Allele Dmel\Lar^5.5

General Information
Symbol	Dmel\Lar^5.5	Species	D. melanogaster
Name		FlyBase ID	FBal0048849
Feature type	allele	Associated gene	Dmel\Lar
Also Known As	Dlar^5.5

Map ( GBrowse )
Allele class
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02	Controlled Vocabulary Terms larval stage NMJ bouton
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class
Mutagen	ethyl methanesulfonate (Krueger et al., 1996, Desai et al., 1997)
Mutations Mapped to the Genome

Type Location Additional Notes References point mutation 2L:19,717,177..19,717,177 reported_pr_change=W?@ pr_change=W552@\|Lar-PA reported_na_change=G1773A evidence=experimental na_change=G19717177A (Krueger et al., 1996)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Protein truncated in FnII domain 3. (Krueger et al., 2003) Introduce termination codons into the extracellular domain. (Desai et al., 1997) Nucleotide substitution: G1773A. (Coordinates refer to cDNA sequence). The substitution causes a W to be replaced by a TGA stop codon, resulting a a protein truncated in the extracellular domain. (Krueger et al., 1996)
Cytology
Phenotypic Data
Phenotypic Class
	behavior defective \| recessive (Krueger et al., 1996) lethal (with Lar^13.2) (Krueger et al., 2003) lethal \| recessive (Krueger et al., 1996) neuroanatomy defective (Kaufmann et al., 2002) neuroanatomy defective (with Lar^13.2) (Fox and Zinn, 2005) neuroanatomy defective \| embryonic stage (Weng et al., 2011) neuroanatomy defective \| larval stage (with Lar^13.2) (Johnson et al., 2006) neurophysiology defective (Desai et al., 1997)
Phenotype Manifest In
	abdominal segmental nerve (Krueger et al., 1996, Desai et al., 1997) actin filament & follicle cell \| somatic clone \| cell non-autonomous (Bateman et al., 2001) anterior fascicle & axon \| ectopic (with Lar^13.2) (Fox and Zinn, 2005) bouton (Kaufmann et al., 2002) dorsal appendage (with Lar^13.2) (Bateman et al., 2001) follicle cell \| cell non-autonomous \| somatic clone (Frydman and Spradling, 2001) intersegmental nerve (Bateman et al., 2000, Wills et al., 1999, Desai et al., 1997) intersegmental nerve (with Lar^13.2) (Krueger et al., 2003) intersegmental nerve (with Lar^13.2), with Lar^{C1929S.Scer\UAS}, Scer\GAL4^elav-C155 (Krueger et al., 2003) intersegmental nerve branch ISNb of A1-7 \| embryonic stage (Weng et al., 2011) longitudinal connective (Krueger et al., 1996) neuromuscular junction (Kaufmann et al., 2002) NMJ bouton \| larval stage (with Lar^13.2) (Johnson et al., 2006) oocyte (with Lar^13.2) (Bateman et al., 2001) oocyte (with Lar^13.2), with Lar^{ΔFn2-9.Scer\UAS}, Scer\GAL4^T155 (Krueger et al., 2003) oocyte (with Lar^13.2), with Lar^{ΔFn123.Scer\UAS}, Scer\GAL4^T155 (Krueger et al., 2003) oocyte (with Lar^13.2), with Lar^{ΔFn456.Scer\UAS}, Scer\GAL4^T155 (Krueger et al., 2003) photoreceptor cell R7 & axon (with Lar²¹²⁷) (Maurel-Zaffran et al., 2001) photoreceptor cell R7 & growth cone (with Lar²¹²⁷) (Maurel-Zaffran et al., 2001) RP1 motor neuron (with Lar^13.2) (Schindelholz et al., 2001) RP3 motor neuron (with Lar^13.2) (Schindelholz et al., 2001) RP4 motor neuron (with Lar^13.2) (Schindelholz et al., 2001) RP5 motor neuron (with Lar^13.2) (Schindelholz et al., 2001) stage S14 oocyte (with Lar^13.2) (Krueger et al., 2003)
Detailed Description
