Dmel\P{lacW}Sema-1a^k13702 Insertion

General Information
Symbol	Dmel\P{lacW}Sema-1a^k13702	Species	D. melanogaster
Name		FlyBase ID	FBti0009850
Feature type	transposable_element_insertion_site
Description
Inserted element	P{lacW}	Expression data
Affected gene(s)	Ecol\lacZ, Sema-1a	Viability / fertility
Causes allele(s)	Ecol\lacZ^{Sema-1a-k13702}, Sema-1a^k13702	Stock availability	2 publicly available
LINE ID	l(2)k13702
Genomic Location
Chromosomal location	2L ( 29E2 )	Sequence location	2L:8,544,219..8,544,219 [+]
Map ( GBrowse )
Member of Large Scale Dataset(s)
Dataset	TI_set_P{lacW}.BDGP A set of mutant stocks derived by insertional mutagenesis using the P-element construct P{lacW}; most lines have a lethal or sterile phenotype. The P{lacW} construct carries a w[+mC] mini-white visible marker, Ecol\lacZ enhancer trap sequences, and bacterial sequences that allow plasmid rescue (FBrf0049800). Insertion lines from this collection were assessed for inclusion in the Gene Disruption Project collection. (Spradling et al., 1999, Bellen et al., 2004)
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
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FB2013_03
FB2013_02	Controlled Vocabulary Terms ISNb
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Detailed Mapping Data
Chromosome (arm)
Sequence Location	2L:8,544,219..8,544,219 [+] (BDGP Project Members, 1994-1999)
Orientation
Cytological location (computed by FlyBase)	29E2 ( inferred by FlyBase from sequence location )
Cytological location (reported)	29E1-29E2 (in situ hybridization reported) (BDGP Project Members, 1994-1999)
Comments concerning location
Sequence Data
Flanking sequence	AQ026063 (FlyBase, 1992-,
Inserted Element
Construct	P{lacW}
Location-dependent role	lacZ enhancer trap (Bier et al., 1989)
Size	10.691Kb
Associated alleles	Ecol\lacZ^P\T.W w^+mC
Molecular map
Affected Gene(s)
Insertion may affect gene	Ecol\lacZ (BDGP Project Members, 1994-1999, Yu et al., 1998) Sema-1a (Yu et al., 1998, BDGP Project Members, 1994-1999, Miller et al., 2011, Yu et al., 2010)
Alleles and Phenotypes
Causes alleles	Ecol\lacZ^{Sema-1a-k13702} (BDGP Project Members, 1994-1999, Yu et al., 1998) Sema-1a^k13702 (BDGP Project Members, 1994-1999, Yu et al., 1998, Spradling et al., 1999, Miller et al., 2011, Yu et al., 2010)

Lethality References lethal \| recessive (Spradling et al., 1999) partially lethal - majority die \| recessive (Yu et al., 1998)
Sterility References
Phenotype Manifest In
	abdominal segmental nerve (Yu et al., 2000) abdominal ventral longitudinal muscle & synapse (Yu et al., 1998) adult olfactory receptor neuron Or23a \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or33c/85e \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or35a \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or42a \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or43a \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or46a \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or47b \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or59c \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or67b \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or71a \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or83c \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) adult olfactory receptor neuron Or88a \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) anterior commissure (Ayoob et al., 2004) axon & alpha\'-lobe \| somatic clone (Komiyama et al., 2007) axon & antennal glomerulus DA1 \| somatic clone (Komiyama et al., 2007) axon & antennal glomerulus DC3 \| somatic clone (Komiyama et al., 2007) axon & antennal glomerulus DL1 \| somatic clone \| cell autonomous (Komiyama et al., 2007) axon & antennal glomerulus VM2 \| somatic clone (Komiyama et al., 2007) axon & beta\'-lobe \| somatic clone (Komiyama et al., 2007) axon & eye photoreceptor cell (Cafferty et al., 2006) axon & eye photoreceptor cell \| somatic clone \| cell autonomous (Cafferty et al., 2006) axon & lamina (Cafferty et al., 2006) axon & lamina \| somatic clone \| somatic clone \| cell autonomous (Cafferty et al., 2006) dendrite & antennal glomerulus DA1 \| somatic clone (Komiyama et al., 2007) dendrite & antennal glomerulus DC3 \| somatic clone (Komiyama et al., 2007) dendrite & antennal glomerulus DL1 \| somatic clone (Komiyama et al., 2007) eye photoreceptor cell & lamina (Cafferty et al., 2006) eye photoreceptor cell & lamina \| somatic clone \| cell autonomous (Cafferty et al., 2006) eye photoreceptor cell \| third instar larval stage (Yu et al., 2010) intersegmental nerve (Terman et al., 2002, Yu et al., 2000) intersegmental nerve \| embryonic stage (Yu et al., 1998) intersegmental nerve branch ISNb of A1-7 (Jeong et al., 2012) lamina (Cafferty et al., 2004) lamina \| third instar larval stage (Yu et al., 2010) lateral longitudinal fascicle (Wu et al., 2011, Jeong et al., 2012) longitudinal connective (Yu et al., 1998) photoreceptor cell R1 & axon (Cafferty et al., 2004) photoreceptor cell R2 & axon (Cafferty et al., 2004) photoreceptor cell R3 & axon (Cafferty et al., 2004) photoreceptor cell R4 & axon (Cafferty et al., 2004) photoreceptor cell R5 & axon (Cafferty et al., 2004) photoreceptor cell R6 & axon (Cafferty et al., 2004) posterior commissure (Ayoob et al., 2004) presumptive embryonic/larval central nervous system (Yu et al., 2000) RP3 neuron & synapse (Yu et al., 2000) RP5 neuron & synapse (Yu et al., 2000) segmental nerve (Terman et al., 2002) segmental nerve \| embryonic stage (Yu et al., 1998) transverse nerve \| embryonic stage (Yu et al., 1998)
Detailed Description
Statement Reference Expression of either Sema-1a[Scer\UAS.cJa], Sema-1a[36G.52A.Scer\UAS] or Sema-1a[Δ31-60.Scer\UAS] under the control of Scer\GAL4[sca-537.4] rescues the central nervous system guidance defects and partially rescues the ISNb guidance defects seen in Sema-1a[k13702] embryos. Expression of either Sema-1a[mICD.Scer\UAS] or Sema-1a[mICD.Scer\UAS.T:Hsap\Fc-IgG] under the control of Scer\GAL4[sca-537.4] significantly but modestly rescues the central nervous system guidance defects seen in Sema-1a[k13702] embryos. Expression of Sema-1a[mEC.Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[sca-537.4] partially rescues the central nervous system guidance defects seen in Sema-1a[k13702] embryos. Expression of Sema-1a[mEC.Scer\UAS.T:Hsap\Fc-IgG,T:Hsap\MYC] under the control of Scer\GAL4[sca-537.4] strongly rescues the central nervous system guidance defects seen in Sema-1a[k13702] embryos. Co-expression of Sema-1a[mEC.Scer\UAS.T:Hsap\Fc-IgG,T:Hsap\MYC] and Sema-1a[mICD.Scer\UAS] under the control of Scer\GAL4[sca-537.4] does not result in additional rescue of the ISNb defects seen in Sema-1a[k13702] embryos compared to either line expressed alone. Co-expression of Sema-1a[mEC.Scer\UAS.T:Hsap\Fc-IgG,T:Hsap\MYC] and Sema-1a[mICD.Scer\UAS.T:Hsap\Fc-IgG] under the control of Scer\GAL4[sca-537.4] does not result in additional rescue of the ISNb defects seen in Sema-1a[k13702] embryos compared to either line expressed alone. (Jeong et al., 2012) Homozygous embryos show defects in ISNb guidance in more than 80% of hemisegments. Guidance defects are often seen in the lateral Fas2-positive longitudinal axon pathways of the central nervous system. (Jeong et al., 2012) Sema-1a[k13702]/+ suppresses the premature ISNb branching seen in embryos expressing RhoGAPp190[dsRNA.N.Scer\UAS] under the control of Scer\GAL4[elav.PLu] from 22.1% to 8.2% of hemisegments, while the total fraction of hemisegments showing ISNb defects is reduced from 36.4% to 21.2% in these animals. Total ISNb guidance defects in embryos doubly heterozygous for Sema-1a[k13702] and pbl[2] are greater than those observed for either single heterozygote. (Jeong et al., 2012) A heterozygous Sema-1a[k13702] background dominantly suppresses the ISNb pathfinding phenotypes from 64% in frac[Δ1] homozygotes to 18% in double mutants. (Miller et al., 2011) The lateral Fas2-positive tract of the central nervous system is often thin and discontinuous in mutant embryos, but the intermediate Fas2-positive tract appears normal. (Wu et al., 2011) R1-R6 