FlyBase Allele Report: Dmel\Sema1a[UAS.cYa]

General Information

Symbol

Dmel\Sema1a^UAS.cYa

Species

D. melanogaster

Name

Saccharomyces cerevisiae UAS construct a of Yu

FlyBase ID

FBal0086345

Feature type

allele

Associated gene

Dmel\Sema1a

Associated Insertion(s)

Carried in Construct

P{UAS-sema-I.Y}

Also Known As

UAS-sema-1a, UAS-sema1a, UAS:Sema-1a

Key Links

Transgenic product class

wild_type

(Yu et al., 1998)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

wild_type

(Yu et al., 1998)

Mutagen

in vitro construct

(Yu et al., 1998)

Progenitor genotype

Carried in construct

P{UAS-sema-I.Y}

Cytology

Description

The entire Sema1a open reading frame is expressed under the control of UASt regulatory sequences.

(Yu et al., 1998)

Allele components

Component

Use(s)

Regulatory region(s)

UASt

binary expression system - regulatory region

Encoded product / tool

Sema1a

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

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 ( 1 )

Disease

Interaction

References

DOES NOT ameliorate Charcot-Marie-Tooth disease type 2D

modeled by GlyRS^P234KY-2.UAS

(Grice et al., 2018)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

axon & eye photoreceptor cell, with Scer\GAL4^GMR.PF

(Cafferty et al., 2006)

axon & lamina, with Scer\GAL4^GMR.PF

(Cafferty et al., 2006)

axon & medulla, with Scer\GAL4^GMR.PF

(Cafferty et al., 2006)

axon | adult stage, with Scer\GAL4^VGlut1-OK371

(Syed et al., 2016)

axon | embryonic stage, with Scer\GAL4^Mef2.PR

(Chak and Kolodkin, 2014)

dendrite & antennal glomerulus | somatic clone, with Scer\GAL4^GH146

(Komiyama et al., 2007)

eye photoreceptor cell & lamina, with Scer\GAL4^GMR.PF

(Cafferty et al., 2006)

eye photoreceptor cell & medulla, with Scer\GAL4^GMR.PF

(Cafferty et al., 2006)

eye photoreceptor cell | third instar larval stage, with Scer\GAL4^GMR.PF

(Yu et al., 2010)

giant fiber neuron | heat sensitive, with Scer\GAL4^c17

(Murphey et al., 2003)

lamina | third instar larval stage, with Scer\GAL4^GMR.PF

(Yu et al., 2010)

larval abdominal intersegmental nerve, with Scer\GAL4^how-24B

(Terman and Kolodkin, 2004)

larval abdominal segmental nerve, with Scer\GAL4^how-24B

(Terman and Kolodkin, 2004)

larval anterior commissure, with Scer\GAL4^P52, Sema1a^k13702

(Ayoob et al., 2004)

larval intersegmental nerve, with Scer\GAL4^F63

(Winberg et al., 1998)

larval intersegmental nerve, with Scer\GAL4^l(3)H94-H94

(Winberg et al., 1998)

larval intersegmental nerve | embryonic stage, with Scer\GAL4^how-24B

(Yu et al., 1998)

larval intersegmental nerve branch ISNb of A1-7 | embryonic stage, with Scer\GAL4^Mef2.PR

(Chak and Kolodkin, 2014)

larval posterior commissure, with Scer\GAL4^P52, Sema1a^k13702

(Ayoob et al., 2004)

larval posterior commissure | embryonic stage, with Scer\GAL4^P52, Sema1a^k13702

(Cho et al., 2012)

larval segmental nerve | embryonic stage, with Scer\GAL4^how-24B

(Yu et al., 1998)

motor neuron, with Scer\GAL4^l(3)H94-H94

(Winberg et al., 2001)

motor neuron | adult stage, with Scer\GAL4^VGlut1-OK371

(Syed et al., 2016)

muscle cell of leg muscle of leg, with Scer\GAL4^VGlut1-OK371

(Syed et al., 2016)

nerve terminal & lamina plexus, with Scer\GAL4^GMR.PF

(Cafferty et al., 2006)

Detailed Description

Statement

Reference

Expression of Sema1a^Scer\UAS.cYa under the control of Scer\GAL4^VGlut-OK371 results in defects in axonal branching in the motoneurons innervating leg muscles in proximal femur (excessive defasciculation, ectopic branches exiting the main nerve and corresponding reduction in thickness of the main nerve trunk) and distal tibia (reduced defasciculation).