	Statement Reference Lar[5.5] homozygous mutant embryos exhibit ISNb bypass phenotypes in 31% of hemisegments. Lar[5.5] heterozygous embryos do not exhibit ISNb guidance defects. (Weng et al., 2011) Lar[5.5]/Lar[13.2] larvae show a reduction in bouton number at the neuromuscular junction compared to wild type. (Johnson et al., 2006) 28% of Lar^13.2/Lar^5.5 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. (Fox and Zinn, 2005) Carefully nurtured Lar^5.5/Lar^13.2 escapers of the lethality can be raised to adulthood. Stage 14 oocytes produced by these adults are abnormally round. (Krueger et al., 2003) Homozygous and heterozygous larvae have fewer boutons (both type Ib and type Is) at the muscle 6/7 neuromuscular junction than wild type. Overall neuromuscular junction (NMJ) ultrastructure looks normal in homozygous larvae, but 61% of individual active zones are larger than the largest active zones found in wild-type NMJs and the mean total area of the mutant active zones is 2.5-fold greater than wild type. (Kaufmann et al., 2002) In Lar^5.5/Lar^13.2 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. In Lar^5.5 somatic clones in the follicle cells, defects are seen in cytoskeletal organisation. In cases where disruption in F-actin are evident, defects are always observed in both mutant cells and in wild-type cells surrounding the clone. Although global organisation of actin polarity is lost around these clones, actin filaments tend to be similarly polarised in adjacent cells. (Bateman et al., 2001) Actin polarisation in Lar^5.5 germ-line clones is almost completely normal. However, egg chambers that contain somatic clones of mutant follicle cells display severely abnormal actin polarisation. These defects affect both mutant and wild-type cells. The genotype od the polar cells is not a determinant - cases of mutant polarisation surrounding wild-type polar cells are seen, the inverse (mutant polar cells surrounded by wild-type polarisation) is also seen. In mutant germline clones, region 2b cysts never fail to become lens-shaped and never contain more than one round of follicle in the process of budding. By contrast, when most of the follicle cells in region 2b and 3 are mutant (a relatively rare phenotype) then 62% of the germaria contain such defects. (Frydman and Spradling, 2001) R7 growth cones extend beyond the R8 termini in Lar²¹²⁷/Lar^5.5 animals 15 hours after pupariation as occurs in wild type, although the R7 growth cones have a compact, club-like shape instead of the normal expanded morphology. Only 52.9% of Lar²¹²⁷/Lar^5.5 R7 axons select their correct target layer. (Maurel-Zaffran et al., 2001) Lar^5.5/Lar^13.2 transheterozygous embryos have a parallel bypass phenotype in the ISNb nerve. (Schindelholz et al., 2001) Homozygotes show an ISNb bypass phenotype at moderate frequency. (Bateman et al., 2000) ISNb axons often show a "bypass" phenotype (failing to enter the normal muscle target domain just outside the ventral nerve cord and instead following the intersegmental nerve towards dorsal targets) in Lar^bypass/Lar^5.5 embryos. (Wills et al., 1999) 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. (Desai et al., 1997) 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 Lar^5.5/Lar^13.2 is overcome by Lar^Scer\UAS.cKa driven by Scer\GAL4^elav-C155. (Krueger et al., 1996)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference Lar^5.5 has neuroanatomy defective \| embryonic stage phenotype, enhanceable by ckn^K.Δ324-331 (Weng et al., 2011)
Enhancer of
Statement Reference Lar^5.5/Lar[+] is an enhancer of neuroanatomy defective \| larval stage phenotype of Sara^Ubi.PJ, Sdc⁴⁸/Sdc^KG06163 (Johnson et al., 2006)
Suppressor of
Statement Reference Lar^5.5/Lar^13.2 is a suppressor of neuroanatomy defective phenotype of Scer\GAL4^how-24B/Scer\GAL4^how-24B, Sdc^Scer\UAS.cJa (Fox and Zinn, 2005)
Other