growth cones scatter around the lamina termination region in homozygous Sema-1a[k13702] third instar larvae, leading to the appearance of a discontinuous termination layer in the lamina. (Yu et al., 2010) Sema-1a^k13702 clones generated in a heterozygous background in either projection neurons or mushroom body α\'/β\' neurons cause axon mistargeting. Sema-1a^k13702 clonal DL1 projection neuron axons in a heterozygous background mistarget dorsally out of the correct areas and show profuse branching. This phenotype is 100% penetrant. Axon mistargeting is also observed for DA1 clones. DC3 and VM2 neuron clones show mild axon mistargeting phenotypes. Dendrites of Sema-1a^k13702 DL1 projection neuron clones mistarget; these dendrites normally target the most dorsolateral glomerulus of the antennal lobe but they mistarget ventromedially and sometimes target outside the antennal lobe. This mistargeting is seen at all stages of development. Dendrites of DA1 projection neuron clones mistarget in the ventromedial direction. Centrally targeting DC3 dendrites show a mild but statistically significant shift in the ventromedial direction. Ventromedially targeting VM2 neurons still target most of their dendrites to the appropriate area. (Komiyama et al., 2007) Homozygous maxillary palp olfactory receptor neuron clones of the Or85e, Or46a, Or42a, Or59c or Or71a expressing classes (where about half or almost all olfactory receptor neurons are mutant) show severe axon-targeting defects. They often fail to enter the antennal lobe and form extra-antennal lobe terminations. Axons that do enter the antennal lobe mistarget to inappropriate areas and form ectopic terminations within the antennal lobe. Small homozygous clones of these classes of maxillary palp olfactory receptor neurons do not show axon targeting defects, indicating that the defects seen when large olfactory receptor neuron clones are present are non-cell-autonomous. Homozygous antennal olfactory receptor neuron clones of the Or10a, Or22a, Or47a, Or92a or Gr21a expressing classes (where about half or almost all olfactory receptor neurons are mutant) do not show axon targeting defects. Homozygous antennal olfactory receptor neuron clones of the Or43a, Or83c, Or88a, Or23a or Or35a expressing classes (where almost all olfactory receptor neurons are mutant) show mild but highly penetrant defects in axon targeting within the antennal lobe; the axons always innervate their correct glomeruli but often also spread slightly beyond their normal targets. No ectopic terminations are found outside the antennal lobe. Homozygous antennal olfactory receptor neuron clones of the Or67b or Or47b expressing classes (where almost all olfactory receptor neurons are mutant) show defects in axon targeting within the antennal lobe; they always innervate their correct glomeruli but occasionally target to more distant regions of the antennal lobe as well. No ectopic terminations are found outside the antennal lobe. (Sweeney et al., 2007) The frequency of axon targeting defects of maxillary palp olfactory receptor neurons in animals expressing plexA[VDRC.cUa] under the control of Scer\GAL4[peb-GAL4] is enhanced if they are also heterozygous for Sema-1a[k13702]. The frequency of both abnormal terminations outside the antennal lobe and of ectopic terminations within the antennal lobe is increased. (Sweeney et al., 2007) In Sema-1a^k13702 homozygous or Sema-1a^k13702/Df(2L)N22-5 late third instar larvae, organisation of developing eye photoreceptor cells in the retina occurs normally and project their axons normally through the a normal looking optic stalk. However, severe defects are seen in the paths taken by these axons after leaving the stalk: R1-R6 growth cones fail to pack into a dense termination layer but instead are scattered around the lamina terminal field and some extend laterally to positions outside the terminal field although few leave the lamina altogether. A similar phenotype is seen in Sema-1a^k13702 homozygous somatic clones but not in surrounding heterozygous or wild-type eye