(Syed et al., 2016)

Expression of Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^Mef2.PR results in a significant increase in ISNb defects in the embryonic muscles, including axon pathfinding defects, bypasses and axon-positioning defects. Embryos with Sema-1a^Scer\UAS.cYa without a GAL4 driver do not exhibit an increase in ISNb defects compared to wild type.

(Chak and Kolodkin, 2014)

Expression of Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^GH146 does not suppress the dendrite targeting defects seen in homozygous meigo¹ projection neuron clones.

(Sekine et al., 2013)

Most posterior commissural axons do not cross the midline in embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 null background.

(Cho et al., 2012)

Expression of one copy of Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^how-24B results in a relatively normal pattern of innervation of the muscles by the ISNb and SNa nerves.

(Yang and Terman, 2012)

Expression of Sema-1a^Scer\UAS.cYa in R-cell axons under the control of Scer\GAL4^GMR.PF induces the formation of thicker R-cell axonal bundles between lamina and medulla. In medulla, R-cell axons form large clumps.

(Yu et al., 2010)

While expression of one copy of Sema-1a^Scer\UAS.cYa, under the control of Scer\GAL4^GH146, in projection neuron clones do not cause a significant effect on the innervation of glomeruli. However, two copies of Sema-1a^Scer\UAS.cYa, under the control of Scer\GAL4^GH146, results in a significant dorsolateral shift of the dendritic field. Rearing flies with Scer\GAL80^ts.αTub84B at a permissive temperature for this transgene, suppresses the overexpression phenotype of two copies of Sema-1a^Scer\UAS.cYa.

(Komiyama et al., 2007)

In late third instar Sema-1a^Scer\UAS.cYa; Scer\GAL4^GMR.PF larvae, the axons of eye photoreceptor cells are hyperfasciculated - forming thick bundles in both the lamina and medulla and large clumps of terminals in the lamina plexus. This phenotype is more severe if multiple copies of Sema-1a^Scer\UAS.cYa are present.

(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)

When expression is driven by Scer\GAL4^how-24B there are low levels of axon guidance errors in SNa, with a slightly greater effect on ISNb (around 25% hemisegments affected).

(Terman and Kolodkin, 2004)

In animals expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^c17 and reared at 18^oC, most of the giant fiber (GF) axons are normal in structure (83% wild type) and function (67& wild type) in the adult. When animals expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^c17 are shifted to 30^oC (for 24 hours) at 37.5% of pupal development, the resulting GF axon usually lacks the bend in the resulting adult flies and physiologically all GF to tergotrochanteral motoneuron contacts show long latencies and/or following frequencies. When animals expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^c17 are shifted to 30^oC (for 24 hours) at 50% of pupal development, only 38% of the GF axons in the resulting adults are wild type, with 62% having a bendless phenotype. Only 7% of the GF axons are physiologically normal. Temperature shift to 30^oC (for 24 hours) of animals expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^c17 at 12.5% or 62.5% pupal development has minor effect on GF anatomy and physiology compared to non-temperature shifted controls.

(Murphey et al., 2003)

When Sema-1a^Scer\UAS.cYa is driven by Scer\GAL4^l(3)H94-H94, drastically reduces the proportion of motor neurons that properly innervate muscles 6 and 13, increasing the proportion with abnormal innervation from 22% (in controls) to 49%.

(Winberg et al., 2001)

Embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^l(3)H94-H94 show abnormal innervation of muscle 13 by the ISNb axons in 52.7% of segments. Embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^F63 show abnormal innervation of the muscle 6/7 cleft by the ISNb axons in 40.3% of segments.

