Protein truncated in FnII domain 8.
Nucleotide substitution: C3280T. (Coordinates refer to cDNA sequence). The substitution causes a Q to be replaced by a TAA stop codon, resulting a a protein truncated in the extracellular domain.
C19727031T
C3208T
Q1055term | Lar-PA; Q1037term | Lar-PB; Q938term | Lar-PD; Q1058term | Lar-PF; Q961term | Lar-PG; Q953term | Lar-PH; Q967term | Lar-PI
Q?term
anterior fascicle & axon | ectopic (with Lar5.5)
egg | maternal effect (with Lar5.5)
larval intersegmental nerve (with Lar5.5), with LarC1929S.UAS, Scer\GAL4elav-C155
NMJ bouton | larval stage (with Lar5.5)
oocyte (with Lar5.5), with LarΔFn2-9.UAS, Scer\GAL4T155
oocyte (with Lar5.5), with LarΔFn123.UAS, Scer\GAL4T155
oocyte (with Lar5.5), with LarΔFn456.UAS, Scer\GAL4T155
oocyte | oogenesis stage S14 (with Lar5.5)
Lar13.2 heterozygous eggs show normal morphology.
Lar13.2 mutant cells in mosaic follicular epithelia exhibit a cell autonomous defect in leading edge protrusion formation, as compared to wild type control cells. Additionally, wild type cells directly ahead of Lar13.2 mutant cells exhibit significantly elongated basal surfaces, indicative of a defect in trailing edge retraction.
Lar5.5/Lar13.2 mutant follicle cells in mosaic egg chambers exhibit a reduction in actin-rich protrusions along the membrane as compared to controls, but only in egg chambers that are completely mutant or in large mutant clones. No defects in global alignment of contractile actin bundles are seen in these egg chambers.
Eggs from Lar5.5/Lar13.2 mutant egg chambers are moderately rounded as compared to wild type.
28% of Lar13.2/Lar5.5 mutants display a motor axon guidance phenotype known as "ISNb bypass" in which ISNb axons successfully split away from the ISN pathway at the exit junction, but can fail to grow into the muscle field at their normal entry point. Instead, such axons travel along parallel to the ISN, underneath the muscles, until they reach the dorsal edge of the VLM field.
Excitatory junctional potentials (EJPs) are reduced 34% in homozygous larvae compared to controls. The mean amplitude and the frequency of unitary mRJPs is normal. The resting potential of the muscle is normal. The quantal content of evoked release is reduced by over 50%.
In Lar5.5/Lar13.2 mutants, some oocytes fail to elongate significantly. This phenotype is moderate in penetrance (14.1% defective stage 14 oocytes). No defects are seen in major aspects of oocyte patterning; both the micropyle and the dorsal appendages are formed in their correct positions, although the latter are often shortened relative to those of the wild-type. Similarly the oocyte nucleus is correctly positioned in the dorsal-anterior compartment in rounded oocytes.
Homozygotes show an ISNb bypass phenotype at moderate frequency.
Truncation phenotypes of the ISN. Most ISNs reach PT1 (persistent twi cell 1) but have small terminal arbors. Combining Ptp69D or Ptp99A mutants increases the penetrance and severity of the ISN defects, the ISN pathway is truncated at specific branchpoint positions. Triple mutants lacking Lar, Ptp69D or Ptp99A exhibit much stronger ISN phenotypes than any single or double mutant. Mutation affects SNb guidance and synaptogenesis within the VLM (ventrolateral muscle) field, a parallel bypass phenotype is observed (SNb axons grow alongside the ISN). SNbs fail to form the normal pattern of synaptic branches and exhibit navigation errors at the muscle field entry point. Growth alongside the ISN is likely to be due to inappropriately active Ptp99A rather than a failure of Lar-mediated VLM recognition. Lar, Ptp69D or Ptp99A triple mutants also exhibit fusion bypass phenotype of the SNb axons. Fusion bypass is seldom observed in any genotype in which Ptp69D is wild type. Removal of Ptp99A or Lar produces a 10- to 20- fold increase in the frequency of fusion bypass and an increase in complete stall phenotypes.
