The expression of fra^Scer\UAS.cKa under the control of Scer\GAL4^Mef2.247 partially suppresses only the reduced filopodial and lamellopodial activities, but not the reduced migration velocity, observed in robo1¹ homozygous embryonic heart cardioblasts; this expression also does not suppress the associated heart lumen formation defects observed in robo1¹ homozygotes.

Overexpression of fra^Scer\UAS.cKa under the control of Scer\GAL4^ppk.1.9 significantly suppresses the Trim9⁴⁶ midline crossing defects.

Re-expression of fra^Scer\UAS.cKa in fra³/fra⁴ mutants reverts the phenotype back to that seen when Abl^Scer\UAS.cHa is expressed alone under the control of Scer\GAL4^insc-Mz1407 : normal anterior and posterior commissure formation.

Co-expression of fra^Scer\UAS.cKa with Rac1^V12.Scer\UAS under the control of Scer\GAL4^ftz.ng results in a strong synergistic increase in the frequency of incorrect axon projections across the midline, compared with Rac1^V12.Scer\UAS-overexpression alone.

The frequency of crossovers across the midline in embryos expressing Rho1^V14.Scer\UAS driven by Scer\GAL4^ftz.ng is significantly increased by co-expression of fra^Scer\UAS.cKa.

Co-expression of sqh^{T20A.S21A.Scer\UAS} under the control of Scer\GAL4^ftz.ng suppresses the midline crossing phenotype in embryos expressing both Rho1^V14.Scer\UAS and fra^Scer\UAS.cKa.

Ventral nerve cord axon bundles of stage 16 embryos overexpressing fra^Scer\UAS.cKa via Scer\GAL4^ftz.ng in a heterozygous Abl⁴ genetic background display few incorrect midline crossings.

Expression of fra^Scer\UAS.cKa in the early stages of axon pathfinding under the control of Scer\GAL4^prd.RG1 rescues axonal defects in even segments of fra¹/Df(2R)en-SFX31 transheterozygous embryos. Approximately 60% of the segments display normal commissures, in contrast to fra¹/Df(2R)en-SFX31 embryos, in which nearly all the segments are affected. A partial rescue of odd segments is also seen. In contrast, overexpression of fra^Scer\UAS.cKa in later stages of development, under the control of Scer\GAL4^elav.PLu does not rescue the the defects in ventral nerve cord architecture seen in fra¹/Df(2R)en-SFX31 mutants.

Overexpression of fra^Scer\UAS.cKa under the control of Scer\GAL4^prd.RG1 does not suppress the abnormal pathfinding phenotype observed in Df(2R)en-SFX31 mutants.

Expression of fra^Scer\UAS.cKa in the early stages of axon pathfinding under the control of Scer\GAL4^prd.RG1 rescues axonal defects in even segments of fra¹/Df(2R)en-SFX31 transheterozygous embryos. Approximately 60% of the segments display normal commissures, in contrast to fra¹/Df(2R)en-SFX31 embryos, in which nearly all the segments are affected. A partial rescue of odd segments is also seen. In contrast, overexpression of fra^Scer\UAS.cKa in later stages of development, under the control of Scer\GAL4^elav.PLu does not rescue the the defects in ventral nerve cord architecture seen in fra¹/Df(2R)en-SFX31 mutants.

Expression of fra^Scer\UAS.cKa in elav⁵ mutant EW and EG neurons (under the control of Scer\GAL4^eg-Mz360) does not modify the proportion of contralateral projection defects in elav⁵ mutant embryos. For example, EW axons fail to cross the midline in 755 of the neuromeres in such embryos.

Expression of fra^Scer\UAS.cKa under the control of Scer\GAL4^elav.PLu does not enhance the sli^E-158 longitudinal tract phenotype.

Re-expression of fra^Scer\UAS.cKa in fra³/fra⁴ mutants reverts the phenotype back to that seen when Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS} is expressed alone under the control of Scer\GAL4^insc-Mz1407 : fuzzy commissures.

fra³/fra⁴ fails to reduce the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4^insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS} when fra^Scer\UAS.cKa is co-expressed.

Co-expression of fra^Scer\UAS.cKa with Ggal\MLCK^ct.Scer\UAS under the control of Scer\GAL4^ftz.ng increases the frequency of axonal midline crossing abnormalities.

Heterozygous Abl⁴ almost completely suppresses the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCK^ct.Scer\UAS with fra^Scer\UAS.cKa under the control of Scer\GAL4^ftz.ng.

Homozygous Abl⁴ enhances the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCK^ct.Scer\UAS with fra^Scer\UAS.cKa under the control of Scer\GAL4^ftz.ng.

The frequency of neuronal crossover projections induced by Scer\GAL4^ftz.ng-driven expression of Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS} is significantly increased by co-expression of fra^Scer\UAS.cKa.

The midline crossover phenotype caused expression of Ggal\MLCK^ct.Scer\UAS under the control of Scer\GAL4^ftz.ng is enhanced by coexpression of fra^Scer\UAS.cKa.