(Winberg et al., 1998)

Embryos carrying two copies of Sema-1a^Scer\UAS.cYa expressed in all muscles under the control of two copies of Scer\GAL4^how-24B in a wild-type background have dramatic motor axon defects. The intersegmental nerve b branch (ISNb) has a bypass phenotype in 24% of hemisegments, including both parallel bypass events (the ISNb fails to enter the ventral muscle field and extends dorsally in close proximity to the ISN as a separate pathway) and fusion bypass events (the ISNb fails to enter the ventral muscle field and extends dorsally along the ISN). A significant number of ISNb stall events are also seen, with the ISNb stalling either between muscles 7 and 6 or between muscles 6 and 13. ISNb pathways with no synaptic arborisations between muscles 6 and 7, or aberrant synaptic arborisations between muscles 6 and 7 or on muscle 12 are also often seen. A significant number of segmental nerve a branch (SNa) stall events are seen. Embryos expressing a single copy of Sema-1a^Scer\UAS.cYa under the control of a single copy of Scer\GAL4^how-24B in a wild-type background do not have significant ISNb or SNa defects. 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 genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by Scer\GAL4^P52/trol^EP1160

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by trol^UAS.RG/Scer\GAL4^P52

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by Scer\GAL4^P52/trol^UAS.RD

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by dally⁸⁰/dally[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by sfl[+]/sfl⁰³⁸⁴⁴

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by sgl[+]/sgl⁰⁸³¹⁰

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by if^unspecified/if[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by mys[+]/mys^unspecified

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by PlexA^+tCa

(Cho et al., 2012)

Sema1a^UAS.cYa has abnormal neuroanatomy phenotype, enhanceable by Df(2R)nvy^PDFKG38/Scer\GAL4^how-24B/nvy[+]

(Terman and Kolodkin, 2004)

Scer\GAL4^c17, Sema1a^UAS.cYa has abnormal neurophysiology | heat sensitive phenotype, enhanceable by Scer\GAL4^c17/shi^1.UAS

(Murphey et al., 2003)

Scer\GAL4^c17, Sema1a^UAS.cYa has abnormal neuroanatomy | heat sensitive phenotype, enhanceable by Scer\GAL4^c17/shi^1.UAS

(Murphey et al., 2003)

NOT Enhanced by

Statement

Reference

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by dlp¹/dlp[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by Sdc¹⁰⁶⁰⁸/Sdc[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by botv⁵¹⁰/botv[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by ttv[+]/ttv^00681b

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by mew[+]/mew^unspecified

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by Ext2[+]/sotv³²⁶

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by Ext2[+]/sotv³²⁶/ttv[+]/ttv^00681b

(Cho et al., 2012)

Suppressed by

Statement

Reference

Scer\GAL4^Mef2.PR, Sema1a^UAS.cYa has abnormal neuroanatomy | embryonic stage phenotype, suppressible | partially by Gyc76C[+]/Gyc76C^KG03723ex173

(Chak and Kolodkin, 2014)

Scer\GAL4^Mef2.PR, Sema1a^UAS.cYa has abnormal neuroanatomy | embryonic stage phenotype, suppressible | partially by Df(4)C3/+

(Chak and Kolodkin, 2014)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, suppressible by Df(4)C3/+

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, suppressible by trol[+]/trol^null

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, suppressible by trol[+]/trol⁸

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy phenotype, suppressible | partially by Df(4)C3/+

(Ayoob et al., 2004)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy phenotype, suppressible | partially by Df(3L)5126/+

(Ayoob et al., 2004)

NOT suppressed by

Statement

Reference

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by dlp¹/dlp[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Sdc¹⁰⁶⁰⁸/Sdc[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by botv⁵¹⁰/botv[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Ext2[+]/sotv³²⁶

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by ttv[+]/ttv^00681b

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Ext2[+]/sotv³²⁶/ttv[+]/ttv^00681b

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by mew[+]/mew^unspecified

(Cho et al., 2012)

Enhancer of

Statement

Reference

Scer\GAL4^c17/Sema1a^UAS.cYa is an enhancer of abnormal neurophysiology | heat sensitive phenotype of Scer\GAL4^c17, shi^1.UAS

(Murphey et al., 2003)