phenotype receptor axons. (Cafferty et al., 2006) Expression of two copies of Sema-1a^Scer\UAS.cYa in midline glial cells, under the control of Scer\GAL4^P52, in a Sema-1a^k13702/Sema-1a^k13702 background, leads to a lack of both anterior and posterior commissures as all commissural axons fail to cross the midline. Expression of one copy of Sema-1a^Scer\UAS.cYa in this background leads to the repulsion of fewer commissural axons from the midline, so that only the posterior commissure and not the anterior commissure is missing from most segments. (Ayoob et al., 2004) Decreasing the levels of plexA via a Df(4)C3/+ background suppresses the lack of posterior commissure in embryos that express one copy of Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52. This phenotype is also partially suppressed in a Df(3L)5126/+ background. Sema-1a^k13702/+; Gyc76C^KG03723ex33/+ double mutant embryos show a motor axon guidance phenotype that is similar in severity to Gyc76C^KG03723ex33 homozygotes, while Gyc76C^KG03723ex33 heterozygotes show a much milder phenotype. (Ayoob et al., 2004) In Sema-1a^k13702 homozygous late third instar larvae, axonal projections from developing eye photoreceptor cells are abnormal: the R1-R6 terminal field in the lamina is severely disrupted, with clumps and loop-like structures frequently observed. Despite this, lamina specific targetting of these axons appears largely normal. (Cafferty et al., 2004) 32.7% of hemisegments in Sema-1a^k13702/+ ; Df(3R)swp2^MICAL/+ double heterozygotes show defects in muscle 6/7 innervation and 37.3% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 51.8% of hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24. 32.4% of hemisegments in Sema-1a^k13702/+ ; Df(4)C3/+ double heterozygotes show defects in muscle 6/7 innervation and 39.8% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 68.5% of hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24. (Terman et al., 2002) 47.4% of homozygous hemisegments show defects in muscle 6/7 innervation and 77.3% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 85.7% of homozygous hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24. (Terman et al., 2002) The intersegmental nerve b (ISNb) phenotypes seen in homozygous Sema-1a^k13702 embryos are suppressed by one copy of Fas2^EB112. Synaptic arborisations on ventral lateral muscles (VLMs) 12 and 6-7 appear normal. The ISNb phenotypes seen in homozygous Sema-1a^k13702 embryos are enhanced by Fas2^Scer\UAS.cLa expressed under the control of Scer\GAL4^elav-C155. The ISNb may fail to defasciculate from the intersegmental nerve (ISN) which results in a fusion bypass with the ISN. ISNb is also seen to stall ventrally on VLMs 6-7. The number of hemisegments showing aberrant or absent RP3 innervation of VLMs 6 and 7 is increased. A failure of RP1, RP4 and RP5 to defasciculate around VLMs 13 and 6, a "stall" phenotype, is also increased. The Sema-1a^k13702 segmental nerve a (SNa) defasciculation defects are not suppressed by Fas2^EB112, Df(3L)Flex14 or Con^Fvex238 alone. However, rescue of the Sema-1a^k13702 SNa stall phenotype is seen in Fas2^EB112/+ ; Sema-1a^k13702 ; Con^Fvex238 triple mutant embryos; the SNa dorsal branches bifurcate at lateral muscles (LMs) 22-23 and extend dorsally. Sema-1a^k13702 SNa phenotypes are dramatically enhanced by Fas2^Scer\UAS.cLa expressed under the control of Scer\GAL4^elav-C155. Failure of all SNa lateral branches to defasciculate from the SNa pathway, resulting in the lack of SNa lateral branches, is seen. An increase in the stall phenotype of the dorsal SNa branch is also seen. Sema-1a^k13702 CNS defects are suppressed by one copy of Fas2^EB112 (they are seen in only 10% of hemisegments, compared to 31% in Sema-1a^k13702 single mutants). (Yu et al., 2000) Intersegmental nerve b (ISNb) is most often stalled at ventral lateral muscles 6-13 in homozygous embryos. RP3 and RP5 synaptic arborisations are absent. The dorsal segmental nerve a (SNa) branch is most often stalled on lateral muscles (LMs) 22-23, where it would normally