Approximately half of the homozygotes die as late instar larvae, and the remainder die attempting to eclose. A striking number of mutant larvae initiate pupation in the food. Mature pupae struggle to eclose and die part way out of the pupal case. Mutant embryos show defects in SNb and SNd motor axon guidance (full and partial bypass phenotypes) and to a lesser extent in the CNS (thinning of the most lateral longitudinal fascicle). The penetrance of these defects in not 100%. The embryonic lethality of Lar5.5/Lar13.2 is overcome by LarScer\UAS.cKa driven by Scer\GAL4elav-C155.
Lar13.2 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by cknA.R305Q
Lar[+]/Lar13.2 is a suppressor | partially of abnormal size | oogenesis phenotype of Sema5cK175
Lar[+]/Lar13.2 is a suppressor | partially of visible | oogenesis phenotype of Sema5cK175
Lar5.5/Lar13.2 is a suppressor of abnormal neuroanatomy phenotype of Scer\GAL4how-24B, SdcUAS.cJa
Lar13.2/Lar13.2 is a suppressor of abnormal neuroanatomy phenotype of Abl1
Lar5.5/Lar13.2, Ptp10D1, Ptp69D1 has abnormal neuroanatomy | embryonic stage phenotype
Df(3R)Ptp99AR3/Ptp99A1, Lar5.5/Lar13.2, Ptp69D1 has abnormal neuroanatomy | embryonic stage 16 phenotype
Df(3R)Ptp99AR3/Ptp99A1, Lar5.5/Lar13.2, Ptp10D1 has abnormal neuroanatomy | embryonic stage 16 phenotype
Df(3R)Ptp99AR3/Ptp99A1, Lar5.5/Lar13.2, Ptp10D1, Ptp69D1 has abnormal neuroanatomy | embryonic stage 16 phenotype
Lar5.5/Lar13.2, Ptp10D1 has abnormal neuroanatomy | embryonic stage phenotype
Lar5.5/Lar13.2, Ptp10D1, Ptp69D1 has abnormal neuroanatomy | embryonic stage 16 phenotype
Lar5.5/Lar13.2 has egg | maternal effect phenotype, enhanceable | maternal effect by Abi[+]/AbiΔ20
Lar13.2 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, enhanceable by cknA.R305Q
Lar13.2 has phenotype, enhanceable by trioS138606/trio[+]
Lar13.2 has larval intersegmental nerve phenotype, enhanceable by trioS138606/trio[+]
Lar13.2 has phenotype, enhanceable by Scer\GAL4elav-C155/Rac1N17.UAS
Larbypass/Lar13.2 has larval intersegmental nerve phenotype, suppressible by Abl1
LarOD16/Lar13.2 has larval intersegmental nerve phenotype, suppressible by Abl2
Lar[+]/Lar13.2 is a suppressor | partially of egg phenotype of Sema5cK175
Lar5.5/Lar13.2 is a suppressor of larval abdominal segmental nerve phenotype of Scer\GAL4how-24B, SdcUAS.cJa
Lar13.2/Lar13.2 is a suppressor of presumptive embryonic/larval central nervous system phenotype of Abl1
Lar[+]/Lar13.2 is a non-suppressor of embryonic/larval neuromuscular junction | larval stage phenotype of DAAMEx68
Lar[+]/Lar13.2 is a non-suppressor of NMJ bouton | larval stage phenotype of DAAMEx68
Lar[+]/Lar13.2 is a non-suppressor of larval LL1 motor neuron | larval stage phenotype of DAAMEx68
Lar5.5/Lar13.2, Ptp10D1, Ptp69D1 has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype
Df(3R)Ptp99AR3/Ptp99A1, Lar5.5/Lar13.2, Ptp69D1 has larval intersegmental nerve | embryonic stage phenotype
Df(3R)Ptp99AR3/Ptp99A1, Lar5.5/Lar13.2, Ptp69D1 has larval ventral nerve cord | embryonic stage 16 phenotype
Df(3R)Ptp99AR3/Ptp99A1, Lar5.5/Lar13.2, Ptp10D1 has larval ventral nerve cord | embryonic stage 16 phenotype
Df(3R)Ptp99AR3/Ptp99A1, Lar5.5/Lar13.2, Ptp10D1, Ptp69D1 has larval intersegmental nerve | embryonic stage phenotype
Df(3R)Ptp99AR3/Ptp99A1, Lar5.5/Lar13.2, Ptp10D1, Ptp69D1 has larval ventral nerve cord | embryonic stage 16 phenotype
Df(3R)Ptp99AR3/Ptp99A1, Lar5.5/Lar13.2, Ptp10D1, Ptp69D1 has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype
