Fmr1Δ50M mutants do not display defects in coordinated behavior (such as in a roll-over assay).
Fmr1Δ50M mutants display significant overbranching in the neuromuscular synapse. Treatment of these mutants with the
mGluR antagonist MPEP, which blocks
mGluR signaling, suppresses the
Fmr1Δ50M overbranching phenotype.
Fmr1Δ50M mutant synaptic terminals display a significant increase in total area, compared to controls.
Fmr1Δ50M mutants treated with the
mGluR antagonist MPEP, which blocks
mGluR signaling, display a significantly decreased synaptic area compared to non-treated mutants. However, MPEP-treated control animals display a similar decrease compared to non-treated controls, leading to the difference between the MPEP-treated wild-type control and the MPEP-treated
Fmr1Δ50M mutant remaining significant, indicating that blocking
mGluR signaling does not significantly rescue the increased synaptic terminal area characteristic of
Fmr1Δ50M mutants.
Fmr1Δ50M mutants display a significant increase in the number of synaptic boutons in the neuromuscular junction. Treatment of these mutants with the
mGluR antagonist MPEP, which blocks
mGluR signaling, does not rescue this increased bouton defect.
At the ultrastructural level, the overall appearance of a bouton and the postsynaptic subsynaptic reticulum in
Fmr1Δ50M mutants appears normal. Quantitatively, there is no significant difference in bouton size, mitochondria size, active zone size/number or the postsynaptic subsynaptic reticulum between
Fmr1Δ50M mutants and control larvae.
Fmr1Δ50M mutants display significant increases of synaptic vesicle density throughout the synaptic bouton clustered vesicle number surrounding active zones and docked vesicle number at the T-bar membrane. overall,
Fmr1Δ50M mutants display a significant ~30% increase in overall vesicle number.
Fmr1Δ50M mutants display a significant ~50% increase in the pool of clustered vesicles around the active zone.
Fmr1Δ50M mutants display a significant ~85% increase in the number of docked vesicles at the active zone.
Fmr1Δ50M mutant mushroom body neurons display axonal overgrowth, with both the axon branch number and the total axon branch length significantly increased in these mutants compared to controls. Treatment of these MARCM clone animals with the
mGluR antagonist MPEP can effectively rescue the axon overgrowth and increased branching defects in these mutants.