|Feature type||allele||Associated gene||Dmel\Fas2|
|Also Known As||fasIIEB112|
|Allele class||loss of function allele, amorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Imprecise excision of the P-element from Ecol\lacZFas2-A31. 1.7kb deletion of Fas2 genomic sequences, including 5' untranslated sequences. The deletion is entirely within the Fas2 gene and is likely to include the start of transcription. Genomic sequences more than 1kb from the 5' end of the Fas2 gene are unaffected.
|Phenotype Manifest In|
fascicle & mushroom body | somatic clone
synapse & aCC neuron
synapse & RP2 neuron
thorax & macrochaeta | somatic clone
thorax & microchaeta | somatic clone
U neuron & growth cone
Fas2[e76]/Fas2[EB112] larval NMJs have fewer synaptic boutons than controls. Fas2[EB112]/+ NMJs have no change in bouton number compared to controls.
Anterior follicle cells in homozygous follicle cell clones undergo normal cell shape changes during oogenesis.
Fas2[EB112]/Fas2[e76] adults display a rough-eye phenotype. Ommatidial photoreceptor and cone cell numbers are disrupted, and in some cases mini-clusters of ommatidia are observed. Fas2[EB112] mutant eye clones show cone cell defects, defects in photoreceptor cell number, and mini-ommatidia are observed. Fas2[EB112] mutant clones in eye disc display abnormal elav-positive cell clusters between ommatidia which resemble R7-like photoreceptor cells. Some of the cells associated with the ectopic clusters are genotypically wild-type. No R8 photoreceptor cells are associated with the ectopic cell clusters. Loss of function clones of Fas2[EB112] in the adult notum display one or more ectopic dorsocentral bristles. other macro- and microchaetae are largely unaffected. Extra sensory organ precursor cells are observed in Fas2[EB112] mutant clones.
There are no obvious abnormalities in the timing and dynamics of the myopodia-filopodia interactions to form the synaptic contact site in Fas2[EB112]/Y embryos. In these mutants, T-shaped presynaptic terminals of normal size form in the prospective synaptic site along the proximal edge of target muscle 12.
Fas2EB112 mutants exhibit amorphous and expanded tracheal tubes, where the luminal chitin does not organise correctly, in comparison to wild-type
The motor neuron that innervates DLMa has a higher number of contact points with the muscle in Fas2e76/Fas2EB112 mutants (6) than in wild type (5). The DLMa is 11% longer in Fas2e76/Fas2EB112 mutants than wild type. Investigation of adult innervation pattern in Fas2e76/Fas2EB112 mutants shows that outgrowth of secondary branches is not affected, but that branch elaboration, which occurs at 18-24 hours APF, is affected. During this stage, the average length of Fas2e76/Fas2EB112 secondary branches is increased, as is the area occupied by the higher order arbors of the secondary branches. Additionally, a higher level of secondary branches are stabilized, as shown by staining for futsch, in Fas2e76/Fas2EB112 mutants at 24 hours APF than wild type.
Fas2[e76]/Fas2[EB112] mutants exhibit normal axon patterns. There are sporadic single BM axon defects, but no OP axon alterations are found.
In a Fas2EB112 mutant background, U motorneuron growth cones exhibit a wide shape that is reminiscent of aCC/RP2 pioneer growth cones.
In stage 14 Fas2EB112 mutants, the lumenal chitin in the developing dorsal trunk of the tracheal system fails to form a filamentous cable running along the tube length, as in wild-type, but instead is amorphous and fills the lumen.
In Fas2EB112 homozygotes, the border follicle cells lose their polarity. Delamination of these cells is delayed, but their migration is accelerated.
Mutant embryos develop long and convoluted tracheal dorsal trunks and the apical cell surface of the dorsal trunk cells appears elongated and expanded. Tubular dilations are seen in the transverse connectives and the lumen of several tracheal branches is discontinuous.
