FlyBase Allele Report: Dmel\CadN[M19]

CadN^M19 R7 photoreceptor clones in the larval medulla leads to axon terminals expanding toward the peripheral part of the column, as compared with controls. CadN^M19 R8 photoreceptor clones also leads to axon terminal expansion, but the column morphology is completely disrupted.

(Trush et al., 2019)

The somatic muscle pattern appears normal in homozygous embryos. The average number of nuclei per segment border muscle is normal.

(Dottermusch-Heidel et al., 2012)

CadN^M19 mutant embryos exhibit minor axonal breaks and defasciculation compared to wild-type embyros (when stained with Fas2).

Loss of CadN in CadN^M19 mutants exhibit mild pathway defects in Sema-2b-expressing axons. These axons cross the midline through the anterior commissure and then project anteriorly to reach the prior segment. In CadN^M19 mutants these axons fail to reach the prior segment.

The early trajectories of pioneer axons in CadN^M19 mutants are similar to that of wild-type embryos.

CadN^M19 mutant embryos occasionally exhibit discontinuous MP1/dMP2 pathways, while the pCC/vMP2 pathway is not obviously affected.

(Ding et al., 2011)

Neurons homozygous mutant for CadN^M19 mistarget to the M10 layer, whereas L5 neurons do not establish a normal arbor in layer M2 and extend ectopic branches into neighboring columns in layer M5.

(Hadjieconomou et al., 2011)

Proximal arborization is occasionally eliminated in neuron clones homozygous for CadN^M19. The defect is adult brains are diverse.

(Hasegawa et al., 2011)

Using MARCM, mistargeting of CadN^M19 mutant L1-L5 cells is seen at the following percentages: 22% of L1 neurons, typically terminating in M10 rather than M5; 0% of L2 neurons; 25% of L3 neuron, typically terminating in M5 and M6 rather than M3; 65% of L4 neurons, terminating in M2 or, less frequently, M8 instead of M4; 0% of L5 terminals, but 100% of L5 interstitial branches fail to extend from M1 into M2. 100% of CadN^M19 mutant R7 cells mistarget. 3% of R8 cells extend significantly deeper into the medulla than the remaining R8 cells, similar to controls.

(Nern et al., 2008)

All of the R7 terminals are found in the R8 layer in CadN^M19 mutant clones. At approximately 35% after pupal formation (APF), 61% of the CadN^M19 mutant R7 growth cones are observed in the appropriate target layer. By 48% APF (this is just before the relocation of R7 terminals from their temporary to their final target layer), this fraction decreases to 38%. At both time points the remaining R7 growth cones terminate in the R8 recipient layer or between the R7 and R8 recipient layers.

(Nern et al., 2005)

When small clones of CadN^M19 homozygous cells are present in the pupal retina (40 hours after puparium formation), mutant primary pigment cells are unaffected, but mutant cone cells are mis-shapen, and packed in a 'cruciform' shape: the length of inter-cone cell interfaces is significantly shorter than wild-type, and the length of cone cell/primary pigment cell interfaces is correspondingly longer; the angle of the interfaces of 2 adjacent cone cells with one primary pigment cell is significantly decreased.

(Hayashi and Carthew, 2004)

Homozygous olfactory projection neurons induced as neuroblast clones in newly hatched larvae (using the MARCM technique) target their dendrites

to approximately the same set of glomeruli appropriate for their lineage,

but a number of defects are seen. Dendrites targeted to a particular

glomerulus are no longer restricted within the confines of that glomerulus;

the general dendritic distribution is more diffuse than controls.

This results in glomeruli that are not appropriate for the lineage

often being partially innervated by the mutant PNs, while glomeruli

that are appropriate for the lineage are often less fully innervated

than normal.

Single cell projection neuron (PN) clones of the DL1 class which are

homozygous for CadN^M19 still target the majority of their dendrites

to the DL1 glomerulus. However, a significant fraction of the dendrites

spread to several neighbouring glomeruli (with a preference for the

DL5 glomerulus) and the density of dendritic mass within DL1 is reduced.

Studies of single cell projection neuron clones of the DL1 class during

development show that at 18 hours after puparium formation (APF) the

homozygous PNs target their dendrites to the same class-specific location

as their wild-type counterparts (although dendritic branches are often

seen shooting out of the developing antennal lobe), but as development

proceeds, the mutant PN dendrites fail to fully refine and do not show

uniglomerular innovation by 50 hours APF (in contrast to wild-type

PNs, which gradually restrict their dendrites to innervate discrete

glomeruli).

