Allele Dmel\Sema-1a^k13702

General Information
Symbol	Dmel\Sema-1a^k13702	Species	D. melanogaster
Name		FlyBase ID	FBal0064125
Feature type	allele	Associated gene	Dmel\Sema-1a
Also Known As	sema-1a^P1, Sema1a^P1, sema^P1

Map ( GBrowse )	Untitled Document
Allele class	loss of function allele
Mutagen	P-element activity
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.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
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.
Nature of the Allele
Allele class	loss of function allele (Yu et al., 1998, Komiyama et al., 2007)
Mutagen	P-element activity (BDGP Project Members, 1994-1999)
Mutations Mapped to the Genome

Type Location Additional Notes References transposable element insertion site 2L:8,544,219..8,544,219 (BDGP Project Members, 1994-1999, Yu et al., 1998, Spradling et al., 1999, Miller et al., 2011, Yu et al., 2010)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference P{lacW} insertion in the 5' untranslated region. (Yu et al., 1998)
Caused by insertion	P{lacW}Sema-1a^k13702 (BDGP Project Members, 1994-1999, Yu et al., 1998, Spradling et al., 1999, Miller et al., 2011, Yu et al., 2010)
Cytology
Phenotypic Data
Phenotypic Class
	lethal \| recessive (Spradling et al., 1999) neuroanatomy defective (Yu et al., 2000) neuroanatomy defective, with Scer\GAL4^P52, Sema-1a^Scer\UAS.cYa (Ayoob et al., 2004) neuroanatomy defective \| adult stage \| cell non-autonomous \| somatic clone (Sweeney et al., 2007) neuroanatomy defective \| embryonic stage (Wu et al., 2011, Jeong et al., 2012) neuroanatomy defective \| recessive (Yu et al., 1998) neuroanatomy defective \| somatic clone (Komiyama et al., 2007) partially lethal - majority die \| recessive (Yu et al., 1998)
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, with Scer\GAL4^P52, Sema-1a^Scer\UAS.cYa (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 (with Df(2L)N22-5) (Cafferty et al., 2006) axon & eye photoreceptor cell \| somatic clone \| cell autonomous (Cafferty et al., 2006) axon & lamina (Cafferty et al., 2006) axon & lamina (with Df(2L)N22-5) (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 (with Df(2L)N22-5) (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, with Scer\GAL4^P52, Sema-1a^Scer\UAS.cYa (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) synapse (Yu et al., 1998) synapse \| ectopic (Yu et al., 1998) transverse nerve \| embryonic stage (Yu et al., 1998)
Detailed Description
	Statement Reference 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) 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) 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) 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) 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) 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)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference Scer\GAL4^P52, Sema-1a^Scer\UAS.cYa, Sema-1a^k13702 has neuroanatomy defective phenotype, suppressible \| partially by Df(3L)5126/+ (Ayoob et al., 2004) Scer\GAL4^P52, Sema-1a^Scer\UAS.cYa, Sema-1a^k13702 has neuroanatomy defective phenotype, suppressible \| partially by Df(4)C3/+ (Ayoob et al., 2004)
Enhancer of
Statement Reference Sema-1a^k13702/Sema-1a[+] is an enhancer of neuroanatomy defective \| adult stage phenotype of Scer\GAL4^peb-GAL4, plexA^VDRC.cUa (Sweeney et al., 2007) Sema-1a^k13702/Sema-1a[+] is an enhancer of neuroanatomy defective \| dominant phenotype of Gyc76C^KG03723ex173 (Ayoob et al., 2004)
Suppressor of
Statement Reference Sema-1a^k13702/Sema-1a[+] is a suppressor of neuroanatomy defective \| embryonic stage phenotype of frac^Δ1 (Miller et al., 2011) Sema-1a^k13702/Sema-1a[+] is a suppressor of neuroanatomy defective \| embryonic stage phenotype of RhoGAPp190^{dsRNA.N.Scer\UAS}, Scer\GAL4^elav.PLu (Jeong et al., 2012)
Other
Statement Reference Df(3R)swp2^MICAL/+, Sema-1a^k13702 has neuroanatomy defective phenotype (Terman et al., 2002) Df(4)C3/+, Sema-1a^k13702 has neuroanatomy defective phenotype (Terman et al., 2002) Sema-1a^k13702, pbl[+]/pbl² has neuroanatomy defective \| dominant \| embryonic stage phenotype (Jeong et al., 2012)
Phenotype Manifest In
Enhanced by
Statement Reference Sema-1a^k13702 has abdominal segmental nerve phenotype, enhanceable by Scer\GAL4^elav-C155/Fas2^Scer\UAS.cLa (Yu et al., 2000) Sema-1a^k13702 has intersegmental nerve phenotype, enhanceable by Scer\GAL4^elav-C155/Fas2^Scer\UAS.cLa (Yu et al., 2000) Sema-1a^k13702 has RP1 motor neuron phenotype, enhanceable by Scer\GAL4^elav-C155/Fas2^Scer\UAS.cLa (Yu et al., 2000) Sema-1a^k13702 has RP3 neuron & synapse phenotype, enhanceable by Scer\GAL4^elav-C155/Fas2^Scer\UAS.cLa (Yu et al., 2000) Sema-1a^k13702 has RP4 motor neuron phenotype, enhanceable by Scer\GAL4^elav-C155/Fas2^Scer\UAS.cLa (Yu et al., 2000) Sema-1a^k13702 has RP5 motor neuron phenotype, enhanceable by Scer\GAL4^elav-C155/Fas2^Scer\UAS.cLa (Yu et al., 2000)