During the first 28hr of wild-type larval life, the frequency of suprathreshold synaptic drive to aCC/RP2 increases considerably. In the absence of Fas2, such as in Fas2EB112, the frequency of synaptic drive to aCC/RP2 still increases during this period, although this increase is significantly less than when Fas2 is present. In Fas2EB112 mutants the number of presynaptic terminals that contact aCC remains unchanged. The ultrastructure of the presynaptic terminals at this stage is qualitatively indistinguishable from those that develop in wild-type.
The initial growth of the pioneer mushroom body (MB) axons is not disturbed in mutants. After converging at the protocerebral neuropil, the MB axons exhibit a normal medial turn and from the primordial medial lobe. When homozygous mutant clones are made in the MB, the axon projections exhibit no gross abnormalities. However dispersed axonal fascicles are seen in 23% of cases, in which axon bundles are randomly scattered throughout the axonal layers of the peduncle and lobes.
Larvae successfully hatch and begin crawling around but within hours begin to behave sluggish and uncoordinated, they ultimately stop moving and die. Synapses form and mature but in the absence of Fas2 they do not grow and then retract, the number of boutons drops to a few or zero.
Transheterozygotes with Fas2e76 exhibit missing postvertical, ocellar, vertical and orbital bristles. At 17oC the phenotype is more penetrant with missing ocelli. Gynandromorph mosaics demonstrate hemizygous male regions fail to differentiate the postvertical, ocellar and vertical bristles and still have some orbital bristles. Ocelli are missing and the compound eye has a rough phenotype. Some macro- and microchaetes in the thorax are missing.
EM analysis of the extent of fasciculation and membrane apposition between various pairs of axons reveals normal neurite outgrowth, extension and guidance in embryos. Some aspects of selective fasciculation and axon-glia interactions appear highly abnormal, the vMP2, MP1 and FN3 pathways defasciculate. Scer\GAL4 driven expression of Fas2 can refasciculate the FN3 axons.
Transheterozygotes for Fas2EB112 and Fas2e76 are sterile. Increased branching of wing sensory axons in discs during metamorphosis. Ectopic sensory neurons are displayed in the wing.
The MP1 pathway does not form in Fas2EB112 mutant embryos: at embryonic stage 12/1 the dMP2 and MP1 growth cones do not turn posteriorly (which happens in the wild-type) but rather project laterally for a short distance. Also, the vMP2 growth cone often turns anteriorly (as in the wild-type) but already shows variability in the precise orientation of its tip. The MP1, dMP2 and vMP2 growth cones stay stalled in the same position through to stage 14 in mutant embryos, in contrast to the wild-type.
|NOT Enhancer of|
Fas2EB112, Scer\GAL4eve.RN2 is a suppressor of neuroanatomy defective phenotype of RdlScer\UAS.cSa, Scer\GAL4eve.RN2
Fas2EB112 is a suppressor | partially of neuroanatomy defective | embryonic stage phenotype of rapie28
|NOT Suppressor of|
|Phenotype Manifest In|
Fas2EB112/Fas2[+] is an enhancer of eye phenotype of EgfrScer\UAS.cBa, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
|NOT Enhancer of|
Fas2EB112, Scer\GAL4eve.RN2 is a suppressor of abdominal intersegmental nerve phenotype of RdlScer\UAS.cSa, Scer\GAL4eve.RN2
Fas2EB112, Scer\GAL4eve.RN2 is a suppressor of intersegmental nerve phenotype of RdlScer\UAS.cSa, Scer\GAL4eve.RN2
Fas2EB112, Scer\GAL4eve.RN2 is a suppressor of mesothoracic intersegmental nerve phenotype of RdlScer\UAS.cSa, Scer\GAL4eve.RN2
Fas2EB112, Scer\GAL4eve.RN2 is a suppressor of metathoracic intersegmental nerve phenotype of RdlScer\UAS.cSa, Scer\GAL4eve.RN2
Fas2EB112, Scer\GAL4eve.RN2 is a suppressor of prothoracic intersegmental nerve phenotype of RdlScer\UAS.cSa, Scer\GAL4eve.RN2
Fas2EB112 is a suppressor of presumptive embryonic/larval central nervous system phenotype of Sema-1ak13702
Fas2EB112 is a suppressor of synapse & aCC neuron phenotype of Ctet\TeTxLCTNT.Scer\UAS, Scer\GAL4eve.RRK
|NOT Suppressor of|
Large follicle cell clones doubly homozygous for Tao[eta] and Fas2[EB112] show cell lethality, while small follicle cell clones doubly homozygous for Tao[eta] and Fas2[EB112] can be recovered in stage 8/9 egg chambers. Anterior follicle cells in these small clones stretch normally.
