FlyBase Allele Report: Dmel\Nos[Δ15]

General Information

Symbol

Dmel\Nos^Δ15

Species

D. melanogaster

Name

FlyBase ID

FBal0267694

Feature type

allele

Associated gene

Dmel\Nos

Associated Insertion(s)

Carried in Construct

Also Known As

dNOS^Δ15

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - molecular evidence

Mutagen

FLPase

Nature of the Allele

Allele class

amorphic allele - molecular evidence

(Yakubovich et al., 2010)

Mutagen

FLPase

(Yakubovich et al., 2010)

Progenitor genotype

PBac{WH}Nos^f02469

(Yakubovich et al., 2010)

PBac{RB}Nos^e02671

(Yakubovich et al., 2010)

Caused by aberration

Df(2L)Nos^Δ15

Cytology

Description

Recombination between the two progenitor chromosomes has resulted in the deletion of the intervening sequence between them. The deletion removes part of the Nos coding sequence (residues 1-757) and also removes the CG6508 and CG17134 genes which are nested within Nos.

(Yakubovich et al., 2010)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

2L:10,809,118..10,837,410 [-]

Comment:

Recombination between the two progenitor chromosomes has resulted in the deletion of the intervening sequence between them.

(Yakubovich et al., 2010)

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 ( 1 )

Disease

Evidence

References

model of lissencephaly

CEA

(Yatsenko et al., 2014)

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal cell number (with Nos¹)

(Cho et al., 2024)

abnormal cell number (with Nos^Δall)

(Cho et al., 2024)

abnormal neuroanatomy

(Yatsenko et al., 2014)

abnormal neuroanatomy | P-stage (with Nos¹)

(Rabinovich et al., 2016)

abnormal neuroanatomy | P-stage (with Nos^C)

(Rabinovich et al., 2016)

abnormal neuroanatomy | P-stage | recessive

(Rabinovich et al., 2016)

abnormal neurophysiology | third instar larval stage

(Robinson et al., 2018)

chemical resistant

(Kanao et al., 2012)

fertile

(Lacin et al., 2014)

fertile (with Nos¹)

(Lacin et al., 2014)

lethal - all die during P-stage, with Nos^{IVS.Syn21.p10.10xUAS}, Scer\GAL4^ey-OK107

(Rabinovich et al., 2016)

lethal - all die during P-stage, with Nos^UAS.cMa, Scer\GAL4^ey-OK107

(Rabinovich et al., 2016)

viable

(Lacin et al., 2014, Yakubovich et al., 2010)

viable (with Nos¹)

(Lacin et al., 2014)

viable (with Nos^C)

(Yakubovich et al., 2010)

Phenotype Manifest In

adult brain

(Yatsenko et al., 2014)

adult mushroom body gamma-lobe | P-stage

(Rabinovich et al., 2016)

adult mushroom body gamma-lobe | P-stage (with Nos¹)

(Rabinovich et al., 2016)

adult mushroom body gamma-lobe | P-stage (with Nos^C)

(Rabinovich et al., 2016)

axon | P-stage

(Rabinovich et al., 2016)

axon | P-stage (with Nos¹)

(Rabinovich et al., 2016)

axon | P-stage (with Nos^C)

(Rabinovich et al., 2016)

embryonic/larval lymph gland (with Nos¹)

(Cho et al., 2024)

embryonic/larval lymph gland (with Nos^Δall)

(Cho et al., 2024)

neuromuscular junction | third instar larval stage

(Robinson et al., 2018)

ventral longitudinal muscle cell | third instar larval stage

(Robinson et al., 2018)

Detailed Description

Statement

Reference

Nos^Δ15 third instar larvae exhibit significantly enhanced mEJC frequencies and significantly increased vesicle pool size in NMJs of ventral longitudinal m6 in abdominal segments 2 and 3 when compared to controls.

(Robinson et al., 2018)

A subset of Nos^Δ15/Nos^Δ15, Nos^Δ15/Nos^C, or Nos^Δ15/Nos¹ mutants display pruning defects and/or precocious regrowth of axons in the mushroom body gamma-lobe, as compared to Nos^Δ15/+, Nos¹/+ or Nos^C/+ controls.

Expression of Nos^Scer\UAS.cMa or Nos^{IVS.Syn21.p10.10xScer\UAS} under the control of Scer\GAL4^ey-OK107 in a Nos^Δ15/Nos^Δ15 background results in early pupal lethality.

(Rabinovich et al., 2016)

Homozygous Nos^Δ15 mutant larvae exhibit normal development and developmental timing, and give rise to viable, fertile and morphologically wild type adult flies. CNS development also appears normal.

Nos¹/Nos^Δ15 mutant larvae exhibit normal development and developmental timing, and give rise to viable, fertile and morphologically wild type adult flies. CNS development also appears normal and there is no overt effect on taste or feeding behavior compared to controls. Nos¹/Nos^Δ15 mutant flies exhibit locomotor defects; flies walk considerably more, and stop considerably less, than control flies.

(Lacin et al., 2014)

The brains of Nos^Δ15 mutants exhibit a weak 'cobblestone-like' phenotype; dense cellular masses (lumps) are seen that overgrow the normal brain contour, protruding above the neural lamina. This phenotype can be partially rescued by nitric oxide treatment.

(Yatsenko et al., 2014)

Homozygous flies show resistance to paraquat compared to controls.

(Kanao et al., 2012)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

Additional Comments

Genetic Interactions

Statement

Reference

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

NOS^Δ15

(Robinson et al., 2018)

Nos^Δ15

(Cho et al., 2024, Song et al., 2019, Kuntz et al., 2017, Wang et al., 2015, Lacin et al., 2014, Yatsenko et al., 2014, Yakubovich et al., 2010)

dNOS^Δ15

(Rabinovich et al., 2016, Kanao et al., 2012)

ΔNOS

(Yatsenko et al., 2014)

Name Synonyms

Secondary FlyBase IDs

References (11)

Report Sections

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