Fmr1³/Fmr1^Δ83M flies have significant locomotor defects (climbing ability) and display excessive grooming behavior compared to rescued controls at 5 days old, getting progressively worse with aging (day 15, 25 and 35). Fmr1³/Fmr1^Δ83M males show significantly decreased courtship behavior compared to rescued controls.

Fmr1^Δ83M mutant mushroom bodies show β-lobe fibers extending across the midline, sometimes sufficient to cause apparaent fusion of the right and left lobes. Fmr1^Δ83M mutant γ-lobe fibers do not extend across the brain midline.

γ-neurons in Fmr1^Δ83M homozygous mutant mushroom bodies do not cross the midline. Retraction of vertical and medial branches of γ-neurons occurs on schedule and to its full extent in young mutant pupae. Given the normal midline phenotype of mutant larval and young pupal γ neurons, the late-stage β-lobe midline-crossing phenotype cannot be blamed on faulty γ-neuron morphology earlier in development.

In homozygous Fmr1^Δ83M mutant brains, the α and β lobes appear as thin Fas2-immunoreactive bundles at head eversion + 16-17 hours, with progressive thickening over the next 30 hours. The medial tips of the β lobes approach the midline at the correct time, but immediately thereafter, fibers can be seen to extend from the β-lobe termini across the midline. By 48 hours, the right and left β lobes appear fused and very similar to the pharate-adult mutant phenotype. Thus, the midline-crossing phenotype is attributable to β-lobe axons failing to stop at the normal lobe terminus and, instead, grow across the brain midline into the contralateral β-lobe. Consistent with the pharate adult, the phenotype usually develops symmetrically.

Homozygous Fmr1^Δ83M mutants exhibit misdirected or missing α-lobes in almost 30% of cases.

Approximately 95% of transheterozygous Fmr1^Δ83M/Fmr1^Δ113M mutants exhibit severe midline crossing in the β-lobe of the mushroom body (defined as a densely strained band equal to or greater in width and thickness than those of the adjacent β-lobes). The rest appear phenotypically normal. No sexual dimorphism in penetrance or expressivity is found.

Slightly over 85% of transheterozygous Fmr1^Δ83M/Fmr1³ mutants exhibit severe midline crossing in the β-lobe of the mushroom body (defined as a densely strained band equal to or greater in width and thickness than those of the adjacent β-lobes). Approximately 5% exhibit moderate midline crossing (defined as when the thickness of the fiber bundle crossing the midline is considerable but less than the width of the β-lobe termini), with another 5% exhibiting mild midline crossing (defined as when a thin band of fibers cross the midline). No sexual dimorphism in penetrance or expressivity is found.

Fmr1^Δ83M heterozygotes do not exhibit midline crossing in the mushroom bodies.

In fewer than 10% of cases, transheterozygous Fmr1^Δ83M/Fmr1³ mutants exhibit misdirected or missing α-lobes.

In over 25% of cases, transheterozygous Fmr1^Δ83M/Fmr1^Δ113M mutants exhibit misdirected or missing α-lobes.

Approximately 8% of Fmr1^Δ83M/Df(3R)by62 mushroom bodies exhibit a mild or moderate β lobe midline-crossing phenotype. One third of Fmr1^Δ83M/Df(3R)by62 mushroom bodies display accessory phenotypes, where the α lobe is misdirected or missing.

In Fmr1^Δ83M/Df(3R)by62 pharate adults, the α and β lobes appear very immature, resembling those seen in wild-type brains at earlier stages of metamorphosis. In many cases, the lobes appear younger than those of pupae whose β lobe fibers are just approaching the midline. The mushroom body α/β immaturity phenotype is characterised by abnormally thin α and β lobes that are very irregular along their lengths, whereas the γ lobes appear normal. Approximately 80-90% of Fmr1^Δ83M/Df(3R)by62 brains show α/β immaturity. In contrast, all Fmr1^Δ83M/In(3LR)TM6B siblings are within normal limits.

Mutants show a fibre extension defect in the DC and LNv neurons. Extension of DC axons from the lobula to the medulla is incomplete, some axons show guidance errors. LNv neurons may over extend, show guidance defects or show aberrant morphology. The LVn defects are less consistent than those in the DC neurons. Homozygotes show only 36.4% of expected eclosion from pupal case. The photoreceptor field in the optic lobes shows no anatomical defects. Analysis of photoreceptor synaptic transmission using ERGs revealed no alteration in either on transient or off transient; this result is contrary to that reported in FBrf0141416, where inappropriate genetic controls were used.

Mutants show no morphological defects. When tested for bang sensitivity, temperature sensitivity and phototaxis there is no detectable difference between wild type and mutant.