Statement Reference Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has neuroanatomy defective \| embryonic stage 16 phenotype (Sun et al., 2001) Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹ has neuroanatomy defective \| embryonic stage 16 phenotype (Sun et al., 2001) Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has neuroanatomy defective \| embryonic stage 16 phenotype (Sun et al., 2001) Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has neuroanatomy defective \| embryonic stage 16 phenotype (Sun et al., 2001) Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has neuroanatomy defective \| embryonic stage phenotype (Sun et al., 2001) Lar^5.5/Lar^13.2, Ptp10D¹ has neuroanatomy defective \| embryonic stage phenotype (Sun et al., 2001)
Phenotype Manifest In
Enhanced by
Statement Reference Lar^5.5/Lar^13.2 has anterior fascicle & axon \| ectopic phenotype, enhanceable by Sdc⁴⁸/Sdc¹⁰⁶⁰⁸ (Fox and Zinn, 2005) Lar^5.5/Lar^13.2 has oocyte phenotype, enhanceable by mys¹/mys[+] (Bateman et al., 2001) Lar^5.5/Lar^13.2 has oocyte phenotype, enhanceable by mys¹⁰/mys[+] (Bateman et al., 2001) Lar^5.5/Lar²¹²⁷ has photoreceptor cell R7 & axon phenotype, enhanceable by ena[+]/ena^GC1 (Maurel-Zaffran et al., 2001) Lar^5.5/Lar²¹²⁷ has photoreceptor cell R7 & axon phenotype, enhanceable by trio¹/trio[+] (Maurel-Zaffran et al., 2001) Lar^5.5 has intersegmental nerve branch ISNb of A1-7 \| embryonic stage phenotype, enhanceable by ckn^K.Δ324-331 (Weng et al., 2011) Lar^5.5 has intersegmental nerve phenotype, enhanceable by trio^S137203/trio[+] (Bateman et al., 2000) Lar^5.5 has phenotype, enhanceable by Scer\GAL4^elav-C155/Rac1^N17.Scer\UAS (Kaufmann et al., 1998) Lar^5.5 has phenotype, enhanceable by trio^S137203/trio[+] (Bateman et al., 2000)
Suppressed by
Statement Reference Lar^5.5/Lar²¹²⁷ has photoreceptor cell R7 & axon phenotype, suppressible by trio^GMR.PN (Maurel-Zaffran et al., 2001) Lar^bypass/Lar^5.5 has intersegmental nerve phenotype, suppressible by Abl¹ (Wills et al., 1999)
Enhancer of
Statement Reference Lar^5.5/Lar[+] is an enhancer of NMJ bouton \| larval stage phenotype of Sara^Ubi.PJ, Sdc⁴⁸/Sdc^KG06163 (Johnson et al., 2006)
Suppressor of
Statement Reference Lar^5.5/Lar^13.2 is a suppressor of abdominal segmental nerve phenotype of Scer\GAL4^how-24B/Scer\GAL4^how-24B, Sdc^Scer\UAS.cJa (Fox and Zinn, 2005) Lar^5.5 is a suppressor of central nervous system phenotype of Ptp52F^18.3 (Schindelholz et al., 2001)
Other
Statement Reference Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has intersegmental nerve \| embryonic stage phenotype (Sun et al., 2001) Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has segmental nerve branch SNa of A1-7 \| embryonic stage phenotype (Sun et al., 2001) Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has ventral nerve cord \| embryonic stage 16 phenotype (Sun et al., 2001) Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹ has segmental nerve branch SNa of A1-7 \| embryonic stage 16 phenotype (Sun et al., 2001) Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹ has ventral nerve cord \| embryonic stage 16 phenotype (Sun et al., 2001) Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has intersegmental nerve \| embryonic stage phenotype (Sun et al., 2001) Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has intersegmental nerve branch ISNb of A1-7 \| embryonic stage phenotype (Sun et al., 2001) Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has ventral nerve cord \| embryonic stage 16 phenotype (Sun et al., 2001) Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has anterior commissure phenotype (Sun et al., 2000, Sun et al., 2000, Sun et al., 2000, Sun et al., 2000) Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has longitudinal connective phenotype (Sun et al., 2000, Sun et al., 2000, Sun et al., 2000, Sun et al., 2000) Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has posterior commissure phenotype (Sun et al., 2000, Sun et al., 2000, Sun et al., 2000, Sun et al., 