bifurcate, in homozygous embryos. CNS defects are seen in 31% of hemisegments in homozygous embryos. (Yu et al., 2000) 1% of homozygotes survive to adulthood. The intersegmental nerve b branch (ISNb) pathway is abnormal in 87% of hemisegments in homozygous embryos. In 49% of hemisegments, the ISNb is stalled, failing to extend from the external surface of ventral lateral muscles (VLMs) 6 and 7 to the internal surface of VLMs 12 and 13. Most of these stalled ISNb branches terminate between muscles 6 and 13, although some are terminated more ventrally, between muscles 6 and 7. In 7% of hemisegments the ISNb undergoes a fusion bypass with the intersegmental nerve (ISN), bypassing the ventral muscle field and extending along the ISN at least to the dorsal level of the lateral muscles. In 35% of hemisegments, synaptic arborisations between muscles 6 and 7 are abnormal, being substantially thinner and smaller compared to wild-type, and 18% of hemisegments lack a muscle 6/7 synapse. The ISNd branch is defective, either being missing or severely truncated and thinner than normal, in 39% of hemisegments. 92% of hemisegments have defects in the segmental nerve a branch (SNa) pathway. These defects primarily affect the dorsal, not the lateral SNa branch. The dorsal SNa branch is stalled between muscles 22 and 23, at the choice point where it would normally bifurcate, in 69% of hemisegments. In 19% of hemisegments the choice point is navigated correctly, but the motor axon that innervates muscle 24 fails to extend dorsally after reaching muscle 24. The SNc branch is defective in 11% of hemisegments. 20% of hemisegments show transverse nerve defects, which sometimes result in the establishment of ectopic synapses on the ventral lateral muscles. The pCC/MP2 and MP1 connectives appear normal, but the third Fas2 expressing longitudinal connective is abnormal in 31% of hemisegments, being discontinuous, thin and wavy. Individual axons from this connective are often misrouted and contact the neighbouring MP1 connective. The overall organisation of the central nervous system (CNS) appears normal. The development of the RP, VUM and Con expressing longitudinal pathways in the CNS is normal. Muscle development and morphology, including the degree of adhesion between neighbouring muscles, appears normal. Homozygous embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^elav-C155 show complete rescue of the ISNb defects, a partial but significant rescue of SNa defects and an almost complete rescue of the CNS phenotype. There is also almost complete rescue of adult lethality. Homozygous embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^sca-537.4 show rescue of the ISNb defects, a partial but significant rescue of SNa defects and an almost complete rescue of the CNS phenotype. There is no rescue of adult lethality. Homozygous embryos expressing Sema-1a^EC.Scer\UAS under the control of Scer\GAL4^elav-C155 or show partial, but significant rescue of neuronal defects. There is also partial, but significant rescue of adult lethality. Homozygous embryos expressing Sema-1a^EC.Scer\UAS under the control of Scer\GAL4^sca-537.4 or show partial, but significant rescue of neuronal defects. There is no rescue of adult lethality. The ISNb and SNa phenotypes seen in homozygous Sema-1a^k13702 embryos are enhanced if the embryos also carry a single copy of Sema-1a^Scer\UAS.cYa expressed under the control of a single copy of Scer\GAL4^how-24B. In addition, SNa fusion bypass events are seen in these embryos, in which the SNa fails to enter the ventral muscle field and extends dorsally along the ISN. The first and second arborisations of the ISN are missing in some hemisegments. (Yu et al., 1998)
Expression Data
Reporter Expression

Additional Information
Statement Reference

Marker for
Reflects expression of
Reporter construct used in assay
External Images
FlyView (LinkOut)
Data on Genetic Line
Line ID	l(2)k13702 (Gene Disruption Project members, 2001-)
Origin as a multiple insertion line
Progenitor(s) within the Genome

Related Aberration or Balancer