Suppressed by
Statement Reference Fas2^EB112, Sema-1a^k13702 has abdominal segmental nerve phenotype, suppressible by Con^Fvex238 (Yu et al., 2000) Scer\GAL4^P52, Sema-1a^Scer\UAS.cYa, Sema-1a^k13702 has posterior commissure phenotype, suppressible \| partially by Df(3L)5126/+ (Ayoob et al., 2004) Scer\GAL4^P52, Sema-1a^Scer\UAS.cYa, Sema-1a^k13702 has posterior commissure phenotype, suppressible \| partially by Df(4)C3/+ (Ayoob et al., 2004) Sema-1a^k13702 has intersegmental nerve phenotype, suppressible by Fas2^EB112/Fas2[+] (Yu et al., 2000) Sema-1a^k13702 has presumptive embryonic/larval central nervous system phenotype, suppressible by Fas2^EB112 (Yu et al., 2000) Sema-1a^k13702 has RP3 neuron & synapse phenotype, suppressible by Fas2^EB112/Fas2[+] (Yu et al., 2000)
NOT suppressed by
Statement Reference Sema-1a^k13702 has abdominal segmental nerve phenotype, non-suppressible by Con^Fvex238 (Yu et al., 2000) Sema-1a^k13702 has abdominal segmental nerve phenotype, non-suppressible by Df(3L)Flex14 (Yu et al., 2000) Sema-1a^k13702 has abdominal segmental nerve phenotype, non-suppressible by Fas2^EB112 (Yu et al., 2000)
Enhancer of
Statement Reference Sema-1a^k13702/Sema-1a[+] is an enhancer of abdominal segmental nerve phenotype of Gyc76C^KG03723ex173 (Ayoob et al., 2004) Sema-1a^k13702/Sema-1a[+] is an enhancer of intersegmental nerve phenotype of Gyc76C^KG03723ex173 (Ayoob et al., 2004) Sema-1a^k13702/Sema-1a[+] is an enhancer of maxillary palp olfactory receptor neuron phenotype of Scer\GAL4^peb-GAL4, plexA^VDRC.cUa (Sweeney et al., 2007)
Suppressor of
Statement Reference Sema-1a^k13702/Df(2L)N22-5 is a suppressor of eye photoreceptor cell \| third instar larval stage phenotype of Scer\GAL4^GMR.PF, plexA^Scer\UAS.cYa (Yu et al., 2010) Sema-1a^k13702/Df(2L)N22-5 is a suppressor of lamina \| third instar larval stage phenotype of Scer\GAL4^GMR.PF, plexA^Scer\UAS.cYa (Yu et al., 2010) Sema-1a^k13702/Sema-1a[+] is a suppressor of intersegmental nerve branch ISNb of A1-7 \| embryonic stage phenotype of frac^Δ1 (Miller et al., 2011) Sema-1a^k13702/Sema-1a[+] is a suppressor of intersegmental nerve branch ISNb of A1-7 phenotype of RhoGAPp190^{dsRNA.N.Scer\UAS}, Scer\GAL4^elav.PLu (Jeong et al., 2012)
Other
Statement Reference Df(3R)swp2^MICAL/+, Sema-1a^k13702 has intersegmental nerve phenotype (Terman et al., 2002) Df(3R)swp2^MICAL/+, Sema-1a^k13702 has segmental nerve phenotype (Terman et al., 2002) Df(4)C3/+, Sema-1a^k13702 has intersegmental nerve phenotype (Terman et al., 2002) Df(4)C3/+, Sema-1a^k13702 has segmental nerve phenotype (Terman et al., 2002) Sema-1a^k13702, pbl[+]/pbl² has intersegmental nerve branch ISNb of A1-7 phenotype (Jeong et al., 2012)
Additional Comments
Genetic Interactions
Statement Reference 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 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) 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) 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) 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)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Fails to complement	Sema-1a^k03509 (Yu et al., 1998, BDGP Project Members, 1994-1999)
Rescued by	Sema-1a^k13702 is rescued by Sema-1a^Scer\UAS.cYa/Scer\GAL4^GH146/Scer\GAL4^GH146 (Komiyama et al., 2007)
Partially rescued by	Sema-1a^k13702/Df(2L)N22-5 is partially rescued by Scer\GAL4^elav-C155/Sema-1a^Scer\UAS.cYa (Cafferty et al., 2006) Sema-1a^k13702 is partially rescued by Scer\GAL4^elav-C155/Sema-1a^Scer\UAS.cYa (Yu et al., 1998) Sema-1a^k13702 is partially rescued by Scer\GAL4^sca-537.4/Sema-1a^{36G.52A.Scer\UAS} (Jeong et al., 2012) Sema-1a^k13702 is partially rescued by Scer\GAL4^sca-537.4/Sema-1a^{mEC.Scer\UAS.T:Hsap\MYC} (Jeong et al., 2012) Sema-1a^k13702 is partially rescued by Sema-1a^EC.Scer\UAS/Scer\GAL4^elav-C155 (Yu et al., 1998) Sema-1a^k13702 is partially rescued by Sema-1a^{mEC.Scer\UAS.T:Hsap\Fc-IgG,T:Hsap\MYC}/Scer\GAL4^sca-537.4 (Jeong et al., 2012) Sema-1a^k13702 is partially rescued by Sema-1a^{mICD.Scer\UAS.T:Hsap\Fc-IgG}/Scer\GAL4^sca-537.4 (Jeong et al., 2012) Sema-1a^k13702 is partially rescued by Sema-1a^{mICD.Scer\UAS}/Scer\GAL4^sca-537.4 (Jeong et al., 2012) Sema-1a^k13702 is partially rescued by Sema-1a^Scer\UAS.cJa/Scer\GAL4^sca-537.4 (Jeong et al., 2012) Sema-1a^k13702 is partially rescued by Sema-1a^Scer\UAS.cYa/Scer\GAL4^sca-537.4 (Yu et al., 1998) Sema-1a^k13702 is partially rescued by Sema-1a^{Δ31-60.Scer\UAS}/Scer\GAL4^sca-537.4 (Jeong et al., 2012)
Not rescued by	Sema-1a^k13702/Df(2L)N22-5 is not rescued by Sema-1a^{Δcyto.Scer\UAS.T:Hsap\MYC}/Scer\GAL4^elav-C155 (Cafferty et al., 2006) Sema-1a^k13702 is not rescued by Sema-1a^{Δcyto.Scer\UAS.T:Hsap\MYC}/Scer\GAL4^GH146/Scer\GAL4^GH146 (Komiyama et al., 2007)
Comments	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)
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⁺
Notes on Origin
Discoverer	I. Kiss.