2000) Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has ventral nerve cord commissure phenotype (Sun et al., 2000, Sun et al., 2000, Sun et al., 2000, Sun et al., 2000) Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has segmental nerve branch SNa of A1-7 \| embryonic stage phenotype (Sun et al., 2001) Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has ventral nerve cord \| embryonic stage 16 phenotype (Sun et al., 2001) Lar^5.5/Lar^13.2, Ptp10D¹ has intersegmental nerve \| embryonic stage phenotype (Sun et al., 2001) Lar^5.5/Lar^13.2, Ptp10D¹ has segmental nerve branch SNa of A1-7 \| embryonic stage phenotype (Sun et al., 2001)
Additional Comments
Genetic Interactions
Statement Reference Lar[5.5] ckn[K.Δ324-331] double mutants exhibit an increase in frequency of the ISNb bypass phenotype from 31% in Lar[5.5] single mutants to 49% in double mutants. Lar[5.5] ckn[K.Δ324-331] double heterozygous embryos display bypass phenotypes with 39% penetrance. (Weng et al., 2011) Lar[5.5]/+ enhances the reduction in bouton number at the neuromuscular junction which is seen in Sdc[KG06163]/Df(2R)48 larvae (carrying Sara[Ubi.PJ] to provide Sara function). (Johnson et al., 2006) Sdc⁴⁸/Sdc¹⁰⁶⁰⁸; Lar^13.2/Lar^5.5 mutants (in which Sara has been rescued by expression of the Sara^Ubi.PJ transgene) display an increased penetrance of the bypass phenotype (43% vs. 28%) relative to the corresponding Lar^13.2/Lar^5.5 transheterozygote. When Sdc^Scer\UAS.cJa is expressed, under the control of Scer\GAL4^how-24B, in a Lar^13.2/Lar^5.5 background, the SNa bifurcation phenotype seen when the transgene is expressed in a wild-type background is suppressed. (Fox and Zinn, 2005) The addition of mys¹⁰/+ or mys¹/+ to Lar^5.5/Lar^13.2 increases the penetrance of the oocyte elongation phenotype from 14.1% to 48.7% and about 40% respectively. (Bateman et al., 2001) Lar[5.5]/Lar[13.2] Ptp69D[1] Ptp99A[1]/Df(3R)Ptp99A[R3] 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 Ptp10D[1] Lar[5.5]/Lar[13.2] Ptp99A[1]/Df(3R)Ptp99A[R3] 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 Ptp10D[1] Lar[5.5]/Lar[13.2] Ptp69D[1] 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 Ptp10D[1] Lar[5.5]/Lar[13.2] Ptp69D[1] Ptp99A[1]/Df(3R)Ptp99A[R3] 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 Ptp10D[1] Lar[5.5]/Lar[13.2] 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 Ptp10D[1] Lar[5.5]/Lar[13.2] Ptp69D[1] triple mutant embryos. Approximately half of the SNa nerves fail to bifurcate in Ptp10D[1] Lar[5.5]/Lar[13.2] Ptp99A[1]/Df(3R)Ptp99A[R3] triple mutant embryos. Approximately half of the SNa nerves either do not reach the bifurcation point at all or are very thin and wandering in Ptp10D[1] Lar[5.5]/Lar[13.2] Ptp69D[1] Ptp99A[1]/Df(3R)Ptp99A[R3] quadruple mutant embryos. Approximately half of the intersegmental nerves terminate at the second lateral branch position in Ptp10D[1] Lar[5.5]/Lar[13.2] 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 Lar[5.5]/Lar[13.2] Ptp69D[1] Ptp99A[1]/Df(3R)Ptp99A[R3] 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 Ptp10D[1] Lar[5.5]/Lar[13.2] Ptp69D[1] Ptp99A[1]/Df(3R)Ptp99A[R3] quadruple mutant embryos. (Sun et al., 2001) Ptp10D¹; Lar^13.2/Lar^5.5; Ptp69D¹ Ptp99A^R3/Ptp69D^8ex25 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; Lar^5.5/Lar^13.2 double mutant embryos. (Sun et al., 2000) The Lar^bypass/Lar^5.5 ISNb "bypass" phenotype is suppressed by Abl¹. (Wills et al., 1999) Mutation causes synergy of the Scer\GAL4^elav-C155, Rac1^N17.Scer\UAS full ISNb bypass phenotype. (Kaufmann et al., 1998)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	Lar^5.5/Lar^13.2 is rescued by Scer\GAL4^elav.PU/Lar^Scer\UAS.cKa (Johnson et al., 2006) Lar^5.5/Lar^13.2 is rescued by Scer\GAL4^T155/Lar^Scer\UAS.cKa (Bateman et al., 2001, Krueger et al., 2003) Lar^5.5/Lar^13.2 is rescued by Scer\GAL4^T155/Lar^{ΔFn789.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.2 is rescued by Scer\GAL4^T155/Lar^{ΔIg123.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar²¹²⁷ is rescued by Lar^Scer\UAS.cKa/Scer\GAL4^hs.2sev (Maurel-Zaffran et al., 2001)
