Bouton numbers are unaffected at the NMJ of Fmr1^Δ50M/+ third instar larvae.

Fmr1^Δ50M and Fmr1^Δ50M/Df(3R)Exel6265 third instar larvae exhibit increased number of presynaptic boutons, namely satellite boutons, at the third instar larval neuromuscular junction, as compared to controls. In Fmr1^Δ50M larval neuromuscular junction, there is a significant decrease in mEPSP amplitude and significant increase in quantal content, but unchanged EPSP amplitude, as compared to controls; there are no apparent changes in active zones and postsynaptic densities, as compared to controls.

Fmr1^Δ50M and Fmr1^Δ50M/Df(3R)Exel6265 transheterozygotes show a progressive increase in grooming behavior (observed in 25-days old individuals, but not in 10-days old individuals). The mushroom bodies of Fmr1^Δ50M/Df(3R)Exel6265 transheterozygotes show highly penetrant defects (α-lobe thinning and malformation), as compared to controls.

Fmr1^Δ50M adult heterozygotes do not display any overt eye morphology defects but display memory defects in an aversive olfactory conditioning assay (their olfactory perception however is not disrupted). Fmr1^Δ50M homozygous adults exhibit mushroom body defects including missing or thinned mushroom body α-lobes and β-lobe fusion.

Fmr1^Δ50M/Fmr1^Δ50M larvae show significant increases in the number of type I boutons at the neuromuscular junction, compared to controls.

Fmr1^Δ50M/Df(3R)Exel6265 and Fmr1^Δ50M/Fmr1³ mutant females display a strong reduction in fertility. Ovaries of Fmr1^Δ50M/Df(3R)Exel6265 mutants, and a subset of Fmr1^Δ50M/Fmr1³ mutants, display developmental defects, including fused egg chambers, aberrant nurse cell numbers, disorganized germaria often fused to an egg chamber, and occasional oocyte misspecification or multiple oocytes per egg chamber.

Fmr1^Δ50M homozygotes are viable, male sterile and female semi-fertile. Fmr1^Δ50M heterozygous males and females are semi-fertile. Fmr1^Δ50M/Fmr1^Δ113M transheterozygotes are male sterile and female semi-fertile.

Fmr1^Δ50M homozygosity and Fmr1^Δ50M/Fmr1^Δ113M transheterozygosity lead to the formation of crystalline aggregates (of Stellate protein) in spermatocytes, which are absent in Fmr1^Δ50M heterozygotes and wild-type controls.

Fmr1^Δ50M/Fmr1^Δ50M, but not Fmr1^Δ50M/+, mutants display a striking expansion of dendritic arbors in MVP2 neurons at day 1 post-eclosion, as compared to controls, with a significant increase in total dendritic arbor volume; the central core of arbors is much wider than that of wild type, with less-pronounced anterior and posterior ends; homozygous mutant arbors occupy a greater dorsoventral depth as compared with wild type. Projection neuron dendritic arbors in Fmr1^Δ50M/Fmr1^Δ50M mutants also exhibit overgrowth, with a significant increase in total dendritic arbor volume, as compared to controls. These dendritic arbor expansion phenotypes are not observed at earlier developmental time points, measured at pupal day 4, and 1 hour post-eclosion.

The presynaptic terminal length of class IV dendritic arborizing neurons in Fmr1^Δ50M/Fmr1^Δ50M MARCM somatic clones in third instar larvae is significantly increased compared to controls.

Fmr1^Δ50M/Fmr1^Δ50M flies do not exhibit any significant difference in the number, distribution or density of GABAergic neurons, or the GABAergic mushroom body calyx innervation, but do show frequent mushroom body beta lobe crossing and fusion at the midline, and absence or loss of mushroom body lobes, most often the alpha lobe, as compared to controls. Fmr1^Δ50M/Fmr1^Δ50M flies exhibit a strong learning deficit in an associative learning assay.

Fmr1^Δ50M/Fmr1^Δ50M GABAergic neuron clones do not show any significant difference in cumulative process length, as compared to control clones, but do exhibit a differential developmental trajectory in process elaboration, with a highly significant increase in process length between days 1 and 5 post-eclosion, and they also show altered depolarization-induced calcium signaling dynamics, in comparison to control neurons. Fmr1^Δ50M/Fmr1^Δ50M GABAergic neuron clones with only a primary process show a significant increase in total length at 5 days post-eclosion, and those with 5 or more processes show a significant decrease in total process length at 1 day post-eclosion, as compared to control neurons. Fmr1^Δ50M/Fmr1^Δ50M GABAergic neuron clones with 2-4 processes do not exhibit any significant difference in total process length as compared to controls. Fmr1^Δ50M/Fmr1^Δ50M GABAergic neuron clones with 5 or more processes show significantly shorter primary and secondary processes and fewer secondary and tertiary branches at 1 day post eclosion, as compared to controls, but these differences are not seen at 5 days post-eclosion.