Comments
	Complements: lmg⁰³⁴²⁴. Complements: raw^k01021. Complements: l(2)k04003^k04003. Complements: l(2)rH280^rH280. (BDGP Project Members, 1994-1999)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 12 )
Reported As
Symbol Synonym	13702 (Yu et al., 1998) l(2)k13702 (Spradling et al., 1999) Sema1a^k13702 (BDGP Project Members, 1994-1999, ) Sema-1a^k13702 Sema1a^P1 (Terman et al., 2002, Yu et al., 2000) sema-1a^P1 (Komiyama et al., 2007, Sweeney et al., 2007) sema1a^P1 (Ayoob et al., 2004) Sema-1a^P1 (Wu et al., 2011, Wu et al., 2011) Sema-1a^PI (Jeong et al., 2012) sema^P1 (Cafferty et al., 2004, Cafferty et al., 2006) sema-I^k13702 SemaI^P1 (Yu et al., 1998)
Name Synonym
Secondary FlyBase IDs

References ( 16 )
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] Wu et al., 2011, Neuron 70(2): 281--298 A combinatorial semaphorin code instructs the initial steps of sensory circuit assembly in the Drosophila CNS. [FBrf0213571] 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] 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]
Supplementary material	Wu et al., 2011, Neuron 70(2): Supplemental Information. [FBrf0217575]
Personal communication to FlyBase	Beaton, 1999.12.12, Alleles of the lines in the P-element paper. Alleles of the lines in the P-element paper. [FBrf0125032] 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]

Allele Dmel\Sema-1ak13702

Allele Dmel\Sema-1a^k13702