Scer\GAL4^c17/Sema1a^UAS.cYa is an enhancer of abnormal neuroanatomy | heat sensitive phenotype of Scer\GAL4^c17, shi^1.UAS

(Murphey et al., 2003)

NOT Suppressor of

Statement

Reference

Sema1a^UAS.cYa/Scer\GAL4^GH146 is a non-suppressor of abnormal neuroanatomy | somatic clone | adult stage phenotype of meigo¹

(Sekine et al., 2013)

Other

Statement

Reference

Scer\GAL4^tey-5053A, Sema1a^UAS.cYa, trol^UAS.RG has abnormal neuroanatomy | embryonic stage phenotype

(Cho et al., 2012)

nvy[+]/Df(2R)nvy^PDFKG1, Sema1a^UAS.cYa has abnormal neuroanatomy phenotype

(Yang and Terman, 2012)

14-3-3ε^j2B10/14-3-3epsilon[+], Sema1a^UAS.cYa has abnormal neuroanatomy phenotype

(Yang and Terman, 2012)

Pka-C1[+]/Pka-C1^DN, Sema1a^UAS.cYa has abnormal neuroanatomy phenotype

(Yang and Terman, 2012)

Sema1a^UAS.cYa, mys¹/mys[+] has abnormal neuroanatomy phenotype

(Yang and Terman, 2012)

Phenotype Manifest In

Enhanced by

Statement

Reference

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, enhanceable by Scer\GAL4^P52/trol^EP1160

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, enhanceable by trol^UAS.RG/Scer\GAL4^P52

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, enhanceable by Scer\GAL4^P52/trol^UAS.RD

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, enhanceable by dally⁸⁰/dally[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, enhanceable by sfl[+]/sfl⁰³⁸⁴⁴

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, enhanceable by sgl[+]/sgl⁰⁸³¹⁰

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, enhanceable by if^unspecified/if[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, enhanceable by mys[+]/mys^unspecified

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, enhanceable by PlexA^+tCa

(Cho et al., 2012)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has eye photoreceptor cell | third instar larval stage phenotype, enhanceable by Rho1^E3.10

(Yu et al., 2010)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has lamina | third instar larval stage phenotype, enhanceable by Rho1^E3.10

(Yu et al., 2010)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has eye photoreceptor cell & medulla phenotype, enhanceable by Fas2^UAS.cLa

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has nerve terminal & lamina plexus phenotype, enhanceable by Fas2^UAS.cLa

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has axon & eye photoreceptor cell phenotype, enhanceable by Fas2^UAS.cLa

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has axon & lamina phenotype, enhanceable by Fas2^UAS.cLa

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has eye photoreceptor cell & lamina phenotype, enhanceable by Fas2^UAS.cLa

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has axon & medulla phenotype, enhanceable by Fas2^UAS.cLa

(Cafferty et al., 2006)

Sema1a^UAS.cYa has larval abdominal segmental nerve phenotype, enhanceable by Df(2R)nvy^PDFKG38/Scer\GAL4^how-24B/nvy[+]

(Terman and Kolodkin, 2004)

Sema1a^UAS.cYa has larval abdominal intersegmental nerve phenotype, enhanceable by Df(2R)nvy^PDFKG38/Scer\GAL4^how-24B/nvy[+]

(Terman and Kolodkin, 2004)

Scer\GAL4^c17, Sema1a^UAS.cYa has giant fiber neuron | heat sensitive phenotype, enhanceable by Scer\GAL4^c17/shi^1.UAS

(Murphey et al., 2003)

NOT Enhanced by

Statement

Reference

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-enhanceable by dlp¹/dlp[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-enhanceable by Sdc¹⁰⁶⁰⁸/Sdc[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-enhanceable by botv⁵¹⁰/botv[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-enhanceable by ttv[+]/ttv^00681b

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-enhanceable by mew[+]/mew^unspecified

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-enhanceable by Ext2[+]/sotv³²⁶

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-enhanceable by Ext2[+]/sotv³²⁶/ttv[+]/ttv^00681b

(Cho et al., 2012)