Homozygotes are viable and do not display obvious growth phenotypes. Fmr1^Δ50M mutant eyes, generated by eyFLP/FRT-mediated mitotic recombination, do not show an increase in ommatidial number.

Neuromuscular junctions in Fmr1^Δ50M/Fmr1^Δ50M mutant larvae exhibit significantly increased branch number and increased type I synaptic bouton number, and significantly increased amplitude of evoked junctional currents, as compared to controls.

A Fmr1^Δ50M mutant C4 ddaC neuron clones causes mild but significant overgrowth of presynaptic terminals.

Homozygous third instar larvae show an increase in bouton number and satellite bouton number at the neuromuscular junction compared to controls.

Fmr1^Δ50M mutant third instar larvae exhibit neuromuscular junction abnormalities in muscle 4. Their synaptic branch and bouton numbers are significantly higher than in wild type flies.

Mutant males and females show an increase in daytime sleep intensity compared to controls.

The Fmr1^Δ50M mutant brain is unaltered in size and gross architecture compared with controls. However synaptogenesis defects can be seen including elevated synaptic area, increased synaptic branching and the formation of supernumerary synaptic boutons. Developmentally arrested satellite boutons also accumulate in Fmr1^Δ50M mutant larvae. Futsch positive loops accumulate in Fmr1^Δ50M mutant synaptic arbors.

The brains of adult Fmr1^Δ50M mutants exhibit strikingly abnormal small ventrolateral (sLN[[v]] neuron synaptic architecture with expanded terminals containing supernumerary synaptic boutons. Fmr1^Δ50M mutant flies have approximately 70 Pdf positive boutons in the dorsal horn and protocerebrum compared to around 40 in controls.

Fmr1^Δ50M mutants display a highly significant decrease in olfactory learning compared to controls.

A particularly prominent defect in Pdf neurons not reported previously is the aberrant appearance of a class of Pdf neurons in the central brain of Fmr1^Δ50M mutants. This class of neurons is a developmentally-transient population of triocerebral Pdf neurons. These neurons are not observe in age-matched adult wild-type brains. In mutants, these neurons are often present at a bilaterally oriented pair with cell body positioning in the tritocerebrum, near the esophageal foramen. Mutant Pdf neurons project their axons upward beyond the posterior optic tract and elaborate a synaptic field in the protocerebral area adjacent to the sLN[[v]] synaptic arbors. Thus, in addition to connectivity defects within the s- and lLN[[v]] neurons, the PDF circuit may be compromised by the encroaching aberrant contributions of the midline PDF tritocerebral (PDF-TRI) neurons present only in Fmr1^Δ50M mutants. Upon eclosion, wild-type and mutant brains show an indistinguishable array of PDF-TRI neurons. However, in the proceeding days, these cells are rapidly lost in control brains, while retained in Fmr1^Δ50M mutants. The inappropriately retained Fmr1^Δ50M mutant PDF-TRI neurons maintain synaptic connectivity at maturity as well as depolarization-dependent Ca[2+] transients.

No evidence of increased proliferation for the abnormally retained neurons is found, but rather clear indication of impaired apoptosis in Fmr1^Δ50M mutant brains.

Examination of crustacean cardioactive peptide (CCAP) and bursicon circuits, which are developmentally-transient and normally eliminated immediately post-eclosion in wild-type, reveal significantly delayed clearance compared with wild-type, however, the CCAP/bursicon neurons are also subsequently eliminated in Fmr1^Δ50M mutants.

The number of NMJ branches (defined as a process with two or more boutons), is significantly higher in Fmr1^Δ50M mutant third instar larvae compared to controls. The number of mature type 1b boutons is significantly increased in the Fmr1^Δ50M null synapse and the number of immature satellite boutons is similarly elevated. The increase in number of mature boutons and the accumulation of satellite neurons are both rescued when the larvae are fed >20uM minocycline. The increase in NMJ arbor branch number is not restored upon treatment with minocycline.

Small ventrolateral (sLN[[v]]) clock neurons in Fmr1^Δ50M brains at three days post eclosion have an increased number and density of synaptic boutons, with overextension of their spatial distribution extending from the dorsal horn bifurcation point. These phenotypes are completely rescued upon feeding with minocycline. However, minocycline-treated Fmr1^Δ50M null sLN[[v]] neurons continue to display a somewhat dispersed bouton array.

In young adult brains (0-4 hours post-eclosion), single cell Fmr1^Δ50M mutant MARCM clones in the adult mushroom body γ lobe show increased axonal length and excess synaptic branching compared to controls. Both of these defects are rescued upon treatment with minocycline.

