Open Close
General Information
Symbol
Dmel\Sema1ak13702
Species
D. melanogaster
Name
FlyBase ID
FBal0064125
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
sema-1aP1, Sema1aP1, sema-1ak13702, semaP1, SemaIP1, Sema-1aPI
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

P{lacW} insertion in the 5' untranslated region.

Insertion components
P{lacW}Sema1ak13702
Product class / Tool use(s)
Encoded product / tool
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

abdominal ventral longitudinal muscle & synapse

axon & alpha'-lobe | somatic clone

axon & antennal glomerulus DA1 | somatic clone

axon & antennal glomerulus DC3 | somatic clone

axon & antennal glomerulus DL1 | somatic clone | cell autonomous

axon & antennal glomerulus VM2 | somatic clone

axon & beta'-lobe | somatic clone

axon & eye photoreceptor cell

axon & eye photoreceptor cell (with Df(2L)N22-5)

axon & eye photoreceptor cell | somatic clone | cell autonomous

axon & lamina

axon & lamina (with Df(2L)N22-5)

axon & lamina | somatic clone | somatic clone | cell autonomous

dendrite & antennal glomerulus DA1 | somatic clone

dendrite & antennal glomerulus DC3 | somatic clone

dendrite & antennal glomerulus DL1 | somatic clone

eye photoreceptor cell & lamina

eye photoreceptor cell & lamina (with Df(2L)N22-5)

eye photoreceptor cell & lamina | somatic clone | cell autonomous

photoreceptor cell R1 & axon

photoreceptor cell R2 & axon

photoreceptor cell R3 & axon

photoreceptor cell R4 & axon

photoreceptor cell R5 & axon

photoreceptor cell R6 & axon

RP3 neuron & synapse

RP5 neuron & synapse

Detailed Description
Statement
Reference

Sema1ak13702 heterozygous embryos show modest increase in the frequency of guidance defects in intersegmental nerve b motor axons compared to controls, these defects are observed in nearly all Sema1ak13702 homozygotes, which also display axon pathfinding defects in the central nervous system.

Sema-1a is not required to prevent dendrite crossing in the class IV dendritic arborizing neurons as Sema-1ak13702 mutant larvae do not display any increase in dendrite self-crossing compared to wild-type controls.

Adult Sema1ak03509 homozygous mutants as well as Sema1ak03509/Sema1ak13702 transheterozygotes display axon mis-projection phenotypes in the leg muscles - lack of innervation of the muscles of the femur and excessive innervation of the muscles of the tibia.

Most posterior commissural axons do not cross the midline in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background.

Homozygous embryos show ISNb motor axon guidance defects (95.5% of hemisegments) and SNa motor axon guidance defects (95.2% of hemisegments). Many ISNb axon bundles stall at the second choice point (between muscles 6 and 7), failing to send remaining ISNb motor axons dorsally, and some fail to defasciculate at the third choice point (between muscles 12 and 13). Axons within the SNa pathway fail to defasciculate between muscles 22 and 23.

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.

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.

R1-R6 growth cones scatter around the lamina termination region in homozygous Sema-1ak13702 third instar larvae, leading to the appearance of a discontinuous termination layer in the lamina.

Sema-1ak13702 homozygous mutant embryos do not exhibit any sensory axon defects.

Sema-1ak13702 clones generated in a heterozygous background in either projection neurons or mushroom body α'/β' neurons cause axon mistargeting.

Sema-1ak13702 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-1ak13702 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.

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.

In Sema-1ak13702 homozygous or Sema-1ak13702/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-1ak13702 homozygous somatic clones but not in surrounding heterozygous or wild-type eye phenotype receptor axons.

Expression of two copies of Sema-1aScer\UAS.cYa in midline glial cells, under the control of Scer\GAL4P52, in a Sema-1ak13702/Sema-1ak13702 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-1aScer\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.

In Sema-1ak13702 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.

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.

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.

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-1aScer\UAS.cYa under the control of

Scer\GAL4elav-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-1aScer\UAS.cYa under the control of

Scer\GAL4sca-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-1aEC.Scer\UAS under the control of

Scer\GAL4elav-C155 or show partial, but significant rescue of neuronal

defects. There is also partial, but significant rescue of adult lethality.