Single cell projection neuron clones of the DA1, VM7 or DL3 class which

are homozygous for CadN^M19 still target their dendrites to the

appropriate glomerulus, but show significant spread to neighbouring

glomeruli and a reduction of dendritic density in the major target

glomerulus.

Animals in which the majority of olfactory receptor neurons (ORNs)

are homozygous for CadN^M19 (generated using the eyFLP technique)

show a severe disruption of antennal glomerular development; glomerular

borders are blurred and individual glomeruli are no longer identifiable.

At 50 hours APF projection neurons appear to have refined normally,

despite the disruption in glomerular development.

Animals in which all projection neurons innervating the VA1lm glomerulus

are homozygous for CadN^M19 (generated using the MARCM technique)

show severe dendritic overspill by the PNs into neighbouring glomeruli.

However, the axonal arborisation of the olfactory receptor neurons

that normally converge onto the VA1lm glomerulus is indistinguishable

from wild type.

Labelled wild-type DL1 projection neurons (PNs) that develop in a background

where other DL1 PN dendrites are homozygous for CadN^M19 (generated

using the reverse MARCM technique) show significant dendritic spillover

into neighbouring glomeruli (including DL5 and DL2). In 6/16 clones

examined, there are also dendritic processes shooting out of the antennal

lobe.

The axons of homozygous olfactory projection neurons induced either

as neuroblast clones or as single cell clones follow the correct trajectory

and arborise in the mushroom body and the lateral horn. The axon arborisations

appear to be less extensive in the lateral horn and more profuse in

the mushroom body calyx compared to wild type.

Single cell projection neuron (PN) clones of the DL1 class that are

homozygous for CadN^M19 invariably lack the dorsal axon branch in

the lateral horn area in adults, although the lateral branch is not

affected. There is a 50% increase in the number of axon terminals

in the mushroom body calyx for homozygous DL1 PN clones compared to

wild type. The increase is not due to an increase in primary branches,

but is due to an increase in the number of higher order branches.

Studies of single cell projection neuron clones of the DL1 class during

development show that at 36 hours APF the dorsal axon branch in the

lateral horn has formed normally (as in wild-type clones), but these

dorsal branches are not seen at 40 or 52 hours APF in the mutant DL1

PN neuron.

Single cell projection neuron clones of the VM7 class that are homozygous

for CadN^M19 lack the more lateral of the two dorsal axon branches

that are normally found in the lateral horn, while the more medial

dorsal branch and the main lateral branch are unaffected.

(Zhu and Luo, 2004)

The ability of mutant flies to detect motion is approximately 5 times worse than wild-type. The response of mutant flies to a UV/Vis choice test is approximately 8 fold worse than wild-type. Mutants perform well, though less well than wild-type, in counter-current fast phototaxis assays. In CadN^M19 mosaic eyes, the layered structure of the medulla is severely disrupted. When homozygous somatic clones are made in the eye so that only mutant R7 cells persist, the response from these flies to a UV/Vis choice test is several times worse than wild-type.

(Lee et al., 2001)

Mutant axon scaffold is slightly less compact in the transverse direction and intersegmental longitudinal connectives are thinner. Loss of CadN does not perturb pathfinding of the pioneers of stage 12 and 13. Pattern alterations are seen in the follower neurons at stage 14, breaks in the MP1 pathway are observed and axon fascicles of vMP2 and MP1 are defective. Transverse portions of ap-expressing neurons do not shift medially, ventral and dorsal ap axons fail to join each other in some hemisegments.

(Iwai et al., 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

CadN^M19 has abnormal neuroanatomy | adult stage | somatic clone phenotype, enhanceable by Sema1a^k13702/Sema1a^k13702

(Pecot et al., 2013)

CadN^M19 has abnormal neuroanatomy phenotype, enhanceable by Scer\GAL4^elav-C155/uzip^RNAi.Sym.UAS

(Ding et al., 2011)

CadN^M19 has abnormal neuroanatomy phenotype, enhanceable by uzip^RNAi.Sym.UAS/Scer\GAL4^repo

(Ding et al., 2011)

CadN^M19 has abnormal neuroanatomy phenotype, enhanceable by uzip^D43/uzip[+]

(Ding et al., 2011)

CadN^M19 has abnormal neuroanatomy phenotype, enhanceable by uzip^D43/uzip²³

(Ding et al., 2011)

CadN^M19 has abnormal neuroanatomy phenotype, enhanceable by uzip^D43

(Ding et al., 2011)