Compared to wild-type, brain size and gross architecture of homozygous Fmr1^Δ50M mutants appear unaltered.

Dorsal projections into the protocerebrum in Fmr1^Δ50M mutants exhibit a highly significant increase in the number of s-LNv Pdf neuron boutons compared with controls.

Fmr1^Δ50M mutants display defects on many levels of neuromuscular junction synaptic architecture, including grossly elevated synaptic area, increased synaptic branching, and the formation of supernumerary synaptic boutons. Most strikingly, developmentally arrested mini (or satellite) boutons accumulate int the mutants.

Fmr1^Δ50M males are completely sterile producing no viable progeny.

In Fmr1^Δ50M mutant spermatids, the central pair of axoneme microtubules is routinely lost, whereas the outer ring microtubule doublets are often deranged.

There is an increase in the total number of branches and the total number of boutons at the neuromuscular junction in mutant larvae compared to controls.

Fmr1^Δ50M/Fmr1^Δ50M, Fmr1^Δ50M/Fmr1^Δ113M and Fmr1^Δ50M/Df(3R)Exel6265 adults sleep significantly longer each day than wild-type controls. The length of time they sleep each day increases with age up to some peak (for Fmr1^Δ50M homozygotes: at 12 days in males, 42 days in females). Increased sleep in these animals is predominantly the result of increased number of sleep episodes and reduced number of brief awakenings, rather than increased average duration of sleep episodes. The increase in daily sleep in these mutants is also seen when animals are kept in permanent darkness.

Fmr1^Δ50M/Fmr1^EP3517 adults sleep significantly longer per day than wild-type, although the effect is more subtle than in Fmr1^Δ50M homozygotes and is more pronounced in females than in males. The increase in daily sleep in these flies is increased further by keeping them in permanent darkness.

Under alternating 12 hours light and 12 hours dark conditions, Fmr1^Δ50M/Fmr1^Δ50M mutants show a circadian cycle of sleep. However, this differs from wild-type in having more sleep under light conditions and in lacking a reduction in sleep in anticipation of the end of dark conditions. Also unlike wild-type, under conditions of total darkness, Fmr1^Δ50M/Fmr1^Δ50M adults show no circadian rhythm in locomotor activity or sleep.

Unlike wild-type flies, Fmr1^Δ50M homozygotes do not recover significant amounts of sleep the day after 24 hours of sleep deprivation. However, following sleep deprivation they show reduced activity in response to a stimulus that causes arousal in wild-type or non-sleep deprived Fmr1^Δ50M homozygotes.

Fmr1^Δ50M homozygotes have a reduced lifespan, with a steady death rate almost from eclosion, rather than a lag with few deaths in the first 28 days as seen in wild-type.

Fmr1³/Fmr1^Δ50M ovaries contain aberrant egg chambers with both increased and decreased numbers of germ cells per chamber compared to the normal number of 16. Fmr1³/Fmr1^Δ50M mutant germaria contain significantly more mitotic cells than controls.

None of the completely mutant egg chambers in Fmr1^Δ50M mosaic ovaries surrounded by heterozygous follicle cells exhibit proliferation defects. They appear morphologically normal.

Fmr1^Δ50M mutant sLN[[v]] synaptic arbors display an overgrowth and over-elaboration phenotype.

Fmr1^Δ50M mutants exhibit an increased number of synaptic boutons throughout the sLN[[v]] terminal, projecting at minimum a further 20υm toward the midline and with a greatly increased average number of boutons beyond 50υm, compared to wild-type. Moreover, the number of synaptic boutons in every concentric ring is significantly elevated in Fmr1^Δ50M mutants throughout the arbor. Both the number and spatial distribution of boutons in the sLN[[v]] synaptic arbor is altered in the absence of Fmr1, with more boutons occupying a larger territory beyond the normal extent of the sLN[[v]] arborization.

Overexpression of Fmr1^Scer\UAS.cZa at the earliest stage of pupal development, under the control of RU486-induced Scer\GAL4^{elav.Switch.PO} exacerbates the Fmr1^Δ50M mutant phenotype resulting in an elevated number of Pdf-positive synaptic boutons redistributed within 30% of the sLN[[v]] axonal arbor. Similarly, induction at pupal stage P2 provides no significant influence upon the synaptic arborization, with no change in the total number of Pdf-positive boutons.

Overexpression of Fmr1^Scer\UAS.cZa in the latter stage of pupal development, under the control of RU486-induced Scer\GAL4^{elav.Switch.PO} ameliorates the Fmr1^Δ50M mutant phenotype, restricting the number and specificity of synaptic connections.

Fmr1^Δ50M mutants do not display defects in coordinated behavior (such as in a roll-over assay).

