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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
lgdd1, l(2)gd1, l(2)gd
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
Additional Notes

A two base pair deletion within amino acid 215 that results in a frameshift and translation termination 14aa downstream. The two deleted bases within the codon were not specified.

Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype

Polytene chromosomes normal (Ashburner).

Nature of the lesion

Carries a frameshift mutation in which two nucleotides have been removed, resulting in a new translational frame and a premature stop codon after the addition of 15 new amino acids.

A 2 bp deletion at amino acid position 215 which results in a frame shift and a translational stop 14 amino acids downstream, leading to a truncated protein containing only the first DM14 domain.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Overgrowing imaginal discs show pattern duplications. In the wing disc the wing pouch extends distally and overgrows as a flat sheet. The third leg disc duplicates the end knob as it overgrows. The imaginal rings in the gut and salivary glands also overgrow. Phenotype is less severe than for l(2)gd1d7. In clones, the cells show retarded growth. Mutant clones in the leg show missing bristles and empty or duplicated sockets. Bristle number is reduced in pharate adults also.

Lethality occurs during late larval and pupal stages. Imaginal discs show extensive hyperplasia during prolonged larval life. Surviving pharate adults display hypertrophy and pattern duplications. l(2)gd11/l(2)gd14 trans-heterozygotes survive to third instar larvae, have an extended larval life and imaginal discs show extensive hyperplasia. Cell death is abundant in homozygous wing imaginal discs. Clones in a Minute background show a loss of venation or abnormal thickening of veins. Occasionally clones have excessive folding of the wing margins and those located in the proximity of the anterior posterior compartment boundary realign the boundary. Clones also have a non-autonomous effect on surrounding wild type cells.

Homozygotes display imaginal disc overgrowth and frequent disc duplication.

Hyperplastic imaginal disc overgrowth, affecting all discs. Discs implanted into wild type hosts for metamorphosis overgrow and differentiate abnormal imaginal structures. l(2)gd11/l(2)gd1d3 mutant larvae grow at a normal rate until end of feeding period of last larval instar, when growth slows and then stops: they eventually reach double the weight of wild type pupariating larvae.

Chimeras with l(2)gd1d3/l(2)gd11 germ cells produce mostly abnormal eggs; half of the eggs are flaccid and slightly reduced in size. The dorsal appendages are often fused at their site of origin and are wilder than wild-type. Some eggs do not collapse and develop into embryos, although the dorsal appendages are still slightly abnormal. Most of the developing larvae die before hatching, some appear normal, but others have severe head defects and abnormal ventral setal belts.

Hyperplastic growth. Imaginal discs show normal gap-junctional communication.

Homozygous l(2)gd11 wing discs, and foregut and salivary gland imaginal rings transplanted into wild-type adults and cultured in vivo show extensive growth, in contrast to the corresponding wild-type structures cultured in vivo. The wing discs often have an abnormal shape and folding pattern similar to that seen in situ in homozygous l(2)gd11 larvae. The hindgut imaginal ring and imaginal histoblast nests continue overgrow in l(2)gd11 homozygous larvae that are delayed in forming pupae.

Homozygous larvae raised under crowded conditions show overgrowth of the wing discs. The discs have convoluted epithelial outgrowths, mainly in the wing pouch region.

The time of pupariation formation in homozygotes is dependent on nutritional conditions, showing greater delay the more overcrowded the conditions. Pupariation in uncrowded larvae is delayed by 18 hours, while under crowded conditions the delay can be up to 9 days. All imaginal discs of homozygous larvae show extreme hyperplasia. The wing discs lack transverse folds in the distal part of the disc. Overgrowth occurs mostly in the distal direction. The haltere discs lack transverse folds in the distal part of the disc. The third and second leg discs show abnormal folding patterns as overgrowth occurs. Extensive overgrowth occurs in the peripheral area of the eye-antennal disc. In many cases the leg and wing discs evert during the pupal stage, but this eversion is abnormal. Approximately 50% of homozygotes form adult structures under uncrowded conditions. These structures are abnormal: legs have abnormal distal segmentation and the segments are joined together by excessive intersegmental membrane, and the animal is deficient in bristles and sensilla. Homozygous mutant discs transplanted into wild-type larvae produce structures with similar deficiences as seen in situ. Transplanted homozygous mutant discs show an abnormally low rate of transdetermination.

