FlyBase Allele Report: Dmel\nub[1]

General Information

Symbol

Dmel\nub¹

Species

D. melanogaster

Name

FlyBase ID

FBal0013178

Feature type

allele

Associated gene

Dmel\nub

Associated Insertion(s)

412{}nub¹

Carried in Construct

Key Links

Allele class

hypomorphic allele - genetic evidence

Mutagen

spontaneous

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Cifuentes and Garcia-Bellido, 1997, Ng et al., 1995)

Mutagen

spontaneous

Progenitor genotype

Associated Insertion(s)

412{}nub¹

Caused by aberration

Df(2L)nub¹

Cytology

Description

The nub¹ chromosome has previously been shown to have an insertion of 412 insertion in the promoter of one of the nub isoforms. In addition, the chromosome contains a 1824bp deletion (Df(2L)nub¹) downstream of nub, in the intergenic region between nub and pdm2. Expression of both nub and pdm2 is affected in the 412{}nub¹ Df(2L)nub¹ chromosome. Analysis of newly generated CRISPR alleles that carry a similar deletion to Df(2L)nub¹ (without a 412 insertion in nub) have a similar phenotype to 412{}nub¹ Df(2L)nub¹ flies, suggesting that the primary cause of the nub¹ phenotype is due to the Df(2L)nub¹ deletion rather than the 412{}nub¹ insertion.

(Loker and Mann, 2022)

A 412 insertion is inserted near the first exon of the α transcription unit, within the first intron of the β transcription unit.

(Ng et al., 1995)

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 ( 1 )

Disease

Evidence

References

model of immune system disease

CEA

(Dantoft et al., 2013)

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 size | adult stage A1

(Terriente et al., 2008)

viable

(Cifuentes and Garcia-Bellido, 1997)

visible

(Perea et al., 2013, Cifuentes and Garcia-Bellido, 1997)

visible | adult stage A1

(Terriente et al., 2008)

Phenotype Manifest In

anterior notal wing process

(Ng et al., 1995)

crossvein

(Cifuentes and Garcia-Bellido, 1997)

dorsal row of triple row of wing sensilla

(Cifuentes and Garcia-Bellido, 1997)

haltere

(Cifuentes and Garcia-Bellido, 1997)

leg

(Cifuentes and Garcia-Bellido, 1997)

medial row of triple row of wing sensilla

(Cifuentes and Garcia-Bellido, 1997)

pleural wing process

(Ng et al., 1995)

posterior notal wing process

(Ng et al., 1995)

sensory mother cell | ectopic

(Neumann and Cohen, 1998)

ventral row of triple row of wing sensilla

(Cifuentes and Garcia-Bellido, 1997)

wing

(Perea et al., 2013, Terriente et al., 2008, Cifuentes and Garcia-Bellido, 1997, Ng et al., 1995)

wing disc

(Cifuentes and Garcia-Bellido, 1997)

wing hinge

(Perea et al., 2013)

wing margin bristle

(Neumann and Cohen, 1998)

wing margin bristle | ectopic

(Neumann and Cohen, 1998)

wing margin bristle | ectopic | somatic clone

(Neumann and Cohen, 1998)

wing vein L2

(Cifuentes and Garcia-Bellido, 1997)

wing vein L4

(Cifuentes and Garcia-Bellido, 1997)

wing vein L5

(Cifuentes and Garcia-Bellido, 1997)

Detailed Description

Statement

Reference

Compared with wild-type, the commensal bacterial load is significantly diminished in guts of nub¹ mutant flies.

(Dantoft et al., 2013)

Mutant flies have strongly reduced wings with a deletion of the wing hinge.

(Perea et al., 2013)

Homozygous nub¹ adults have wings that are deformed and are reduced in size.

(Terriente et al., 2008)

nub¹/ft^k07918 somatic clones are small and cause overgrowth, as in ft^k07918 clones, but retain the extreme accommodation phenotype of nub¹.

