FlyBase Allele Report: 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

Associated Insertion(s)

Carried in Construct

Also Known As

Dlar^5.5

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

Mutagen

ethyl methanesulfonate

(Desai et al., 1997, Krueger et al., 1996)

Progenitor genotype

Cytology

Description

Protein truncated in FnII domain 3.

(Krueger et al., 2003)

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)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2L:19,717,177..19,717,177 [+]

Nucleotide change:

G19717177A

Reported nucleotide change:

G1773A

Amino acid change:

Reported amino acid change:

W?term

(Krueger et al., 1996)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

actin-based cell projection | oogenesis | somatic clone (with Lar^13.2)

(Squarr et al., 2016)

actin filament & follicle cell | somatic clone | cell non-autonomous

(Bateman et al., 2001)

adult mushroom body beta-lobe | somatic clone

(Kurusu and Zinn, 2008)

anterior fascicle & axon | ectopic (with Lar^13.2)

(Fox and Zinn, 2005)

axon | adult stage | somatic clone

(Kurusu and Zinn, 2008)

axon | somatic clone | third instar larval stage

(Kurusu and Zinn, 2008)

axon | third instar larval stage (with Lar^13.2)

(Kurusu and Zinn, 2008)

bouton

(Kaufmann et al., 2002)

centripetal follicle cell | somatic clone (with Lar^13.2)

(Squarr et al., 2016)

dorsal appendage (with Lar^13.2)

(Bateman et al., 2001)

egg | maternal effect (with Lar^13.2)

(Squarr et al., 2016)

embryonic/larval mushroom body | third instar larval stage (with Lar^13.2)

(Kurusu and Zinn, 2008)

follicle cell | cell non-autonomous | somatic clone

(Frydman and Spradling, 2001)

larval abdominal segmental nerve

(Desai et al., 1997, Krueger et al., 1996)

larval intersegmental nerve

(Bateman et al., 2000, Wills et al., 1999, Desai et al., 1997)

larval intersegmental nerve (with Lar^13.2)

(Krueger et al., 2003)

larval intersegmental nerve (with Lar^13.2), with Lar^C1929S.UAS, Scer\GAL4^elav-C155

(Krueger et al., 2003)

larval intersegmental nerve branch ISNb of A1-7 | embryonic stage

(Weng et al., 2011)

larval longitudinal connective

(Krueger et al., 1996)

larval RP5 motor neuron (with Lar^13.2)

(Schindelholz et al., 2001)

larval VL3/4 motor neuron (with Lar^13.2)

(Schindelholz et al., 2001)

larval VO1 motor neuron (with Lar^13.2)

(Schindelholz et al., 2001)

larval VO2 motor neuron (with Lar^13.2)

(Schindelholz et al., 2001)

medial lobe of larval mushroom body | somatic clone | third instar larval stage

(Kurusu and Zinn, 2008)

medial lobe of larval mushroom body | third instar larval stage (with Lar^13.2)

(Kurusu and Zinn, 2008)

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.UAS, Scer\GAL4^T155

(Krueger et al., 2003)

oocyte (with Lar^13.2), with Lar^ΔFn123.UAS, Scer\GAL4^T155

(Krueger et al., 2003)

oocyte (with Lar^13.2), with Lar^ΔFn456.UAS, Scer\GAL4^T155

(Krueger et al., 2003)

oocyte | oogenesis stage S14 (with Lar^13.2)

(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)

vertical lobe of larval mushroom body | third instar larval stage (with Lar^13.2)

(Kurusu and Zinn, 2008)

Detailed Description

Statement

Reference

Lar^5.5/Lar^13.2 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 Lar^5.5/Lar^13.2 mutant egg chambers are moderately rounded as compared to wild type.

(Squarr et al., 2016)

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 genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Lar^5.5 has abnormal neuroanatomy | 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 abnormal neuroanatomy | 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 abnormal neuroanatomy phenotype of Scer\GAL4^how-24B, Sdc^UAS.cJa

(Fox and Zinn, 2005)

Other

Statement

Reference

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has abnormal neuroanatomy | embryonic stage phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has abnormal neuroanatomy | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹ has abnormal neuroanatomy | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has abnormal neuroanatomy | embryonic stage 16 phenotype

(Sun et al., 2001)

Lar^5.5/Lar^13.2, Ptp10D¹ has abnormal neuroanatomy | embryonic stage phenotype

(Sun et al., 2001)

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has abnormal neuroanatomy | embryonic stage 16 phenotype

(Sun et al., 2001)

Phenotype Manifest In

Enhanced by

Statement

Reference

Lar^5.5/Lar^13.2 has egg | maternal effect phenotype, enhanceable | maternal effect by Abi[+]/Abi^Δ20

(Squarr et al., 2016)

Lar^5.5 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, enhanceable by ckn^K.Δ324-331

(Weng et al., 2011)

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 phenotype, enhanceable by trio^S137203/trio[+]

(Bateman et al., 2000)

Lar^5.5 has larval 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.UAS

(Kaufmann et al., 1998)

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 larval 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 larval abdominal segmental nerve phenotype of Scer\GAL4^how-24B, Sdc^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

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has larval 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, Ptp69D¹ has larval intersegmental nerve | embryonic stage phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has larval 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 larval ventral nerve cord | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹ has larval ventral nerve cord | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹ has larval 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, Ptp69D¹ has larval intersegmental nerve | embryonic stage phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has larval ventral nerve cord | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype

(Sun et al., 2001)

Lar^5.5/Lar^13.2, Ptp10D¹ has larval intersegmental nerve | embryonic stage phenotype

(Sun et al., 2001)

Lar^5.5/Lar^13.2, Ptp10D¹ has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype

(Sun et al., 2001)

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has larval 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 larval longitudinal connective phenotype

(Sun et al., 2000)

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has larval ventral nerve cord commissure phenotype

(Sun et al., 2000)

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has larval anterior commissure phenotype

(Sun et al., 2000)

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has larval posterior commissure phenotype

(Sun et al., 2000)

Additional Comments

Genetic Interactions

Statement

Reference

Abi^Δ20/+ strongly enhances the rounded egg phenotype of Lar^5.5/Lar^13.2 mutants.

