Commissures in embryos expressing Scer\GAL4insc-Mz1407>AblScer\UAS.cHa are similar to that of wild-type.
Overexpression of AblScer\UAS.cHa by Scer\GAL4elav.PLu or Scer\GAL4ftz.ng results in occasional abnormal crossovers in less than 14% of embryos examined.
Co-expression of AblScer\UAS.cHa and AblKN.Scer\UAS in the Scer\GAL4ftz.ng pattern suppresses all abnormal axonal crossovers.
Scer\GAL4insc-Mz1407/AblUAS.cHa is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of fra3/fra4
AblUAS.cHa/Scer\GAL4ftz.ng is an enhancer of abnormal neuroanatomy | embryonic stage 16 | dominant phenotype of robo11
AblUAS.cHa/Scer\GAL4elav.PLu is an enhancer of abnormal neuroanatomy | embryonic stage 16 | dominant phenotype of sli1
AblUAS.cHa/Scer\GAL4ftz.ng is a suppressor of abnormal neuroanatomy phenotype of comm1
AblUAS.cHa/Scer\GAL4elav.PLu is a suppressor of abnormal neuroanatomy phenotype of comm1
AblUAS.cHa, Scer\GAL4insc-Mz1407, fra3/fra4 has abnormal neuroanatomy | embryonic stage phenotype
AblUAS.cHa, Scer\GAL4insc-Mz1407, fra3/fra[+] has abnormal neuroanatomy | embryonic stage phenotype
Scer\GAL4insc-Mz1407/AblUAS.cHa is an enhancer of larval ventral nerve cord commissure phenotype of fra3/fra4
AblUAS.cHa/Scer\GAL4ftz.ng is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of robo11
AblUAS.cHa/Scer\GAL4elav.PLu is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of sli1
AblUAS.cHa/Scer\GAL4ftz.ng is a suppressor of symmetrical commissure phenotype of comm1
AblUAS.cHa/Scer\GAL4elav.PLu is a suppressor of symmetrical commissure phenotype of comm1
AblUAS.cHa, Scer\GAL4insc-Mz1407, fra3/fra4 has tract | ectopic | embryonic stage phenotype
AblUAS.cHa, Scer\GAL4insc-Mz1407, fra3/fra[+] has larval ventral nerve cord commissure phenotype
Over-expression of AblScer\UAS.cHa using Scer\GAL4insc-Mz1407 enhances the degree of thinning and missing posterior commissures in fra3/fra4 embryos, and many anterior commissures disappear. Large bundles of axons are observed ectopically exiting the central nervous system (CNS), often extending beyond the CNS/PNS boundary.
A rare commissure may be malformed in heterozygous fra3 embryos expressing Scer\GAL4insc-Mz1407>AblScer\UAS.cHa.
Re-expression of fraScer\UAS.cKa in fra3/fra4 mutants reverts the phenotype back to that seen when AblScer\UAS.cHa is expressed alone under the control of Scer\GAL4insc-Mz1407 : normal anterior and posterior commissure formation.
Commissure formation is restored in fra3/fra4 mutants expressing both fraΔP1.Scer\UAS and AblScer\UAS.cHa under the control of Scer\GAL4insc-Mz1407.
Commissure formation is restored in fra3/fra4 mutants expressing both fraΔP2.Scer\UAS and AblScer\UAS.cHa under the control of Scer\GAL4insc-Mz1407.
Commissure formation is restored in fra3/fra4 mutants expressing both fraΔP3.Scer\UAS and AblScer\UAS.cHa under the control of Scer\GAL4insc-Mz1407.
Nearly a third of hemi-segments in fra3/fra4 embryos expressing Scer\GAL4insc-Mz1407>AblScer\UAS.cHa exhibit defects characterised by Fas2-positive axons ectopically exiting the central nervous system (CNS).
Compared with heterozygous robo1 mutants alone, overexpression of AblScer\UAS.cHa using Scer\GAL4ftz.ng enhances the frequency of abnormal axonal crossovers.
Compared with heterozygous sli1 mutants alone, pan-neural overexpression of AblScer\UAS.cHa using Scer\GAL4elav.PLu enhances the frequency of abnormal axonal crossovers. Scer\GAL4elav.PLu>AblScer\UAS.cHa expression causes axons to cross the midline inappropriately in most segments of all embryos in sli1 heterozygous mutants.
Using Scer\GAL4ftz.ng, expression of AblScer\UAS.cHa in a subset of neurons in a comm1 background causes a few thin commissures to reform.
Pan-neural expression of AblScer\UAS.cHa under the control of Scer\GAL4elav.PLu partially suppresses the comm1 commissure phenotype.