Fmr1^Δ50M mutants display significant overbranching in the neuromuscular synapse. Treatment of these mutants with the mGluR antagonist MPEP, which blocks mGluR signaling, suppresses the Fmr1^Δ50M overbranching phenotype.

Fmr1^Δ50M mutant synaptic terminals display a significant increase in total area, compared to controls.

Fmr1^Δ50M 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 Fmr1^Δ50M mutant remaining significant, indicating that blocking mGluR signaling does not significantly rescue the increased synaptic terminal area characteristic of Fmr1^Δ50M mutants.

Fmr1^Δ50M 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 Fmr1^Δ50M mutants appears normal. Quantitatively, there is no significant difference in bouton size, mitochondria size, active zone size/number or the postsynaptic subsynaptic reticulum between Fmr1^Δ50M mutants and control larvae.

Fmr1^Δ50M 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, Fmr1^Δ50M mutants display a significant ~30% increase in overall vesicle number. Fmr1^Δ50M mutants display a significant ~50% increase in the pool of clustered vesicles around the active zone. Fmr1^Δ50M mutants display a significant ~85% increase in the number of docked vesicles at the active zone.

Fmr1^Δ50M 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.

At prepupal stage 4, but not stage 3, Fmr1^Δ50M homozygous gamma neuron clones in a Fmr1^Δ50M heterozygous background show longer axons with the same number of., but larger, branches, as compared to controls. Mutant neurons show a normal increase in size before eclose but show delayed pruning at eclosion, as they exhibit a decrease in axon branching only at day 4 after eclosion instead of at eclosion.

In 4 days old adults reared under sensory deprivation, Fmr1^Δ50M homozygous gamma neuron clones (in a Fmr1^Δ50M heterozygous background) display a more pronounced increase in axon branch number, a significant increase in axon branch length and a failure in pruning, as compared to controls.

In just under 10% of homozygous Fmr1^Δ50M mutants, the β lobe of the mushroom body is misdirected or missing. Just under 20% of homozygous Fmr1^Δ50M mutants display a misdirected or missing α-lobe. In just under 70%, both the α- and β lobes of the mushroom body are either misdirected or missing. Where the β-lobe is present, just under 10% display severe midline crossing (defined as a densely strained band equal to or greater in width and thickness than those of the adjacent β-lobes), with approximately 25% displaying 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). Just under 10% display mild midline crossing phenotypes in the β lobe (defined as when a thin band of fibers cross the midline).

Approximately 10% of Fmr1^Δ50M/Fmr1^Δ113M transheterozygotes display misdirecting or missing α lobes.

Approximately just over 70% of transheterozygous Fmr1^Δ50M/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.

Mutant adults have normal gross brain morphology, including an architecturally normal mushroom body. Mild β lobe overgrowth is seen at a slightly higher frequency than wild type. Single cell mutant clones in the mushroom body (in a wild-type background) produce additional cell body processes compared to wild-type single cell clones (converting the characteristic unipolar mushroom body neurons seen in wild-type into multipolar neurons); there is a 3-fold increase in the number of cell body processes in the mutant cells. The mutant cells show a more complex and disordered dendritic structure compared to wild type; primary dendrites display clear secondary branches and the fine dendritic processes that are normally restricted to the termini spread aberrantly along the primary branches. Single cell mutant γ neurons in the mushroom body always have significantly increased axonal branching and significantly more and longer axonal branches than control cells. The large, extra branches do not follow the main axon trajectory, but instead extend in apparently random directions to invade inappropriate territory. Neurons in large mutant clones in the mushroom body show a significantly enlarged average bouton area and more variable distribution of bouton sizes than wild type. The mutant presynaptic boutons are almost filled with vesicles; the average area of the bouton occupied by vesicles is increased 50% in mutant boutons to nearly 75% of the bouton.

When mutant female are mated with wild-type males, only 21% of the expected progeny produced. Mutant males have enlarged testes. The diameter of the tip of the testis is similar to controls, but the diameter in the middle of the testis is about 50% larger than wild-type. This phenotype is 100% penetrant in newly enclosed flies, but it abates with aging. Other than this the morphology of mutant testes appears normal. The testis phenotype appears to be caused by the accumulation of misarranged spermatid bundles within the testis lumen. The coiled spermatid bundles normally seen at the testis base are missing in mutants. Instead of mature spermatids, degenerated cell debris fill the base of mutant testes. The early individualisation process of spermatogenesis does appear to progress largely as normal (occasional defects are seen). However, the orientation of spermatid tails within a cyst is often arranged in an irregular fashion in mutants. In addition the configuration of mitochondria and axoneme within a sperm flagellum is variably skewed, as well as some unknown ring structures present at the inner-space between spermatid tails which is not seen in controls. There is also a specific disruption of the microtubule axoneme structure in the sperm flagellum which becomes progressively more pronounced at spermatid differentiation proceeds. The central pair microtubules are missing in mutant axonemes, although the outer microtubules are still present. this phenotype is progressive, 30% of early stage spermatids, and 56% of late-stage spermatid.