(Squarr et al., 2016)

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 Ptp69D¹ Ptp99A¹/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 Ptp10D¹ Lar^5.5/Lar^13.2 Ptp99A¹/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 Ptp10D¹ Lar^5.5/Lar^13.2 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 Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/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 Ptp10D¹ 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 Ptp10D¹ Lar^5.5/Lar^13.2 Ptp69D¹ triple mutant embryos.

Approximately half of the SNa nerves fail to bifurcate in Ptp10D¹ Lar^5.5/Lar^13.2 Ptp99A¹/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 Ptp10D¹ Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 quadruple mutant embryos.

Approximately half of the intersegmental nerves terminate at the second lateral branch position in Ptp10D¹ 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 Ptp69D¹ Ptp99A¹/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 Ptp10D¹ Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/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 and Rescue Data

Rescued by

Lar^5.5/Lar^13.2 is rescued by Scer\GAL4^elav.PU/Lar^UAS.cKa

(Johnson et al., 2006)

Lar^5.5/Lar^13.2 is rescued by Scer\GAL4^T155/Lar^ΔFn789.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is rescued by Scer\GAL4^T155/Lar^ΔIg123.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is rescued by Scer\GAL4^T155/Lar^UAS.cKa

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is rescued by Scer\GAL4^T155/Lar^UAS.cKa

(Bateman et al., 2001)

Lar^5.5/Lar²¹²⁷ is rescued by Lar^UAS.cKa/Scer\GAL4^hs.2sev

(Maurel-Zaffran et al., 2001)

Partially rescued by

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav.PU/Lar^ΔFn2-9.UAS

(Johnson et al., 2006)

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^ΔFn789.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^ΔFn456.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^C1638S.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^C1929S.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^ΔFn2-9.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^CSX2.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^UAS.cKa

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^ΔFn123.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is partially rescued by Scer\GAL4^elav-C155/Lar^ΔPTP-D2.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.1 is partially rescued by Scer\GAL4^elav-C155/Lar^C1638S.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.1 is partially rescued by Scer\GAL4^elav-C155/Lar^UAS.cKa

(Krueger et al., 2003)

Lar^5.5/Lar^5.2 is partially rescued by Scer\GAL4^elav-C155/Lar^C1638S.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^5.2 is partially rescued by Scer\GAL4^elav-C155/Lar^C1929S.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^5.2 is partially rescued by Scer\GAL4^elav-C155/Lar^UAS.cKa

(Krueger et al., 2003)

Lar^5.5/Lar^5.2 is partially rescued by Scer\GAL4^elav-C155/Lar^ΔPTP-D2.UAS

(Krueger et al., 2003)

Lar^5.5/Lar²¹²⁷ is partially rescued by Lar^UAS.cKa/Scer\GAL4^sca-109-68

(Maurel-Zaffran et al., 2001)

Lar^5.5/Lar²¹²⁷ is partially rescued by Lar^{ΔC.UAS.Tag:SS(wg),Tag:HA}/Scer\GAL4^sca-109-68

(Maurel-Zaffran et al., 2001)

Not rescued by

Lar^5.5/Lar^13.2 is not rescued by Lar^UAS.cKa/Scer\GAL4^how-24B

(Johnson et al., 2006)

Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^how-24B/Lar^ΔFn2-9.UAS

(Johnson et al., 2006)

Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^elav.PU/Lar^CSX2.UAS

(Johnson et al., 2006)

Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^how-24B/Lar^CSX2.UAS

(Johnson et al., 2006)

Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^elav.PU/Lar^ΔIg123.UAS

(Johnson et al., 2006)

Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^how-24B/Lar^ΔIg123.UAS

(Johnson et al., 2006)

Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^elav-C155/Lar^ΔIg123.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^T155/Lar^ΔFn2-9.UAS

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is not rescued by Scer\GAL4^elav-C155/Lar^UAS.cKa

(Krueger et al., 2003)

Lar^5.5/Lar^13.2 is not rescued by Lar^UAS.cKa/Scer\GAL4^198Y

(Bateman et al., 2001)

Lar^5.5/Lar²¹²⁷ is not rescued by Scer\GAL4^hs.2sev/Lar^{ΔC.UAS.Tag:SS(wg),Tag:HA}

(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)

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Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

Dlar^5.5

(Han et al., 2020, Jeon et al., 2008, Johnson et al., 2006, Krueger et al., 2003, Kaufmann et al., 2002, Sun et al., 2001, Bateman et al., 2000, Sun et al., 2000, Wills et al., 1999)

La^r5.5

(Jeon et al., 2008)

Lar^5.5

(Weng et al., 2011, Viktorinová et al., 2009, Kurusu and Zinn, 2008)

dlar^5.5

(Squarr et al., 2016)

lar^5.5

(Fox and Zinn, 2005)

Name Synonyms

Secondary FlyBase IDs

References (22)

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