhanceable by Rho1V14.UAS, Scer\GAL4ftz.ng
Abl4/Abl[+], Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval ventral nerve cord commissure | embryonic stage 16 phenotype, enhanceable by Rho1V14.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has commissure | embryonic stage 16 phenotype, enhanceable by fraUAS.cKa, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval ventral nerve cord commissure | embryonic stage 16 phenotype, enhanceable by fraUAS.cKa, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has dMP2 neuron phenotype, enhanceable by Rac1V12.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has pCC neuron phenotype, enhanceable by Rac1V12.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has vMP2 neuron phenotype, enhanceable by Rac1V12.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has dMP2 neuron phenotype, enhanceable by Rho1N19.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has vMP2 neuron phenotype, enhanceable by Rho1N19.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has pCC neuron phenotype, enhanceable by Rho1N19.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has dMP2 neuron phenotype, enhanceable by Rho1V14.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has pCC neuron phenotype, enhanceable by Rho1V14.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has vMP2 neuron phenotype, enhanceable by Rho1V14.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has dMP2 neuron phenotype, enhanceable by Cdc42V12.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has pCC neuron phenotype, enhanceable by Cdc42V12.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has vMP2 neuron phenotype, enhanceable by Cdc42V12.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval longitudinal connective phenotype, enhanceable by fraUAS.cKa, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval longitudinal connective phenotype, enhanceable by robo[+]/robo11
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval longitudinal connective phenotype, enhanceable by sli2/sli[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval longitudinal connective phenotype, enhanceable by sqhE20.E21
Ggal\MLCKct.UAS, Rho1V14.UAS, Scer\GAL4ftz.ng has commissure | embryonic stage 16 phenotype, suppressible by sqhT20A.S21A.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Rho1V14.UAS, Scer\GAL4ftz.ng has larval ventral nerve cord commissure | embryonic stage 16 phenotype, suppressible by sqhT20A.S21A.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has commissure | embryonic stage 16 phenotype, suppressible by Abl4/Abl[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval ventral nerve cord commissure | embryonic stage 16 phenotype, suppressible by Abl4/Abl[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa has commissure | embryonic stage 16 phenotype, suppressible by Abl4/Abl[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng, fraUAS.cKa has larval ventral nerve cord commissure | embryonic stage 16 phenotype, suppressible by Abl4/Abl[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has pCC neuron phenotype, suppressible | partially by Cdc42N17.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has pCC neuron phenotype, suppressible | partially by Rac1N17.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has vMP2 neuron phenotype, suppressible | partially by Cdc42N17.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has vMP2 neuron phenotype, suppressible | partially by Rac1N17.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has dMP2 neuron phenotype, suppressible | partially by Cdc42N17.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has dMP2 neuron phenotype, suppressible | partially by Rac1N17.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval longitudinal connective phenotype, suppressible by fra3/fra[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval longitudinal connective phenotype, suppressible | partially by fra4/fra[+]
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval longitudinal connective phenotype, suppressible | partially by sqh1
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng has larval longitudinal connective phenotype, suppressible | partially by sqhA20.A21.Tag:FLAG
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng is an enhancer of commissure | embryonic stage 16 phenotype of Rac1V12.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng is an enhancer of larval ventral nerve cord commissure | embryonic stage 16 phenotype of Rac1V12.UAS, Scer\GAL4ftz.ng
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng is an enhancer of commissure | embryonic stage 16 phenotype of Rho1V14.UAS, Scer\GAL4ftz.ng, fraUAS.cKa
Ggal\MLCKct.UAS, Scer\GAL4ftz.ng is an enhancer of larval ventral nerve cord commissure | embryonic stage 16 phenotype of Rho1V14.UAS, Scer\GAL4ftz.ng, fraUAS.cKa
Ggal\MLCKct.UAS/Scer\GAL4ftz.ng is an enhancer of larval longitudinal connective phenotype of robo11
Ggal\MLCKct.UAS/Scer\GAL4ftz.ng is an enhancer of larval longitudinal connective phenotype of sli2
Ggal\MLCKct.UAS/Scer\GAL4e22c is a suppressor of amnioserosa | maternal effect phenotype of Rho172O/Rho1[+], dia2
Ggal\MLCKct.UAS/Scer\GAL4elav.PLu is a suppressor of symmetrical commissure phenotype of comm1
Ggal\MLCKct.UAS/Scer\GAL4ftz.ng is a suppressor of symmetrical commissure phenotype of comm1
The abnormal cell protrusions that are seen extending from amnioserosa cells in the progeny of dia2 Rho172O double heterozygous females during dorsal closure are suppressed by expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4e22c.
Co-expression of Ggal\MLCKct.Scer\UAS with Rac1V12.Scer\UAS under the control of Scer\GAL4ftz.ng results in a synergistic increase in the frequency of incorrect axon projections across the midline, compared with Rac1V12.Scer\UAS-overexpression alone.
When fraScer\UAS.cKa is co-expressed with both Rho1V14.Scer\UAS and Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng, all embryos exhibit severe defects in scaffold formation. Many ventral nerve cord axons either cross the midline or collapse into the midline region.
Co-expression of sqhT20A.S21A.Scer\UAS under the control of Scer\GAL4ftz.ng suppresses the midline crossing phenotype in embryos expressing both Rho1V14.Scer\UAS and Ggal\MLCKct.Scer\UAS.
No embryos heterozygous for Abl4 and expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng exhibit axonal midline crossing defects.
Co-expression of fraScer\UAS.cKa with Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng increases the frequency of axonal midline crossing abnormalities.
Heterozygous Abl4 almost completely suppresses the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCKct.Scer\UAS with fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng.
Homozygous Abl4 enhances the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCKct.Scer\UAS with fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng.
The heterozygous Abl4-dependent suppression of the axonal midline crossing phenotype in embryos expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is lost if Rho1V14.Scer\UAS is also expressed.
The addition of Rho1N19.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 28% of embryos exhibit the phenotype. An average of 1.3 crossovers are seen per embryo. The addition of Rho1V14.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 45% of embryos exhibit the phenotype. An average of 2.1 crossovers are seen per embryo. The addition of Rac1N17.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos partially suppresses the midline crossover phenotype seen in the pCC/MP2 pathway axons. 4.0% of embryos exhibit the phenotype. An average of 1.o crossovers are seen per embryo. The addition of Rac1V12.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 95% of embryos exhibit the phenotype. An average of 4.2 crossovers are seen per embryo. The addition of Cdc42N17.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos partially suppresses the midline crossover phenotype seen in the pCC/MP2 pathway axons. 4.4% of embryos exhibit the phenotype. An average of 1.3 crossovers are seen per embryo. The addition of Cdc42V12.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 97% of embryos exhibit the phenotype. An average of 7.8 crossovers are seen per embryo.
The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is partially suppressed by sqh1 or sqhA20.A21.T:Zzzz\FLAG and is enhanced by sqhE20.E21. Fas2-positive axon bundles cross the midline in about 83% or 88% of robo1/+ embryos which are also expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng. Fas2-positive axon bundles cross the midline in 100% of sli2/+ embryos which are also expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng. The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is partially suppressed by fra4/+ and completely suppressed by fra3/+. The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is enhanced by coexpression of fraScer\UAS.cKa. Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng in comm1 embryos results in 49% of embryos showing some axons crossing the midline and in many cases thin commissures are present. Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4elav.PLu in comm1 embryos results in partial commissure formation in 71% of embryos.