The glial cell migration defects of rap[ie28] embryos are significantly suppressed by Fas2[EB112] (54.7% of hemisegments show normal migration, 27.9% of hemisegments show partial migration). However, the increase in glial cell number and the axonal defects seen in rap[ie28] embryos is not suppressed by Fas2[EB112].
rho[hs.sev] rough eye phenotype is enhanced in the presence of Fas2[EB112]/+ at 18[o]C. Expression of Egfr[Scer\UAS.cBa] under the control of Scer\GAL4[GMR.PF] results in a rough-eye phenotype, which is enhanced by the presence of Fas2[EB112]/+. The rough-eye phenotype observed in Fas2[EB112]/Fas2[e76] flies is enhanced by the presence of argos[Δ7]/+. The rough-eye phenotype observed in flies expressing sty[Scer\UAS.cHa] under the control of Scer\GAL4[sev.EP] is suppressed in the presence of Fas2[EB112]/+.
Intersegmental nerves are co-arrested upon expression of RdlScer\UAS.cSa in the aCC/RP2 neurons (under the control of Scer\GAL4eve.RN2) in a Fas2EB112 mutant background in 36% of cases, compared with 70% in a wild-type background.
In the absence of Fas2, in Fas2EB112 mutants, the effect of Ctet\TeTxLCTNT.Scer\UAS expression in aCC/RP2 neurons (under the control of Scer\GAL4eve.RRK) on the frequency of synaptic inputs is significantly diminished compared to Ctet\TeTxLCTNT.Scer\UAS expression in wild-type.
Fas2EB112/+, Kr1/+ double heterozygotes (that also carry KrmCD) exhibit an axon guidance phenotype. The SNb enters the ventral muscle field normally in most cases but the nerve stops at the second choice point by forming a growth cone-like structure. No individual RP axons are observed.
The intersegmental nerve b (ISNb) phenotypes seen in homozygous Sema-1ak13702 embryos are suppressed by one copy of Fas2EB112. Synaptic arborisations on ventral lateral muscles (VLMs) 12 and 6-7 appear normal. The Sema-1ak13702 segmental nerve a (SNa) defasciculation defects are not suppressed by Fas2EB112 alone. However, rescue of the Sema-1ak13702 SNa stall phenotype is seen in Fas2EB112/+ ; Sema-1ak13702 ; ConFvex238 triple mutant embryos; the SNa dorsal branches bifurcate at lateral muscles (LMs) 22-23 and extend dorsally. Sema-1ak13702 CNS defects are suppressed by one copy of Fas2EB112 (they are seen in only 10% of hemisegments, compared to 31% in Sema-1ak13702 single mutants).
|Complementation & Rescue Data|
Scer\GAL4elav.PLu or Scer\GAL4Mhc.PW mediated expression of Fas2Scer\UAS.cLa rescues larval lethality. Scer\GAL4A51 mediated expression of Fas2Scer\UAS.cLa causes mosaic rescued larvae, rescue of boutons in the segments Scer\GAL4 is expressed (muscles 6 and 7) and elimination of boutons in segments where it is not expressed.
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 14 )|
|Secondary FlyBase IDs|
|References ( 31 )|
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|Recent research papers ( 2 )|
|Recent reviews (0)|
|All reviews listed in FlyBase were published before 2011|