Homozygous embryos expressing Sema-1aEC.Scer\UAS under the control of

Scer\GAL4sca-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-1ak13702 embryos

are enhanced if the embryos also carry a single copy of Sema-1aScer\UAS.cYa

expressed under the control of a single copy of Scer\GAL4how-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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
NOT Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

Sema1ak13702 has axon | embryonic stage phenotype, enhanceable by vari[+]/vari327

Sema1ak13702 has axon | embryonic stage phenotype, enhanceable by vari[+]/vari48EP

Sema1ak13702 has axon | embryonic stage phenotype, enhanceable by cher[+]/cherQ1042X

Sema1ak13702 has axon | embryonic stage phenotype, enhanceable by cherEPSΔ5/cher[+]

Sema1ak13702 has RP3 neuron & synapse phenotype, enhanceable by Scer\GAL4elav-C155/Fas2UAS.cLa

NOT Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

The moderate guidance defects observed in intersegmental nerve b motor axons of Sema1ak13702 heterozygous embryos are exacerbated by combination with a single copy of any of the following: vari327, vari48EP, cherQ1042X (which on its own also produces weak defasciculation defects) or cherEPSΔ5. The very strong defects observed in Sema1ak13702 homozygotes cannot be worsened further by either vari327 or cherEPSΔ5 homozygosity.

kermitex31/+, Sema-1ak13702/+ double mutants exhibit an increased number of defects in both ISNb and SNa motor neuron axon pathways as compared to kermitex31/+ mutant embryos.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is significantly suppressed if the embryos are also heterozygous for either Df(4)C3, trolnull or trol8.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is significantly enhanced if the embryos also carry one copy of plexA+tCa.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is significantly enhanced if the embryos are also heterozygous for either dally80, sfl03844 or sgl08310.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is not affected if the embryos are also doubly heterozygous for Ext2326 and ttv00681b.

Co-expression of trolEP1160 significantly enhances the commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background.

Co-expression of either trolScer\UAS.RG or trolScer\UAS.RD strongly enhances the commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is not affected if the embryos are also heterozygous for either dlp1, Sdc10608, botv510, Ext2326 or ttv00681b.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is significantly enhanced if the embryos are also heterozygous for ifunspecified or mysunspecified.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is not affected if the embryos are also heterozygous for mewunspecified.

trol8/+ ; Sema-1ak13702/+ double heterozygous embryos show ISNb motor axon guidance defects (50.5% of hemisegments) and SNa motor axon guidance defects (44.8% of hemisegments).

trolnull/+ ; Sema-1ak13702/+ double heterozygous embryos show ISNb motor axon guidance defects (51.0% of hemisegments) and SNa motor axon guidance defects (41.8% of hemisegments).

Sema-1ak13702/+ ; Sdc10608/+ double heterozygous embryo do not show significant ISNb or SNa motor axon guidance defects compared to controls.

The defects seen in the Fas2-positive longitudinal fascicles of embryos expressing FakScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4sca-537.4 are partially suppressed if the embryos are also heterozygous for Sema-1ak13702.

Sema-1ak13702/+ suppresses the premature ISNb branching seen in embryos expressing RhoGAPp190dsRNA.N.Scer\UAS under the control of Scer\GAL4elav.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-1ak13702 and pbl2 are greater than those observed for either single heterozygote.

A heterozygous Sema-1ak13702 background dominantly suppresses the ISNb pathfinding phenotypes from 64% in fracΔ1 homozygotes to 18% in double mutants.

One copy of Sema-1ak13702 moderately enhances the detached posterior crossvein phenotype seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU.

One copy of Sema-1ak13702 moderately enhances the detached posterior crossvein phenotype seen when DysdsRNA.C.Scer\UAS is expressed under the control of Scer\GAL4tub.PU but produces extra wing vein material.

One copy of Sema-1ak13702 suppresses the posterior crossvein phenotype seen when DgdsRNA.Scer\UAS is expressed under the control of Scer\GAL4tub.PU.

Sema-1ak13702 Sema-2a03021 double mutants exhibit sensory axon mis-projections in the same frequency as Sema-2a03021 homozygotes.

The frequency of axon targeting defects of maxillary palp olfactory receptor neurons in animals expressing plexAVDRC.cUa under the control of Scer\GAL4peb-GAL4 is enhanced if they are also heterozygous for Sema-1ak13702. The frequency of both abnormal terminations outside the antennal lobe and of ectopic terminations within the antennal lobe is increased.