Suppressed by

Statement

Reference

Scer\GAL4^Mef2.PR, Sema1a^UAS.cYa has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, suppressible | partially by Gyc76C[+]/Gyc76C^KG03723ex173

(Chak and Kolodkin, 2014)

Scer\GAL4^Mef2.PR, Sema1a^UAS.cYa has axon | embryonic stage phenotype, suppressible | partially by Gyc76C[+]/Gyc76C^KG03723ex173

(Chak and Kolodkin, 2014)

Scer\GAL4^Mef2.PR, Sema1a^UAS.cYa has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, suppressible | partially by Df(4)C3/+

(Chak and Kolodkin, 2014)

Scer\GAL4^Mef2.PR, Sema1a^UAS.cYa has axon | embryonic stage phenotype, suppressible | partially by Df(4)C3/+

(Chak and Kolodkin, 2014)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, suppressible by Df(4)C3/+

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, suppressible by trol[+]/trol^null

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, suppressible by trol[+]/trol⁸

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure phenotype, suppressible | partially by Df(4)C3/+

(Ayoob et al., 2004)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure phenotype, suppressible | partially by Df(3L)5126/+

(Ayoob et al., 2004)

Scer\GAL4^l(3)H94-H94, Sema1a^UAS.cYa has motor neuron phenotype, suppressible by otk³/otk[+]

(Winberg et al., 2001)

Scer\GAL4^l(3)H94-H94, Sema1a^UAS.cYa has larval intersegmental nerve phenotype, suppressible by Df(4)C3/+

(Winberg et al., 1998)

Scer\GAL4^F63, Sema1a^UAS.cYa has larval intersegmental nerve phenotype, suppressible by Df(4)C3/+

(Winberg et al., 1998)

NOT suppressed by

Statement

Reference

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-suppressible by botv⁵¹⁰/botv[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-suppressible by Ext2[+]/sotv³²⁶

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-suppressible by ttv[+]/ttv^00681b

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-suppressible by Ext2[+]/sotv³²⁶/ttv[+]/ttv^00681b

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-suppressible by mew[+]/mew^unspecified

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-suppressible by dlp¹/dlp[+]

(Cho et al., 2012)

Scer\GAL4^P52, Sema1a^UAS.cYa, Sema1a^k13702 has larval posterior commissure | embryonic stage phenotype, non-suppressible by Sdc¹⁰⁶⁰⁸/Sdc[+]

(Cho et al., 2012)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has eye photoreceptor cell | third instar larval stage phenotype, non-suppressible by ena^GC1

(Yu et al., 2010)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has lamina | third instar larval stage phenotype, non-suppressible by ena^GC1

(Yu et al., 2010)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has axon & eye photoreceptor cell phenotype, non-suppressible | somatic clone by Df(3R)swp2^MICAL/Df(3R)swp2^MICAL

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has axon & lamina phenotype, non-suppressible | somatic clone by Df(3R)swp2^MICAL/Df(3R)swp2^MICAL

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has eye photoreceptor cell & lamina phenotype, non-suppressible | somatic clone by Df(3R)swp2^MICAL/Df(3R)swp2^MICAL

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has axon & medulla phenotype, non-suppressible | somatic clone by Df(3R)swp2^MICAL/Df(3R)swp2^MICAL

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has eye photoreceptor cell & medulla phenotype, non-suppressible | somatic clone by Df(3R)swp2^MICAL/Df(3R)swp2^MICAL

(Cafferty et al., 2006)

Scer\GAL4^GMR.PF, Sema1a^UAS.cYa has nerve terminal & lamina plexus phenotype, non-suppressible | somatic clone by Df(3R)swp2^MICAL/Df(3R)swp2^MICAL

(Cafferty et al., 2006)

Enhancer of

Statement

Reference

Scer\GAL4^c17/Sema1a^UAS.cYa is an enhancer of giant fiber neuron | heat sensitive phenotype of Scer\GAL4^c17, shi^1.UAS

(Murphey et al., 2003)

NOT Suppressor of

Statement

Reference

Sema1a^UAS.cYa/Scer\GAL4^GH146 is a non-suppressor of adult antennal lobe projection neuron | somatic clone phenotype of meigo¹

