A single nucleotide substitution in the coding sequence of mam results in a truncated protein of 83 amino acids from the N-terminus.
In homozygous mamk1514 mutant AM29+ paired MARCM clones, both axons adopt a ventromedial trajectory and target to DM6.
In mamk1514 mutants, the axonal projection to glomerulus DL4 is abolished, while the projection to DM6 remains. mamk1514 mutants autonomously switch both the axonal pathway and the target glomerulus of the olfactory neurons projecting to DL4 to those of the olfactory neurons projecting to DM6.
In mamk1514 mutants, the axonal projections to glomeruli VL1, VM4, VC3l, VM1, VC3m, VC5, VC1, VA4, VC2, VC4, DL1, DM1, V, DM4, DM2, DM3, DA4l, DC1, DA3, and DA1 are abolished.
mamk1514 olfactory organ cell clones induced at 30 hours before puparium formation and analyzed at 20-24 hours after puparium formation contain eight cells that stain with sens indicating they are pNb progeny, suggesting that all the progenies of PIIa and pIIB transform to pNb-like cells.
mamk1514 has abnormal neuroanatomy | somatic clone phenotype, suppressible | partially by Sema2bf02042
mamk1514 has olfactory receptor neuron | somatic clone phenotype, suppressible | partially by Sema2bf02042
In Sema-2bf02042, mamk1514 double mutant paired axon clones (generated through expression of Scer\FLP1hs.PG, Scer\GAL80ts.αTub84B and Scer\GAL4AM29), both neurons chose a dorsolateral axon trajectory, a phenotype opposite to that of mamk1514 paired clones. Sema-2b removal only partially reverts the mamk1514 phenotype in glomerular targeting, as double-mutant axons skip the DL4 glomerulus in 46% of clones despite taking the correct dorsolateral trajectory that passes by the target DL4 glomerulus.