Partially rescued by	Lar^5.5/Lar^5.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{C1638S.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^5.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{C1929S.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^5.2 is partially rescued by Scer\GAL4^elav-C155/Lar^Scer\UAS.cKa (Krueger et al., 2003) Lar^5.5/Lar^5.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{ΔPTP-D2.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.1 is partially rescued by Scer\GAL4^elav-C155/Lar^{C1638S.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.1 is partially rescued by Scer\GAL4^elav-C155/Lar^Scer\UAS.cKa (Krueger et al., 2003) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav.PU/Lar^{ΔFn2-9.Scer\UAS} (Johnson et al., 2006) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{C1638S.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{C1929S.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{CSX2.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^Scer\UAS.cKa (Krueger et al., 2003) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{ΔFn2-9.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{ΔFn123.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{ΔFn456.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{ΔFn789.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^{ΔPTP-D2.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar²¹²⁷ is partially rescued by Lar^Scer\UAS.cKa/Scer\GAL4^sca-109-68 (Maurel-Zaffran et al., 2001) Lar^5.5/Lar²¹²⁷ is partially rescued by Lar^{ΔC.Scer\UAS.T:SS-wg,T:Ivir\HA1}/Scer\GAL4^sca-109-68 (Maurel-Zaffran et al., 2001)
Not rescued by	Lar^5.5/Lar^13.2 is not rescued by Lar^Scer\UAS.cKa/Scer\GAL4^198Y (Bateman et al., 2001) Lar^5.5/Lar^13.2 is not rescued by Lar^Scer\UAS.cKa/Scer\GAL4^how-24B (Johnson et al., 2006) Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^elav.PU/Lar^{CSX2.Scer\UAS} (Johnson et al., 2006) Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^elav.PU/Lar^{ΔIg123.Scer\UAS} (Johnson et al., 2006) Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^elav-C155/Lar^Scer\UAS.cKa (Krueger et al., 2003) Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^elav-C155/Lar^{ΔIg123.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^how-24B/Lar^{CSX2.Scer\UAS} (Johnson et al., 2006) Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^how-24B/Lar^{ΔFn2-9.Scer\UAS} (Johnson et al., 2006) Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^how-24B/Lar^{ΔIg123.Scer\UAS} (Johnson et al., 2006) Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^T155/Lar^{ΔFn2-9.Scer\UAS} (Krueger et al., 2003) Lar^5.5/Lar²¹²⁷ is not rescued by Scer\GAL4^hs.2sev/Lar^{ΔC.Scer\UAS.T:SS-wg,T:Ivir\HA1} (Maurel-Zaffran et al., 2001)
Comments	Expression of Lar[Scer\UAS.cKa] under the control of Scer\GAL4[elav.PU] rescues the reduction in bouton number at the neuromuscular junction seen in Lar[5.5]/Lar[13.2] larvae, while expression under the control of Scer\GAL4[how-24B] does not rescue the mutant phenotype. Expression of Lar[ΔFn2-9.Scer\UAS] under the control of Scer\GAL4[elav.PU] partially rescues the reduction in bouton number at the neuromuscular junction seen in Lar[5.5]/Lar[13.2] larvae. Expression of either Lar[CSX2.Scer\UAS] or Lar[ΔIg123.Scer\UAS] under the control of Scer\GAL4[elav.PU] fails to rescue the reduction in bouton number at the neuromuscular junction seen in Lar[5.5]/Lar[13.2] larvae. (Johnson et al., 2006)