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. Stereotypical grid-like array of neurites entering the medulla is disrupted in mutant flies - short and thin branches fail to connect. This occurs even for neurons that do cross towards the distal medulla. Homozygotes show 0% eclosion from pupal case.

Mutants show no morphological defects. When tested for bang sensitivity, temperature sensitivity and phototaxis there is no detectable difference between wild type and mutant. However there are defects in coordination in a simple flight test. Synaptic transmission is reduced (as indicated by a reduction in off-transient mean amplitude as assayed by ERG). Null mutants show pronounced synaptic overgrowth and overelaboration of synaptic terminals. Muscle 4 has 51% increase in number of boutons over controls. Arboreal branching is increased - with muscle 4 showing 50% more branches than wild type. Evoked synaptic transmission at the NMJ is elevated. Mean EJC amplitude is increased. Average synaptic efficacy is upregulated.

Fmr1^Δ50M has neuroanatomy defective | larval stage phenotype, non-enhanceable by Scer\GAL4^αTub84B.PL/Torsin^{dsRNA.UAS.WIZ}

Fmr1^Δ50M has semi-sterile phenotype, non-enhanceable by futsch^N94

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by wnd³

Fmr1^Δ50M has neurophysiology defective | third instar larval stage phenotype, suppressible by wnd³

Fmr1^Δ50M/Df(3R)Exel6265 has neuroanatomy defective | third instar larval stage phenotype, suppressible by wnd³/wnd¹

Fmr1^Δ50M/Df(3R)Exel6265 has neuroanatomy defective | adult stage phenotype, suppressible by wnd³/wnd¹

Fmr1^Δ50M/Df(3R)Exel6265 has size defective | adult stage phenotype, suppressible by wnd³/wnd¹

Fmr1^Δ50M/Df(3R)Exel6265 has grooming behavior defective | progressive phenotype, suppressible by wnd³/wnd¹

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/bsk^HMS04479

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/kay^Fbz.UAS

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by wnd^GL00282/Scer\GAL4^elav.PU

Fmr1^Δ50M has neurophysiology defective | third instar larval stage phenotype, suppressible by wnd^GL00282/Scer\GAL4^elav.PU

Fmr1^Δ50M has neuroanatomy defective | adult stage phenotype, suppressible | partially by Nab2^ex3/Nab2[+]

Fmr1^Δ50M/Fmr1³ has cell number defective | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Fmr1³ has female semi-sterile phenotype, suppressible | partially by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Df(3R)Exel6265 has cell number defective | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Df(3R)Exel6265 has female semi-sterile phenotype, suppressible | partially by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Fmr1^Δ113M has sterile phenotype, suppressible by aub^sting-1/aub[+]

Fmr1^Δ50M has partially lethal - majority die phenotype, suppressible by CenG1A[+]/CenG1A^EY01217

Fmr1^Δ50M has neuroanatomy defective phenotype, suppressible by CenG1A[+]/CenG1A^EY01217

Fmr1^Δ50M has neuroanatomy defective | somatic clone | third instar larval stage phenotype, suppressible by Abl¹/Abl[+]

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP3248/rin² has lethal - all die during pupal stage phenotype, suppressible by rin^mCherry

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP5420/rin² has short lived phenotype, suppressible by rin^mCherry

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by dlp[+]/dlp^A187

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by dlp[+]/Sdc[+]/dlp^A187/Sdc²³

Fmr1^Δ50M has neurophysiology defective | third instar larval stage phenotype, suppressible by dlp[+]/Sdc[+]/dlp^A187/Sdc²³

Fmr1^Δ50M has neuroanatomy defective phenotype, suppressible by Dscam1¹⁸

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible | partially by Top3β²⁶

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500D.UAS.Tag:MYC}

Fmr1^Δ50M has learning defective | adult stage phenotype, suppressible by Scer\GAL4^ey-OK107/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has learning defective | adult stage phenotype, suppressible by Scer\GAL4^ey-OK107/Hsap\FMR1^{S500D.UAS.Tag:MYC}

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible | partially by Scer\GAL4^da.G32/Timp^UAS.cPa

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, suppressible | partially by Mmp1^Q112stop

Fmr1^Δ50M has neuroanatomy defective phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has male sterile phenotype, suppressible by Scer\GAL4^VP16.nos.UTR/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has male sterile phenotype, suppressible by Scer\GAL4^VP16.nos.UTR/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has male sterile phenotype, suppressible by Hsap\FXR2^UAS.Tag:MYC/Scer\GAL4^VP16.nos.UTR

Fmr1^Δ50M has neuroanatomy defective | larval stage phenotype, suppressible by RanBPM^k05201/l(2)k05201[+]