Aberration
Balancer
Stocks ( 2 )
Bloomington	11097 y¹ w^67c23; P{lacW}Sema-1a^k13702/CyO
Kyoto	111328 y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{GMR-lacZ.C(38.1)}TPN1; P{lacW}Sema-1a^k13702 P{neoFRT}40A/CyO y⁺
Linkouts
Comments
	Location 2L:8544219-8544220 confirmed by FlyBase alignment of dbGSS accession AQ026063 to D. melanogaster arm Release_4 and heterochromatin Release_3.2b. Insertion orientation confirmed. (FlyBase, 2005)
Synonyms & Secondary IDs
Reported As
Symbol Synonym	P{lacW}l(2)k13702^k13702 (BDGP Project Members, 1994-1999, FlyBase, 1992-) P{lacW}Sema-1a^k13702 (FlyBase, 2005, FlyBase, 1992-, ) P{lacW}Sema1a^k13702 (FlyBase, 1992-) P{lacW}sema-I^k13702 (Yu et al., 1998, FlyBase, 1992-) Sema1a^P1 (Miller et al., 2011) sema1a^P1 (Yu et al., 2010)
Secondary FlyBase IDs
	FBti0006430
References ( 20 )
Research paper	Jeong et al., 2012, Neuron 76(4): 721--734 The Control of Semaphorin-1a-Mediated Reverse Signaling by Opposing Pebble and RhoGAPp190 Functions in Drosophila. [FBrf0219982] Miller et al., 2011, J. Neurosci. 31(14): 5335--5347 Drosophila mmp2 regulates the matrix molecule faulty attraction (frac) to promote motor axon targeting in Drosophila. [FBrf0213409] Yu et al., 2010, J. Neurosci. 30(36): 12151--12156 Plexin a-semaphorin-1a reverse signaling regulates photoreceptor axon guidance in Drosophila. [FBrf0211784] Komiyama et al., 2007, Cell 128(2): 399--410 Graded expression of Semaphorin-1a cell-autonomously directs dendritic targeting of olfactory projection neurons. [FBrf0199080] Sweeney et al., 2007, Neuron 53(2): 185--200 Temporal target restriction of olfactory receptor neurons by Semaphorin-1a/PlexinA-mediated axon-axon interactions. [FBrf0193588] Cafferty et al., 2006, J. Neurosci. 26(15): 3999--4003 Semaphorin-1a functions as a guidance receptor in the Drosophila visual system. [FBrf0191042] Ayoob et al., 2004, J. Neurosci. 24(30): 6639--6649 The Drosophila receptor guanylyl cyclase Gyc76C is required for semaphorin-1a-plexin A-mediated axonal repulsion. [FBrf0179119] Bellen et al., 2004, Genetics 167(2): 761--781 The BDGP gene disruption project: single transposon insertions associated with 40% of Drosophila genes. [FBrf0179132] Cafferty et al., 2004, Development 131(21): 5287--5295 The receptor tyrosine kinase Off-track is required for layer-specific neuronal connectivity in Drosophila. [FBrf0180165] Terman et al., 2002, Cell 109(7): 887--900 MICALs, a family of conserved flavoprotein oxidoreductases, function in plexin-mediated axonal repulsion. [FBrf0151231] Yu et al., 2000, Genetics 156(2): 723--731 Semaphorin-1a acts in concert with the cell adhesion molecules fasciclin II and connectin to regulate axon fasciculation in Drosophila. [FBrf0130183] Spradling et al., 1999, Genetics 153(1): 135--177 The Berkeley Drosophila genome project gene disruption project. Single P-element insertions mutating 25% of vital Drosophila genes. [FBrf0111489] Yu et al., 1998, Neuron 20(2): 207--220 The transmembrane Semaphorin Sema I is required in Drosophila for embryonic motor and CNS axon guidance. [FBrf0100649] Bier et al., 1989, Genes Dev. 3: 1273--1287 Searching for pattern and mutation in the Drosophila genome with a P-lacZ vector. [FBrf0049800]
Supplementary material	Wu et al., 2011, Neuron 70(2): Supplemental Information. [FBrf0217575]
Personal communication to FlyBase	Gene Disruption Project members, 2001-, (Computer file) (Computer file) [FBrf0132177] BDGP Project Members, 1994-1999, BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file) BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file) [FBrf0067338]
FlyBase analysis	FlyBase Curators, 2013, Members of BDGP/GDP insertion collections: P{hsneo}, P{PZ}, P{lacW}. Members of BDGP/GDP insertion collections: P{hsneo}, P{PZ}, P{lacW}. [FBrf0220600] FlyBase, 2005, Assessment of transgenic construct insertion sites. Assessment of transgenic construct insertion sites. [FBrf0184339] FlyBase, 1992-, FlyBase curation. FlyBase curation. [FBrf0105495]

Dmel\P{lacW}Sema-1ak13702 Insertion

Dmel\P{lacW}Sema-1a^k13702 Insertion