All imaginal discs become hypertrophied in the third instar larva, some (e.g. the wing disc) to twice their normal linear dimension. The discs retain their characteristic folded structure. Eversion of the discs is abnormal, and the animals die approximately 24 hours after puparium formation. Imaginal discs transplanted into host larvae metamorphose fairly normally. The brain is enlarged in old larvae, and brain fragments transplanted into adult abdomens give rise to tumorous tissue.

Pupariation delayed, up to nine days in crowded cultures; pupariation is but one day in uncrowded cultures. Discs continue to grow, becoming very large with long delays. Mutant discs transplanted into normal larval hosts metamorphose; cuticular patterns normal but bristles and to a greater degree sensillae and bracts missing; unguis missing from tarsal claws; tarsi two jointed. Mutant discs yield low incidence of trans-determination.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by

l(2)gd11 has imaginal disc phenotype, enhanceable by ft8

l(2)gd11 has wing disc phenotype, enhanceable by ft8

l(2)gd11 has haltere disc phenotype, enhanceable by ft8

l(2)gd11 has genital disc phenotype, enhanceable by ft8

l(2)gd11 has macrochaeta phenotype, enhanceable by ft8

l(2)gd11 has wing vein phenotype, enhanceable by ft8

Suppressed by
Additional Comments
Genetic Interactions

Clones double mutant for l(2)gd11 and ft8 or ftG show extensive overgrowth. Wing discs bend at the hinge region and show many extra folds that probably result from excess proliferation. Discs are initially smaller than wild type or either single mutant but eventually outgrow them. Leg discs are greatly overgrown, approximating the size of a wild type wing disc, and show no sign of duplications, except for the first leg disc. Haltere disc is also overgrown with an occasional duplication of the capitellum pouch. The eye-antennal disc is massively overgrown and becomes the largest disc, with duplications and triplications of the antenna knob and the retinal field. Genital discs duplicate and show many extra folds. Double mutants do not survive to pharate adults. Clones double mutant for l(2)gd11 and ft8 produce very few bristles. The cuticle of clones produced in the head or notum is usually twisted or rough. Clones induced in the wings interfere with wing vein formation. Internal vesicles form but do not form bristles. Double mutant clones are larger than for either single mutant. Wing discs from l(2)gd11, ds38k double mutants are large and have variable morphology, often with a series of frill-like folds on the edges of the discs. Leg discs are larger and thicker than for ds38k alone. The haltere disc duplicates, triplicates or quadruplicates. The eye antenna disc shows a pair of knob-like structures in the anterior of the antenna field that probably represent presumptive antennae. Animals usually die in the larval or early pupal stage, and never reach the pharate adult stage. Clones double mutant for ds38k and ds38k form protrusions due to abnormal morphogenesis that might result from an excess of cells. Wing discs from l(2)gd11, cg1 double mutants show a variety of extra folds and extensive overgrowth. The second and third leg, haltere, female genital and eye-antenna discs all show duplication of various structures. These animals fail to form pharate adults and die as larvae or pupae. dppd5 suppresses the duplicative ability of second leg discs in ft8, l(2)gd11/l(2)gd11 mutants. Imaginal discs from ds38k l(2)gd11/l(2)gd11 larvae resemble those of ft8 l(2)gd11/l(2)gd11 rather than l(2)gd11/l(2)gd11 in that wing, haltere, second and third leg discs are duplicated.

Pharate adult wings of l(2)gd11 vg1 double mutants are partially restored compared to the single homozygotes. Clones in a vg1 homozygous background are recognisable by growths protuding from the wing blade, thus partially restoring the wing pattern by extensions of the wing blade areas (three-fold increase in wing blade area) and a span of clonal tissue in both dorsal and ventral wing surfaces.

wgNZ l(2)gd11/l(2)gd11 larvae show duplication of the third leg disc, wgl-16 l(2)gd11 homozygous larvae display an overgrowth phenotype but not third leg duplicate discs and dppd5 l(2)gd11 larvae show an overgrowth phenotype but not duplicate third leg disc.

Xenogenetic Interactions
Complementation and Rescue Data
Images (0)
Stocks (1)
Notes on Origin

Pole cell transplantation indicates that the l(2)gd1 product is required for normal germ-line development and/or subsequent embryogenesis.

Preliminary experiments using a P element-borne copy of the wild type Gyc32E 12kb genomic region failed to rescue either abo1 or l(2)gd11 phenotypes.

Strong allele.

l(2)gd11, l(2)gd14, l(2)gd1d7 and l(2)gd1d10 all harbor the same lesion.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (18)