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-1aScer\UAS.cYa under the control of Scer\GAL4P52. This phenotype is also partially suppressed in a Df(3L)5126/+ background.

Sema-1ak13702/+; Gyc76CKG03723ex33/+ double mutant embryos show a motor axon guidance phenotype that is similar in severity to Gyc76CKG03723ex33 homozygotes, while Gyc76CKG03723ex33 heterozygotes show a much milder phenotype.

32.7% of hemisegments in Sema-1ak13702/+ ; Df(3R)swp2MICAL/+ 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-1ak13702/+ ; 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.

The intersegmental nerve b (ISNb) phenotypes seen in homozygous Sema-1ak13702 embryos are suppressed by one copy of Fas2EB112. Synaptic arborisations on ventral lateral muscles (VLMs) 12 and 6-7 appear normal. The ISNb phenotypes seen in homozygous Sema-1ak13702 embryos are enhanced by Fas2Scer\UAS.cLa expressed under the control of Scer\GAL4elav-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-1ak13702 segmental nerve a (SNa) defasciculation defects are not suppressed by Fas2EB112, Df(3L)Flex14 or ConFvex238 alone. However, rescue of the Sema-1ak13702 SNa stall phenotype is seen in Fas2EB112/+ ; Sema-1ak13702 ; ConFvex238 triple mutant embryos; the SNa dorsal branches bifurcate at lateral muscles (LMs) 22-23 and extend dorsally. Sema-1ak13702 SNa phenotypes are dramatically enhanced by Fas2Scer\UAS.cLa expressed under the control of Scer\GAL4elav-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-1ak13702 CNS defects are suppressed by one copy of Fas2EB112 (they are seen in only 10% of hemisegments, compared to 31% in Sema-1ak13702 single mutants).

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

The axon guidance defects characteristic for Sema1ak13702 homozygous embryos can be partially rescued (to a varying extent) by expression of any of the following: Sema1aScer\UAS.cJa, Sema1aScer\UAS.T:Hsap\MYC, Sema1aΔ1-40.Scer\UAS or Sema1aΔ5.Scer\UAS under the control of Scer\GAL4sca-537.4. Whereas the defects in the central nervous system are efficiently suppressed by all these transgenes, the frequency of defasciculation irregularities in the intersegmental nerve b is only partially decreased (and not at all with the Sema1aΔ1-40.Scer\UAS) and remains elevated compared to wild-type controls.

Expression of either Sema-1aScer\UAS.cJa, Sema-1a36G.52A.Scer\UAS or Sema-1aΔ31-60.Scer\UAS under the control of Scer\GAL4sca-537.4 rescues the central nervous system guidance defects and partially rescues the ISNb guidance defects seen in Sema-1ak13702 embryos.

Expression of either Sema-1amICD.Scer\UAS or Sema-1amICD.Scer\UAS.T:Hsap\Fc-IgG under the control of Scer\GAL4sca-537.4 significantly but modestly rescues the central nervous system guidance defects seen in Sema-1ak13702 embryos.

Expression of Sema-1amEC.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4sca-537.4 partially rescues the central nervous system guidance defects seen in Sema-1ak13702 embryos.

Expression of Sema-1amEC.Scer\UAS.T:Hsap\Fc-IgG,T:Hsap\MYC under the control of Scer\GAL4sca-537.4 strongly rescues the central nervous system guidance defects seen in Sema-1ak13702 embryos.

Co-expression of Sema-1amEC.Scer\UAS.T:Hsap\Fc-IgG,T:Hsap\MYC and Sema-1amICD.Scer\UAS under the control of Scer\GAL4sca-537.4 does not result in additional rescue of the ISNb defects seen in Sema-1ak13702 embryos compared to either line expressed alone.

Co-expression of Sema-1amEC.Scer\UAS.T:Hsap\Fc-IgG,T:Hsap\MYC and Sema-1amICD.Scer\UAS.T:Hsap\Fc-IgG under the control of Scer\GAL4sca-537.4 does not result in additional rescue of the ISNb defects seen in Sema-1ak13702 embryos compared to either line expressed alone.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Complements: lmg03424. Complements: rawk01021. Complements: l(2)k04003k04003. Complements: l(2)rH280rH280.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (18)
References (31)