(Sekine et al., 2013)

Other

Statement

Reference

Scer\GAL4^tey-5053A, Sema1a^UAS.cYa, trol^UAS.RG has larval RP5 motor neuron | embryonic stage phenotype

(Cho et al., 2012)

nvy[+]/Df(2R)nvy^PDFKG1, Sema1a^UAS.cYa has larval intersegmental nerve branch ISNb of A1-7 phenotype

(Yang and Terman, 2012)

Sema1a^UAS.cYa, mys¹/mys[+] has larval intersegmental nerve branch ISNb of A1-7 phenotype

(Yang and Terman, 2012)

Sema1a^UAS.cYa, mys¹/mys[+] has larval segmental nerve branch SNa of A1-7 phenotype

(Yang and Terman, 2012)

nvy[+]/Df(2R)nvy^PDFKG1, Sema1a^UAS.cYa has larval segmental nerve branch SNa of A1-7 phenotype

(Yang and Terman, 2012)

14-3-3ε^j2B10/14-3-3epsilon[+], Sema1a^UAS.cYa has larval intersegmental nerve branch ISNb of A1-7 phenotype

(Yang and Terman, 2012)

14-3-3ε^j2B10/14-3-3epsilon[+], Sema1a^UAS.cYa has larval segmental nerve branch SNa of A1-7 phenotype

(Yang and Terman, 2012)

Pka-C1[+]/Pka-C1^DN, Sema1a^UAS.cYa has larval intersegmental nerve branch ISNb of A1-7 phenotype

(Yang and Terman, 2012)

Pka-C1[+]/Pka-C1^DN, Sema1a^UAS.cYa has larval segmental nerve branch SNa of A1-7 phenotype

(Yang and Terman, 2012)

Additional Comments

Genetic Interactions

Statement

Reference

The ISNb axon pathfinding, positioning and bypass defects caused by expression of Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^Mef2.PR are significantly reduced in Gyc76C^KG03723ex173/+ embryos.

The ISNb axon pathfinding, positioning and bypass defects caused by expression of Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^Mef2.PR are significantly reduced in Df(4)C3/+ embryos.

(Chak and Kolodkin, 2014)

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 null background is significantly suppressed if the embryos are also heterozygous for either Df(4)C3, trol^null or trol⁸.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 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-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 null background is significantly enhanced if the embryos are also heterozygous for either dally⁸⁰, sfl⁰³⁸⁴⁴ or sgl⁰⁸³¹⁰.

Co-expression of trol^EP1160 significantly enhances the commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 null background.

Co-expression of either trol^Scer\UAS.RG or trol^Scer\UAS.RD strongly enhances the commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 null background.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 null background is not affected if the embryos are also heterozygous for either dlp¹, Sdc¹⁰⁶⁰⁸, botv⁵¹⁰, Ext2³²⁶ or ttv^00681b.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 null background is significantly enhanced if the embryos are also heterozygous for if^unspecified or mys^unspecified.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 null background is not affected if the embryos are also heterozygous for mew^unspecified.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^P52 in a Sema-1a^k13702 null background is not affected if the embryos are also doubly heterozygous for Ext2³²⁶ and ttv^00681b.

Co-expression of both trol^Scer\UAS.RG and Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^tey-5053A results in significant RP5 neuron defasciculation defects at the final choice point between muscles 12 and 13. Targeting defects are also seen, resulting in premature bifurcations.

(Cho et al., 2012)

Expression of one copy of Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^how-24B in embryos that are also heterozygous for one of nvy^PDFKG1, 14-3-3ε^j2B10, Pka-C1^DN or mys¹ results in axon guidance defects in the ISNb and SNa nerves, resulting in reduced muscle innervation.

(Yang and Terman, 2012)

A ena^GC1 background does not affect the Sema-1a^Scer\UAS.cYa overexpression-induced hyperfasciculation phenotype.

A Rho1^E3.10 background significantly enhances the Sema-1a^Scer\UAS.cYa overexpression-induced hyperfasciculation phenotype.