Lar5.5/Lar13.2, Ptp10D1 has larval intersegmental nerve | embryonic stage phenotype
Lar5.5/Lar13.2, Ptp10D1 has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype
Lar5.5/Lar13.2, Ptp10D1, Ptp69D1 has larval ventral nerve cord | embryonic stage 16 phenotype
Lar5.5/Lar13.2, Ptp10D1, Ptp69D1/Ptp69D8ex25, Ptp99AR3/Ptp99A1 has larval longitudinal connective phenotype
Lar5.5/Lar13.2, Ptp10D1, Ptp69D1/Ptp69D8ex25, Ptp99AR3/Ptp99A1 has larval ventral nerve cord commissure phenotype
Lar5.5/Lar13.2, Ptp10D1, Ptp69D1/Ptp69D8ex25, Ptp99AR3/Ptp99A1 has larval anterior commissure phenotype
Lar5.5/Lar13.2, Ptp10D1, Ptp69D1/Ptp69D8ex25, Ptp99AR3/Ptp99A1 has larval posterior commissure phenotype
Lar13.2 cknA.R305Q double mutants exhibit an increase in frequency of the ISNb bypass phenotype compared to Lar13.2 single mutants to 46% in double mutants.
Sdc48/Sdc10608; Lar13.2/Lar5.5 (in which Sara has been rescued by expression of the SaraUbi.PJ transgene) display an increased penetrance of the bypass phenotype (43% vs. 28%) relative to the corresponding Lar13.2/Lar5.5 transheterozygote. When SdcScer\UAS.cJa is expressed, under the control of Scer\GAL4how-24B, in a Lar13.2/Lar5.5 background, the SNa bifurcation phenotype seen when the transgene is expressed in a wild-type background is suppressed.
Lar5.5/Lar13.2 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 triple mutant embryos show severe motor axon defects. The two inner bundles of the ventral nerve cord are very similar to that of wild-type, but the outer bundle, which develops later, is often discontinuous in late stage 16 triple mutant embryos. In addition, about one third of the ISNb nerves fail to leave the intersegmental nerve at the exit junction and continue to grow out along the common intersegmental nerve pathway in these triple mutant embryos. In most of these bypass hemisegments, only one intersegmental nerve branch is visible, and it is usually thicker than normal.
In Ptp10D1 Lar5.5/Lar13.2 Ptp99A1/Df(3R)Ptp99AR3 triple mutant embryos the two inner bundles of the ventral nerve cord are very similar to that of wild-type, but the outer bundle, which develops later, is often discontinuous.
The Ptp10D1 Lar5.5/Lar13.2 Ptp69D1 triple mutant embryonic phenotype involves ectopic midline crossing and longitudinal bundle fusion by the ventral nerve cord. The axons that abnormally cross the midline in the triple mutant embryos often grow diagonally to the other side without respecting the normal borders of the anterior and posterior commissures. In many cases, all of the connective axons appear to be rerouted across the midline, producing complete connective breaks.
Most of the ventral nerve cord axons abnormally cross the midline and the longitudinal bundles are almost absent in Ptp10D1 Lar5.5/Lar13.2 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 quadruple mutant embryos. The longitudinal tracts are depleted of axons and the commissures are completely fused and much thicker than normal. No axons are ever observed to enter the ventrolateral muscle field in the quadruple mutant embryos.
In Ptp10D1 Lar5.5/Lar13.2 double mutant embryos, the normal SNa bifurcation is not observed in some hemisegments. This phenotype is only observed at low frequency.
Approximately half of the SNa nerves fail to bifurcate in Ptp10D1 Lar5.5/Lar13.2 Ptp69D1 triple mutant embryos.
Approximately half of the SNa nerves fail to bifurcate in Ptp10D1 Lar5.5/Lar13.2 Ptp99A1/Df(3R)Ptp99AR3 triple mutant embryos.