(Garoia et al., 2000)

The bristles of the wing margin form in a broader domain than in wild type. The DV identity of the bristles is ambiguous, possibly because clones fail to respect the DV lineage restriction. Ectopic wing margin bristles occur in clones induced in the wing. Rarely, ectopic bristle precursors occur outside the clone.

(Neumann and Cohen, 1998)

Wings are smaller and shorter than normal and are abnormally folded and bent. Wing size reduction is due to reduced number of wing cells. Bristles of the triple row are incorrectly differentiated. Bracteated bristles can be seen in distal position, indicating a failure in proximo-distal specification. Wing veins L4 and L5 and crossveins are missing. Haltere is smaller than wild type. Legs may appear shortened and gnarled. Third larval instar mutant wings exhibit conspicuous cell mortality. Clones in the wing are small and cause reduction of the whole wing size. Clones covering the proximal wing vein L2 causes thickening and those covering the triple row cause bracteated bristles.

(Cifuentes and Garcia-Bellido, 1997)

Wing blade reduced to a tiny stump, wing hinge is partially deleted. A portion of the wing margin is still present. Clonal analysis reveals that mutant clones are considerably smaller than wild type clones, though the autonomous reduction in size is insufficient to explain the overall reduction in size of mutant wings. Clones which occupy a portion of the wing hinge cause a non-autonomous reduction in the size of the wing.

(Ng et al., 1995)

Wings very small, opaque, curved spoonlike up or down; inflated at eclosion. Wing margins interrupted. Only one vein (L2 or L3) present. Halteres somewhat reduced. Viability excellent. RK1.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Other

Statement

Reference

Scer\GAL4^NP1550, nub¹, zfh2^RNAi.UAS has partially lethal - majority die phenotype

(Terriente et al., 2008)

Scer\GAL4^NP1550, nub¹, zfh2^RNAi.UAS has partially lethal - majority die | pupal stage phenotype

(Terriente et al., 2008)

dpp^αTub84B.PZ, nub¹ has visible phenotype

(Cifuentes and Garcia-Bellido, 1997)

dpp^d12/dpp^s8, nub¹ has visible phenotype

(Cifuentes and Garcia-Bellido, 1997)

dpp^d12, nub¹ has visible phenotype

(Cifuentes and Garcia-Bellido, 1997)

dpp^s8, nub¹ has visible phenotype

(Cifuentes and Garcia-Bellido, 1997)

elA¹, nub¹ has visible phenotype

(Cifuentes and Garcia-Bellido, 1997)

Phenotype Manifest In

Suppressed by

Statement

Reference

nub¹ has wing margin bristle | ectopic | somatic clone phenotype, suppressible by wg^l-17

(Neumann and Cohen, 1998)

Other

Statement

Reference

dpp^αTub84B.PZ, nub¹ has wing phenotype

(Cifuentes and Garcia-Bellido, 1997)

dpp^d12/dpp^s8, nub¹ has wing phenotype

(Cifuentes and Garcia-Bellido, 1997)

dpp^d12, nub¹ has wing phenotype

(Cifuentes and Garcia-Bellido, 1997)

dpp^s8, nub¹ has wing phenotype

(Cifuentes and Garcia-Bellido, 1997)

elA¹, nub¹ has wing phenotype

(Cifuentes and Garcia-Bellido, 1997)

Additional Comments

Genetic Interactions

Statement

Reference

Most individuals with the genetic combination of nub¹, Scer\GAL4^NP1550/nub¹;zfh2^{dsRNA.Scer\UAS} die as late pupae, though very rare escapers are found.

(Terriente et al., 2008)

Clones of cells that are simultaneously mutant for wg^l-17 and nub¹ do not form ectopic bristle precursors.

(Neumann and Cohen, 1998)

Double mutant clones with dpp^d12/dpp^s8 or elA¹ cause dramatic reduction of cell number in the wing pouch. Clones of dpp-expressing cells (dpp^αTub84B.PZ) cause some overgrowth but exclusively of dpp-expressing cells.

(Cifuentes and Garcia-Bellido, 1997)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (1)

Holtzman, S. and Kaufman, T. (2013)

Mutant

Wild-type