Suppressed by

Statement

Reference

CadN^M19 has abnormal neuroanatomy phenotype, suppressible by Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4^repo/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19 has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4^elav-C155/uzip^UAS.CFP

(Ding et al., 2011)

NOT Enhancer of

Statement

Reference

CadN[+]/CadN^M19 is a non-enhancer of abnormal cell polarity phenotype of Scer\GAL4^hs.2sev, shg^{dCR3h.UAS.sgGFP}

(Mirkovic and Mlodzik, 2006)

CadN^M19 is a non-enhancer of visible phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

CadN^M19 is a non-enhancer of visible phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

Suppressor of

Statement

Reference

CadN^M19 is a suppressor of abnormal neuroanatomy phenotype of Wnt5⁴⁰⁰

(Ding et al., 2011)

NOT Suppressor of

Statement

Reference

CadN[+]/CadN^M19 is a non-suppressor of abnormal cell polarity phenotype of Scer\GAL4^hs.2sev, shg^{dCR3h.UAS.sgGFP}

(Mirkovic and Mlodzik, 2006)

CadN^M19 is a non-suppressor of visible phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

CadN^M19 is a non-suppressor of visible phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

Phenotype Manifest In

Enhanced by

Statement

Reference

CadN^M19 has lamina monopolar neuron L3 | adult stage | somatic clone phenotype, enhanceable by Sema1a^k13702/Sema1a^k13702

(Pecot et al., 2013)

CadN^M19 has MP1 tract phenotype, enhanceable by Scer\GAL4^elav-C155/uzip^RNAi.Sym.UAS

(Ding et al., 2011)

CadN^M19 has larval anterior commissure phenotype, enhanceable by uzip^RNAi.Sym.UAS/Scer\GAL4^repo

(Ding et al., 2011)

CadN^M19 has presumptive embryonic/larval central nervous system phenotype, enhanceable by uzip^RNAi.Sym.UAS/Scer\GAL4^repo

(Ding et al., 2011)

CadN^M19 has larval MP1 neuron phenotype, enhanceable by uzip^RNAi.Sym.UAS/Scer\GAL4^repo

(Ding et al., 2011)

CadN^M19 has dMP2 neuron phenotype, enhanceable by uzip^RNAi.Sym.UAS/Scer\GAL4^repo

(Ding et al., 2011)

CadN^M19 has MP1 tract phenotype, enhanceable by uzip^RNAi.Sym.UAS/Scer\GAL4^repo

(Ding et al., 2011)

CadN^M19 has larval anterior commissure phenotype, enhanceable by uzip^D43/uzip[+]

(Ding et al., 2011)

CadN^M19 has presumptive embryonic/larval central nervous system phenotype, enhanceable by uzip^D43/uzip[+]

(Ding et al., 2011)

CadN^M19 has larval MP1 neuron phenotype, enhanceable by uzip^D43/uzip[+]

(Ding et al., 2011)

CadN^M19 has dMP2 neuron phenotype, enhanceable by uzip^D43/uzip[+]

(Ding et al., 2011)

CadN^M19 has MP1 tract phenotype, enhanceable by uzip^D43/uzip[+]

(Ding et al., 2011)

CadN^M19 has larval anterior commissure phenotype, enhanceable by uzip^D43/uzip²³

(Ding et al., 2011)

CadN^M19 has presumptive embryonic/larval central nervous system phenotype, enhanceable by uzip^D43/uzip²³

(Ding et al., 2011)

CadN^M19 has larval MP1 neuron phenotype, enhanceable by uzip^D43/uzip²³

(Ding et al., 2011)

CadN^M19 has dMP2 neuron phenotype, enhanceable by uzip^D43/uzip²³

(Ding et al., 2011)

CadN^M19 has MP1 tract phenotype, enhanceable by uzip^D43/uzip²³

(Ding et al., 2011)

CadN^M19 has larval anterior commissure phenotype, enhanceable by uzip^D43

(Ding et al., 2011)

CadN^M19 has presumptive embryonic/larval central nervous system phenotype, enhanceable by uzip^D43

(Ding et al., 2011)

CadN^M19 has larval anterior commissure phenotype, enhanceable by Scer\GAL4^elav-C155/uzip^RNAi.Sym.UAS

(Ding et al., 2011)

CadN^M19 has presumptive embryonic/larval central nervous system phenotype, enhanceable by Scer\GAL4^elav-C155/uzip^RNAi.Sym.UAS

(Ding et al., 2011)

CadN^M19 has larval MP1 neuron phenotype, enhanceable by Scer\GAL4^elav-C155/uzip^RNAi.Sym.UAS