Approximately half of the intersegmental nerves terminate at the second lateral branch position in Ptp10D1 Lar5.5/Lar13.2 double mutant embryos. The remainder of the intersegmental nerves either terminate between the second lateral branch and the terminal arbor or make an abnormally small terminal arbor in these double mutant embryos.
Approximately half of the intersegmental nerves terminate at the first lateral branch point position and most of the remainder stop at the second lateral branch point in Lar5.5/Lar13.2 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 triple mutant embryos.
Only about 15% of the intersegmental nerves terminate at the first lateral branch point position and most of the remainder stop at the second lateral branch point in Ptp10D1 Lar5.5/Lar13.2 Ptp69D1 Ptp99A1/Df(3R)Ptp99AR3 quadruple mutant embryos.
Ptp10D1; Lar13.2/Lar5.5; Ptp69D1 Ptp99AR3/Ptp69D8ex25 Ptp99A1 quadruple mutants have severely disrupted longitudinal tracts and most axons cross the midline. The bundles that cross the midline do not respect the normal boundaries of the commissures and the anterior and posterior commissures appear fused. No central nervous system abnormalities (by Fas2 staining) are seen in Ptp10D1; Lar5.5/Lar13.2 double mutant embryos.
Mutation causes synergy of the Scer\GAL4elav-C155, Rac1N17.Scer\UAS full ISNb bypass phenotype.
Lar5.5/Lar13.2 is rescued by Scer\GAL4elav.PU/LarUAS.cKa
Lar5.5/Lar13.2 is rescued by Scer\GAL4T155/LarΔFn789.UAS
Lar5.5/Lar13.2 is rescued by Scer\GAL4T155/LarΔIg123.UAS
Lar5.5/Lar13.2 is rescued by Scer\GAL4T155/LarUAS.cKa
Lar5.5/Lar13.2 is rescued by Scer\GAL4T155/LarUAS.cKa
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav.PU/LarΔFn2-9.UAS
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav-C155/LarΔFn789.UAS
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav-C155/LarΔFn456.UAS
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav-C155/LarC1638S.UAS
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav-C155/LarC1929S.UAS
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav-C155/LarΔFn2-9.UAS
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav-C155/LarCSX2.UAS
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav-C155/LarUAS.cKa
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav-C155/LarΔFn123.UAS
Lar5.5/Lar13.2 is partially rescued by Scer\GAL4elav-C155/LarΔPTP-D2.UAS
Lar5.5/Lar13.2 is not rescued by LarUAS.cKa/Scer\GAL4how-24B
Lar5.5/Lar13.2 is not rescued by Scer\GAL4how-24B/LarΔFn2-9.UAS
Lar5.5/Lar13.2 is not rescued by Scer\GAL4elav.PU/LarCSX2.UAS
Lar5.5/Lar13.2 is not rescued by Scer\GAL4how-24B/LarCSX2.UAS
Lar5.5/Lar13.2 is not rescued by Scer\GAL4elav.PU/LarΔIg123.UAS
Lar5.5/Lar13.2 is not rescued by Scer\GAL4how-24B/LarΔIg123.UAS
Lar5.5/Lar13.2 is not rescued by Scer\GAL4elav-C155/LarΔIg123.UAS
Lar5.5/Lar13.2 is not rescued by Scer\GAL4T155/LarΔFn2-9.UAS
Lar5.5/Lar13.2 is not rescued by Scer\GAL4elav-C155/LarUAS.cKa
Lar5.5/Lar13.2 is not rescued by LarUAS.cKa/Scer\GAL4198Y
Expression of LarScer\UAS.cKa under the control of Scer\GAL4elav.PU rescues the reduction in bouton number at the neuromuscular junction seen in Lar5.5/Lar13.2 larvae, while expression under the control of Scer\GAL4how-24B does not rescue the mutant phenotype.
Expression of LarΔFn2-9.Scer\UAS under the control of Scer\GAL4elav.PU partially rescues the reduction in bouton number at the neuromuscular junction seen in Lar5.5/Lar13.2 larvae.
Expression of either LarCSX2.Scer\UAS or LarΔIg123.Scer\UAS under the control of Scer\GAL4elav.PU fails to rescue the reduction in bouton number at the neuromuscular junction seen in Lar5.5/Lar13.2 larvae.