Fmr1^Δ50M/Fmr1³ has endomitotic cell cycle defective phenotype, suppressible | partially by Cbl^F165/Cbl[+]

Fmr1^Δ50M has neuroanatomy defective phenotype, suppressible | partially by mGluR^112b

Fmr1^Δ50M has neurophysiology defective phenotype, suppressible by futsch^N94

Fmr1^Δ50M has neuroanatomy defective phenotype, suppressible by futsch^N94

Fmr1^Δ50M has neurophysiology defective | third instar larval stage phenotype, non-suppressible by dlp[+]/dlp^A187

Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500A.UAS.Tag:MYC}

Fmr1^Δ50M has learning defective | adult stage phenotype, non-suppressible by Scer\GAL4^ey-OK107/Hsap\FMR1^{S500A.UAS.Tag:MYC}

Fmr1^Δ50M has neuroanatomy defective phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has neuroanatomy defective phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

Fmr1^Δ50M has semi-sterile phenotype, non-suppressible by futsch^N94

Fmr1^Δ50M/Fmr1[+] is an enhancer of neuroanatomy defective | adult stage phenotype of Nab2^ex3

Fmr1^Δ50M/Fmr1[+] is an enhancer of eye color defective | adult stage phenotype of Hsap\TARDBP^UAS.YFP.cEa, Scer\GAL4^GMR.PU

Fmr1^Δ50M/Fmr1[+] is an enhancer of locomotor behavior defective | third instar larval stage phenotype of Hsap\TARDBP^UAS.YFP.cEa, Scer\GAL4^Toll-6-D42

Fmr1^Δ50M/Fmr1[+] is an enhancer of eye color defective | adult stage phenotype of Hsap\TARDBP^{G298S.UAS.YFP}, Scer\GAL4^GMR.PU

Fmr1^Δ50M/Fmr1[+] is an enhancer of locomotor behavior defective | third instar larval stage phenotype of Hsap\TARDBP^{G298S.UAS.YFP}, Scer\GAL4^Toll-6-D42

Fmr1^Δ50M/Df(3R)by62 is a non-enhancer of neuroanatomy defective phenotype of Hsap\ATXN8OS^CTG112.UAS, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF

Fmr1^Δ50M is a non-enhancer of visible phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF

Fmr1^Δ50M/Fmr1[+] is a suppressor of visible | adult stage phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

Fmr1^Δ50M/Fmr1[+] is a suppressor of eye color defective phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

Fmr1^Δ50M/Fmr1[+] is a suppressor of size defective | adult stage phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

Fmr1^Δ50M is a suppressor | partially of neuroanatomy defective | third instar larval stage phenotype of Top3β²⁶

Fmr1^Δ50M is a suppressor of lethal - all die before end of pupal stage phenotype of Mmp1^Q112stop

Fmr1^Δ50M is a suppressor of some die during pupal stage phenotype of Mmp1^Q112stop

Fmr1^Δ50M is a suppressor of some die during third instar larval stage phenotype of Mmp1^Q112stop

Fmr1^Δ50M is a suppressor | partially of lethal - all die before end of pupal stage phenotype of Timp^UAS.cPa

Fmr1^Δ50M is a suppressor | partially of some die during embryonic stage phenotype of Timp^UAS.cPa

Fmr1^Δ50M is a suppressor | partially of some die during larval stage phenotype of Timp^UAS.cPa

Fmr1^Δ50M is a suppressor of locomotor behavior defective phenotype of mGluR^112b

Fmr1^Δ50M is a suppressor of neurophysiology defective phenotype of futsch^N94

Fmr1^Δ50M is a suppressor of neuroanatomy defective phenotype of futsch^N94

Fmr1^Δ50M/Df(3R)by62 is a non-suppressor of neuroanatomy defective phenotype of Hsap\ATXN8OS^CTG112.UAS, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF

Fmr1^Δ50M is a non-suppressor of visible phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF

Abi⁵, Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype

Abl⁴, Fmr1^Δ50M has neuroanatomy defective | third instar larval stage phenotype

Fmr1^Δ50M, Rac1^J11 has neuroanatomy defective | third instar larval stage phenotype

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP5420/rin² has size defective | pupal stage phenotype

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP3248/rin² has lethal - all die during pupal stage phenotype

Fmr1^Δ50M/Fmr1^Δ113M, rin^NP5420/rin² has short lived phenotype

Fmr1^Δ50M, spartin[+]/spartin¹ has neuroanatomy defective | dominant | third instar larval stage phenotype

Dad^j1E4/Dad[+], Fmr1^Δ50M has neuroanatomy defective | dominant | third instar larval stage phenotype