(Ding et al., 2011)

CadN^M19 has dMP2 neuron phenotype, enhanceable by Scer\GAL4^elav-C155/uzip^RNAi.Sym.UAS

(Ding et al., 2011)

Suppressed by

Statement

Reference

CadN^M19, uzip^D43 has vMP2 tract phenotype, suppressible by Scer\GAL4^repo/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19, uzip^D43 has larval MP1 neuron phenotype, suppressible by Scer\GAL4^elav-C155/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19, uzip^D43 has dMP2 neuron phenotype, suppressible by Scer\GAL4^elav-C155/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19, uzip^D43 has pCC neuron phenotype, suppressible by Scer\GAL4^elav-C155/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19, uzip^D43 has MP1 tract phenotype, suppressible by Scer\GAL4^elav-C155/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19, uzip^D43 has vMP2 tract phenotype, suppressible by Scer\GAL4^elav-C155/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19 has larval MP1 neuron phenotype, suppressible by Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 has dMP2 neuron phenotype, suppressible by Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 has pCC neuron phenotype, suppressible by Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 has MP1 tract phenotype, suppressible by Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 has vMP2 tract phenotype, suppressible by Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19, uzip^D43 has larval MP1 neuron phenotype, suppressible by Scer\GAL4^repo/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19, uzip^D43 has dMP2 neuron phenotype, suppressible by Scer\GAL4^repo/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19, uzip^D43 has pCC neuron phenotype, suppressible by Scer\GAL4^repo/uzip^UAS.CFP

(Ding et al., 2011)

CadN^M19, uzip^D43 has MP1 tract phenotype, suppressible by Scer\GAL4^repo/uzip^UAS.CFP

(Ding et al., 2011)

NOT Enhancer of

Statement

Reference

CadN[+]/CadN^M19 is a non-enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, shg^{dCR3h.UAS.sgGFP}

(Mirkovic and Mlodzik, 2006)

CadN^M19 is a non-enhancer of wing phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

CadN^M19 is a non-enhancer of wing phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

Suppressor of

Statement

Reference

CadN^M19 is a suppressor | partially of embryonic myoblast phenotype of Iqsec^U112/Iqsec^C1-28

(Dottermusch-Heidel et al., 2012)

CadN^M19 is a suppressor of fascicle phenotype of Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 is a suppressor of presumptive embryonic/larval central nervous system phenotype of Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 is a suppressor of lateral longitudinal fascicle phenotype of Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 is a suppressor of larval MP1 neuron phenotype of Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 is a suppressor of MP1 tract phenotype of Wnt5⁴⁰⁰

(Ding et al., 2011)

CadN^M19 is a suppressor of vMP2 tract phenotype of Wnt5⁴⁰⁰

(Ding et al., 2011)

NOT Suppressor of

Statement

Reference

CadN[+]/CadN^M19 is a non-suppressor of ommatidium phenotype of Scer\GAL4^hs.2sev, shg^{dCR3h.UAS.sgGFP}

(Mirkovic and Mlodzik, 2006)

CadN^M19 is a non-suppressor of wing phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

CadN^M19 is a non-suppressor of wing phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

Other

Statement

Reference

Arf1^v37, CadN^M19 has larval somatic muscle cell phenotype

(Dottermusch-Heidel et al., 2012)

Additional Comments

Genetic Interactions

Statement

Reference

The defects in myoblast fusion seen in siz^C1-28/siz^U112 embryos are partially suppressed by CadN^M19 and multinucleate muscles are formed.

CadN^M19 Arf79F^v37 double mutant embryos lack some muscles, while other muscles look thinner than normal and do not attach properly.

(Dottermusch-Heidel et al., 2012)

Neuronal knockdown of uzip through expression of uzip^{dsRNA.Sym.Scer\UAS} under the control of Scer\GAL4^elav-C155 slightly (but not significantly) increases axonal defects in CadN^M19 mutants. Glial knockdown through expression of uzip^{dsRNA.Sym.Scer\UAS} under the control of Scer\GAL4^repo, increases the axonal defects found in CadN^M19 mutants.

A uzip^D43 heterozygous background increases the axonal defects found in CadN^M19 mutants.

A uzip^D43/uzip²³ background increases the axonal defects found in CadN^M19 mutants.

CadN^M19 uzip^D43 double mutants exhibit extensive axonal defects, including broken fascicles in the three longitudinal pathways.