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	Dlar^5.5 (Krueger et al., 2003, Kaufmann et al., 2002, Bateman et al., 2000, Sun et al., 2000, Wills et al., 1999, Jeon et al., 2008, Sun et al., 2001, Johnson et al., 2006) La^r5.5 (Jeon et al., 2008) lar^5.5 (Fox and Zinn, 2005) Lar^5.5 (Weng et al., 2011, Viktorinová et al., 2009)
Name Synonym
Secondary FlyBase IDs

References ( 19 )
Research paper	Weng et al., 2011, J. Neurosci. 31(12): 4421--4433 The Cytoplasmic Adaptor Protein Caskin Mediates Lar Signal Transduction during Drosophila Motor Axon Guidance. [FBrf0213321] Viktorinová et al., 2009, Development 136(24): 4123--4132 The cadherin Fat2 is required for planar cell polarity in the Drosophila ovary. [FBrf0209333] Jeon et al., 2008, Neural Dev. 3: 3 Redundancy and compensation in axon guidance: genetic analysis of the Drosophila Ptp10D/Ptp4E receptor tyrosine phosphatase subfamily. [FBrf0205151] Johnson et al., 2006, Neuron 49(4): 517--531 The HSPGs Syndecan and Dallylike bind the receptor phosphatase LAR and exert distinct effects on synaptic development. [FBrf0191320] Fox and Zinn, 2005, Curr. Biol. 15(19): 1701--1711 The heparan sulfate proteoglycan syndecan is an in vivo ligand for the Drosophila LAR receptor tyrosine phosphatase. [FBrf0190011] Krueger et al., 2003, Mol. Cell. Biol. 23(19): 6909--6921 Functions of the ectodomain and cytoplasmic tyrosine phosphatase domains of receptor protein tyrosine phosphatase Dlar in vivo. [FBrf0162244] Kaufmann et al., 2002, Neuron 34(1): 27--38 Drosophila liprin-alpha and the receptor phosphatase Dlar control synapse morphogenesis. [FBrf0147174] Bateman et al., 2001, Curr. Biol. 11(17): 1317--1327 The receptor tyrosine phosphatase Dlar and integrins organize actin filaments in the Drosophila follicular epithelium. [FBrf0138265] Frydman and Spradling, 2001, Development 128(16): 3209--3220 The receptor-like tyrosine phosphatase Lar is required for epithelial planar polarity and for axis determination within Drosophila ovarian follicles. [FBrf0139630] Maurel-Zaffran et al., 2001, Neuron 32(2): 225--235 Cell-autonomous and -nonautonomous functions of LAR in R7 photoreceptor axon targeting. [FBrf0139775] Schindelholz et al., 2001, Development 128(21): 4371--4382 Regulation of CNS and motor axon guidance in Drosophila by the receptor tyrosine phosphatase DPTP52F. [FBrf0139642] Sun et al., 2001, Mol. Cell. Neurosci. 17(2): 274--291 Complex genetic interactions among four receptor tyrosine phosphatases regulate axon guidance in Drosophila. [FBrf0134771] Bateman et al., 2000, Neuron 26(1): 93--106 The guanine nucleotide exchange factor trio mediates axonal development in the Drosophila embryo. [FBrf0127003] Sun et al., 2000, Development 127(4): 801--812 Receptor tyrosine phosphatases regulate axon guidance across the midline of the Drosophila embryo. [FBrf0125454] Wills et al., 1999, Neuron 22(2): 301--312 The tyrosine kinase Abl and its substrate enabled collaborate with the receptor phosphatase Dlar to control motor axon guidance. [FBrf0108074] Kaufmann et al., 1998, Development 125(3): 453--461 Drosophila Rac1 controls motor axon guidance. [FBrf0100716] Desai et al., 1997, Development 124(10): 1941--1952 Competition and cooperation among receptor tyrosine phosphatases control motoneuron growth cone guidance in Drosophila. [FBrf0093417] Krueger et al., 1996, Cell 84(4): 611--622 The transmembrane tyrosine phosphatase DLAR controls motor axon guidance in Drosophila. [FBrf0086508]
Supplementary material	Fox and Zinn, 2005, Curr. Biol. 15(19): Supplemental data. [FBrf0191745]

Allele Dmel\Lar5.5

Allele Dmel\Lar^5.5