Fmr1^Δ50M, Scer\GAL4^da.G32, Timp^UAS.cPa has viable phenotype

Fmr1^Δ50M, ban[+]/mir-ban¹² has female sterile phenotype

Fmr1^Δ50M, mir-ban¹² has sterile phenotype

Fmr1^Δ50M has type I bouton | larval stage phenotype, non-enhanceable by Scer\GAL4^αTub84B.PL/Torsin^{dsRNA.UAS.WIZ}

Fmr1^Δ50M has protocerebrum phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has bouton phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has protocerebrum phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

Fmr1^Δ50M has bouton phenotype, non-enhanceable by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by wnd³

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by wnd³

Fmr1^Δ50M/Df(3R)Exel6265 has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by wnd³/wnd¹

Fmr1^Δ50M/Df(3R)Exel6265 has adult mushroom body alpha-lobe phenotype, suppressible by wnd³/wnd¹

Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/bsk^HMS04479

Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/kay^Fbz.UAS

Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by wnd^GL00282/Scer\GAL4^elav.PU

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by wnd^GL00282/Scer\GAL4^elav.PU

Fmr1^Δ50M has adult mushroom body alpha-lobe | adult stage phenotype, suppressible | partially by Nab2^ex3/Nab2[+]

Fmr1^Δ50M/Fmr1³ has ovary | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Fmr1³ has egg chamber | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Fmr1³ has nurse cell | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Fmr1³ has germarium | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Df(3R)Exel6265 has ovary | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Df(3R)Exel6265 has egg chamber | adult stage phenotype, suppressible | partially by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Df(3R)Exel6265 has nurse cell | adult stage phenotype, suppressible by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M/Df(3R)Exel6265 has germarium | adult stage phenotype, suppressible | partially by Zfrp8[+]/Zfrp8^SM206

Fmr1^Δ50M has spermatocyte | spermatogenesis phenotype, suppressible by aub^sting-1/aub[+]

Fmr1^Δ50M has adult mushroom body beta-lobe phenotype, suppressible by CenG1A[+]/CenG1A^EY01217

Fmr1^Δ50M has larval multidendritic class IV neuron | somatic clone | third instar larval stage phenotype, suppressible by Abl¹/Abl[+]

Fmr1^Δ50M has type I bouton | third instar larval stage phenotype, suppressible by dlp[+]/dlp^A187

Fmr1^Δ50M has type I bouton | third instar larval stage phenotype, suppressible by dlp[+]/Sdc[+]/dlp^A187/Sdc²³

Fmr1^Δ50M has larval dorsal multidendritic neuron ddaC phenotype, suppressible by Dscam1¹⁸

Fmr1^Δ50M has synapse phenotype, suppressible by Dscam1¹⁸

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible | partially by Top3β²⁶

Fmr1^Δ50M has NMJ bouton | third instar larval stage phenotype, suppressible | partially by Top3β²⁶

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has s-LNv Pdf neuron | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500D.UAS.Tag:MYC}

Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500D.UAS.Tag:MYC}

Fmr1^Δ50M has s-LNv Pdf neuron | supernumerary | third instar larval stage phenotype, suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500D.UAS.Tag:MYC}

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4^da.G32/Timp^UAS.cPa

Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible | partially by Scer\GAL4^da.G32/Timp^UAS.cPa

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible | partially by Mmp1^Q112stop

Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, suppressible by Mmp1^Q112stop

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has bouton phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has protocerebrum phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has embryonic/larval neuromuscular junction phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has spermatid axoneme phenotype, suppressible by Scer\GAL4^VP16.nos.UTR/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has axonemal microtubule phenotype, suppressible by Scer\GAL4^VP16.nos.UTR/Hsap\FMR1^UAS.Tag:MYC

Fmr1^Δ50M has spermatid axoneme phenotype, suppressible by Scer\GAL4^VP16.nos.UTR/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has axonemal microtubule phenotype, suppressible by Scer\GAL4^VP16.nos.UTR/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has spermatid axoneme phenotype, suppressible by Hsap\FXR2^UAS.Tag:MYC/Scer\GAL4^VP16.nos.UTR

Fmr1^Δ50M has axonemal microtubule phenotype, suppressible by Hsap\FXR2^UAS.Tag:MYC/Scer\GAL4^VP16.nos.UTR

Fmr1^Δ50M has embryonic/larval neuromuscular junction phenotype, suppressible by RanBPM^k05201/l(2)k05201[+]

Fmr1^Δ50M has NMJ bouton phenotype, suppressible by RanBPM^k05201/l(2)k05201[+]

Fmr1^Δ50M/Fmr1³ has nurse cell phenotype, suppressible | partially by Cbl^F165/Cbl[+]

Fmr1^Δ50M has neuromuscular junction phenotype, suppressible | partially by mGluR^112b