CadN^M19 defects in Sema-2b-expressing neurons are enhanced by heterozygosity and homozygosity of uzip^D43. In the CadN^M19 uzip^D43 double mutant, Sema-2b axons can successfully reach the contralateral side and combine mild defasciculation in commissures. After reaching the contralateral side, some axons stall and some axons turn posteriorly but not anteriorly.

The early trajectories of pioneer axons in CadN^M19 Wnt5⁴⁰⁰ double mutants are similar to that of wild-type embryos.

CadN^M19 uzip^D43 double mutants exhibit more defects in MP1/dMP2 and pCC/vMP2 pathways than CadN^M19 single mutants. They do not form normally where defasciculation is supposed to occur, but become fuzzy, thinning or broken, indicating that uzip and CadN cooperatively affect the axonal growth of pioneer axons.

Defects in MP1/dMP2 and pCC/vMP2 pathways mutant for CadN^M19 uzip^D43 can be partially rescued by expression of uzip^{Scer\UAS.T:Avic\GFP-CFP} in glia (under the control of Scer\GAL4^repo) and in neurons (under the control of Scer\GAL4^elav-C155).

(Ding et al., 2011)

A CadN^M19/+ background does not affect the Scer\GAL4^hs.2sev>shg^{dCR3h.Scer\UAS.T:Avic\GFP-rs} ommatidial phenotype.

(Mirkovic and Mlodzik, 2006)

When small clones of cells homozygous for shg^R69 are present in the retina of CadN^M19/CadN^M12 pupae (40 hours after puparium formation), cone cells in the mutant clones fail to adhere to their cone cell or primary pigment cell neighbours, and some lose all apical contact with other cells. The mutant cells round up, and the remaining wild-type cone cells in mosaic ommatidia pack into configurations typical for soap bubble aggregates.

(Hayashi and Carthew, 2004)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

CadN^M19 is rescued by Scer\GAL4^GH146/CadN^UAS.cIa

(Zhu and Luo, 2004)

CadN^M19 is rescued by Scer\GAL4^sca-537.4/CadN^UAS.cIa

(Iwai et al., 1997)

Partially rescued by

CadN⁴⁰⁵/CadN^M19 is partially rescued by Scer\GAL4^elav.PU/CadN^{7b-13a-18a.UAS}

(Hsu et al., 2009)

CadN⁴⁰⁵/CadN^M19 is partially rescued by Scer\GAL4^elav.PU/CadN^{7b-13b-18a.UAS}

(Hsu et al., 2009)

Not rescued by

CadN⁴⁰⁵/CadN^M19 is not rescued by Scer\GAL4^how-24B/CadN^{7b-13a-18a.UAS}

(Hsu et al., 2009)

CadN⁴⁰⁵/CadN^M19 is not rescued by Scer\GAL4^how-24B/CadN^{7b-13b-18a.UAS}

(Hsu et al., 2009)

Comments

Scer\GAL4^how-24B-mediated expression of CadN^{7b-13a-18a.Scer\UAS} or CadN^{7b-13b-18a.Scer\UAS} has no effect on the lethality of CadN^M19/CadN⁴⁰⁵.

Scer\GAL4^elav.PU-mediated expression of CadN^{7b-13a-18a.Scer\UAS} or CadN^{7b-13b-18a.Scer\UAS} partially rescues the lethality of CadN^M19/CadN⁴⁰⁵ - animals now survive through to the adult stage, but fail to produce progeny.

(Hsu et al., 2009)

CNS phenotype can be rescued in part by Scer\GAL4^sca-537.4-mediated expression of CadN^Scer\UAS.cIa.

(Iwai et al., 1997)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (9)

Reported As

Symbol Synonym

CadN³

CadN^M19

(Pecot et al., 2013, Dottermusch-Heidel et al., 2012, Koper et al., 2012, Ding et al., 2011, Hadjieconomou et al., 2011, Nern et al., 2008, Seppa et al., 2008)

CadN^m19

(Mora et al., 2013)

N-cad^M19

(Hummel and Zipursky, 2004)

N-cadherin^M19

(Hamp et al., 2016)

NCad^M19

(Schäfer et al., 2014, Hasegawa et al., 2011, Tajiri et al., 2007)

Ncad^M19

(Trush et al., 2019, Chan et al., 2017, Hsu et al., 2009, Mirkovic and Mlodzik, 2006, Ting et al., 2005, Zhu and Luo, 2004)

l(2)36Da³

l(2)36Da^M19

(Hartenstein et al., 2017, Iwai et al., 1997)

Name Synonyms

Secondary FlyBase IDs

References (26)

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