(Yu et al., 2010)

The hyperfasciculation phenotype seen in the axons of eye photoreceptor cells in ate third instar Sema-1a^Scer\UAS.cYa; Scer\GAL4^GMR.PF larvae is enhanced by Fas2^Scer\UAS.cLa - axons are clustered into relatively few large bundles in the lamina and medulla. This phenotype is not suppressed in Df(3R)swp2^MICAL homozygous somatic clones.

(Cafferty et al., 2006)

Decreasing the levels of plexA via a Df(4)C3/+ background partially 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.

(Ayoob et al., 2004)

When expression is driven by Scer\GAL4^how-24B in a heterozygous Df(2R)nvy^PDFKG38 background motor axons fail to defasciculate and innervate their muscle targets.

(Terman and Kolodkin, 2004)

shi^1.Scer\UAS and Sema-1a^Scer\UAS.cYa show an interaction when expressed under the control of Scer\GAL4^c17; even in the absence of a temperature shift to the restrictive temperature only half the adults have anatomically normal giant fiber (GF) axons, with the remainder having either a bendless phenotype or failing to reach the target area. Only 45% of the GF axons are physiologically normal. When shi^1.Scer\UAS and Sema-1a^Scer\UAS.cYa are co-expressed under the control of Scer\GAL4^c17 and animals are shifted to the restrictive temperature (for 24 hours) at 37.5% of pupal development, 44% of the GF axons in the resulting adults terminate in the thorax and are anatomically defective and most of the reamining GF axons terminate in the brain. None of the GF axons are physiologically normal in these adults. When shi^1.Scer\UAS and Sema-1a^Scer\UAS.cYa are co-expressed under the control of Scer\GAL4^c17 and animals are shifted to the restrictive temperature (for 24 hours) at 50% of pupal development, most of the GF axons in the resulting adults exit the brain but the presynaptic terminals in the thorax are defective. The disrupted axon terminals are unusually large and are often filled with membrane-bound vesicles. None of the GF axons are physiologically normal in these adults. When shi^1.Scer\UAS and Sema-1a^Scer\UAS.cYa are co-expressed under the control of Scer\GAL4^c17 and animals are shifted to the restrictive temperature (for 24 hours) at 62.5% of pupal development, none of the GF axons show a bend when examined immediately after the temperature shift, suggesting that all immature synapses have retracted.

(Murphey et al., 2003)

The addition of otk³/+ to Sema-1a^Scer\UAS.cYa, Scer\GAL4^l(3)H94-H94 flies reduces the proportion with of motor neurons abnormally innervating to from 49% to 26%.

(Winberg et al., 2001)

The abnormal innervation of muscles by the ISNb axons caused by expression of Sema-1a^Scer\UAS.cYa under the control of Scer\GAL4^l(3)H94-H94 or Scer\GAL4^F63 is dominantly suppressed by Df(4)C3.

(Winberg et al., 1998)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescues

Sema1a^UAS.cYa/Scer\GAL4^GH146 rescues Sema1a^k13702

(Komiyama et al., 2007)

Partially rescues

Scer\GAL4^elav-C155/Sema1a^UAS.cYa partially rescues Sema1a^k13702/Df(2L)N22-5

(Cafferty et al., 2006)

Scer\GAL4^elav-C155/Sema1a^UAS.cYa partially rescues Sema1a^k13702

(Yu et al., 1998)

Sema1a^UAS.cYa/Scer\GAL4^sca-537.4 partially rescues Sema1a^k13702

(Yu et al., 1998)

Comments

The photoreceptor axon projection phenotype seen in the optic lobes of late third instar Sema-1a^k13702/Df(2L)N22-5 larvae is largely rescued by Sema-1a^Scer\UAS.cYa; Scer\GAL4^elav-C155.

(Cafferty 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

Sema-1a^Scer\UAS.cYa

Sema1a^Scer\UAS.cYa

Sema1a^UAS.cYa

sema-I^UAS.cYa

Name Synonyms

Saccharomyces cerevisiae UAS construct a of Yu

(Yu et al., 1998)

Secondary FlyBase IDs

References (18)

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