Fmr1^Δ50M has synaptic vesicle phenotype, suppressible by mGluR^112b

Fmr1^Δ50M has bouton phenotype, suppressible by futsch^N94

Fmr1^Δ50M has neuromuscular junction phenotype, suppressible by futsch^N94

Fmr1^Δ50M has synapse phenotype, suppressible by futsch^N94

Fmr1^Δ50M has adult mushroom body beta-lobe | adult stage phenotype, non-suppressible by Nab2^ex3/Nab2[+]

Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500A.UAS.Tag:MYC}

Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500A.UAS.Tag:MYC}

Fmr1^Δ50M has s-LNv Pdf neuron | supernumerary | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav.PU/Hsap\FMR1^{S500A.UAS.Tag:MYC}

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has bouton phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has protocerebrum phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has embryonic/larval neuromuscular junction phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR1^UAS.Tag:MYC

Fmr1^Δ50M has s-LNv Pdf neuron phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

Fmr1^Δ50M has bouton phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

Fmr1^Δ50M has protocerebrum phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

Fmr1^Δ50M has embryonic/larval neuromuscular junction phenotype, non-suppressible by Scer\GAL4^elav-C155/Hsap\FXR2^UAS.Tag:MYC

Fmr1^Δ50M/Fmr1³ has nurse cell | supernumerary phenotype, non-suppressible by Cbl^F165/Cbl[+]

Fmr1^Δ50M has synapse phenotype, non-suppressible by mGluR^112b

Fmr1^Δ50M has presynaptic active zone phenotype, non-suppressible by mGluR^112b

Fmr1^Δ50M/Fmr1[+] is an enhancer of adult mushroom body alpha-lobe | adult stage phenotype of Nab2^ex3

Fmr1^Δ50M/Fmr1[+] is an enhancer of eye | adult stage phenotype of Hsap\TARDBP^UAS.YFP.cEa, Scer\GAL4^GMR.PU

Fmr1^Δ50M/Fmr1[+] is an enhancer of eye | adult stage phenotype of Hsap\TARDBP^{G298S.UAS.YFP}, Scer\GAL4^GMR.PU

Fmr1^Δ50M/Fmr1[+] is a non-enhancer of adult mushroom body beta-lobe | adult stage phenotype of Nab2^ex3

Fmr1^Δ50M is a non-enhancer of eye phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF

Fmr1^Δ50M is a non-enhancer of ommatidium phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF

Fmr1^Δ50M/Fmr1[+] is a suppressor of eye phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

Fmr1^Δ50M/Fmr1[+] is a suppressor of ommatidium | adult stage phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

Fmr1^Δ50M is a suppressor | partially of embryonic/larval neuromuscular junction | third instar larval stage phenotype of Top3β²⁶

Fmr1^Δ50M is a suppressor | partially of NMJ bouton | third instar larval stage phenotype of Top3β²⁶

Fmr1^Δ50M is a suppressor of trachea phenotype of Scer\GAL4^da.G32, Timp^UAS.cPa

Fmr1^Δ50M is a suppressor of trachea phenotype of Mmp1^Q112stop

Fmr1^Δ50M is a suppressor of synapse phenotype of futsch^N94

Fmr1^Δ50M is a suppressor of bouton phenotype of futsch^N94

Fmr1^Δ50M is a suppressor of neuromuscular junction phenotype of futsch^N94

Fmr1^Δ50M is a non-suppressor of eye phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF

Fmr1^Δ50M is a non-suppressor of ommatidium phenotype of Hsap\MAPT^V337M.UAS, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF

Abi⁵, Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype

Abi⁵, Fmr1^Δ50M has NMJ bouton | third instar larval stage phenotype

Abl⁴, Fmr1^Δ50M has embryonic/larval neuromuscular junction | third instar larval stage phenotype

Abl⁴, Fmr1^Δ50M has NMJ bouton | third instar larval stage phenotype

Fmr1^Δ50M, Rac1^J11 has embryonic/larval neuromuscular junction | third instar larval stage phenotype

Fmr1^Δ50M, Rac1^J11 has NMJ bouton | third instar larval stage phenotype

Fmr1^Δ50M, dlp[+]/dlp^A187 has embryonic/larval neuromuscular junction | third instar larval stage phenotype

Fmr1^Δ50M, Sdc[+]/Sdc²³, dlp[+]/dlp^A187 has embryonic/larval neuromuscular junction | third instar larval stage phenotype

Fmr1^Δ50M, spartin[+]/spartin¹ has NMJ bouton | supernumerary | third instar larval stage phenotype

Dad^j1E4/Dad[+], Fmr1^Δ50M has NMJ bouton | supernumerary | third instar larval stage phenotype

Fmr1^Δ50M, ban[+]/mir-ban¹² has female germline stem cell phenotype