FB2024_03 , released June 25, 2024
Allele: Dmel\H2
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General Information
Symbol
Dmel\H2
Species
D. melanogaster
Name
FlyBase ID
FBal0005293
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
Nature of the Allele
Progenitor genotype
Cytology

Polytene chromosomes normal.

Description

6.9kb insertion (identity unknown) very close to the site of the hobo insertion in HB8.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

H2 heterozygous adults display loss of one or more thoracic sensory bristles, as compared o controls.

H2 heterozygotes show a partial loss of wing vein L5

The wings of H2/+ mutant adults are significantly larger than those of wild type flies.

H2 wings are larger than wild type.

Homozygous intestinal stem cell clones lose self-renewing capacity over time, and fail to form large clones at 14 days after clone induction, in contrast to wild-type controls.

36% of H2 heterozygous mutant flies display shortened L2 and L4 longitudinal wing veins.

Flies heterozygous for H2 exhibit defects in sensory organ formation. On the notum, approximately 17% of the hairs are absent. This is due to increased N-signaling causing a failure in SOP cell specification or transformation of the hair daughter cell into an extra socket cell.

Heterozygotes show a weak suppression of notum macrochaetae and an essentially normal pattern of microchaetae.

H1/H2 flies produce nota that are bald.

Homozygotes lack most sensory organs and wing veins. Heterozygotes lack a few sensory organs and the distal part of wing vein L5.

Dorsal mitotic clone in the wing reduces vein differentiation in wing vein LV.

Loss of neuron mutant.

Lethal phase is at the transition from 1st to 2nd instar, and larval development preceding lethality is slightly delayed. Heteroallelic combinations with other alleles can allow development of pharate adults, therefore this allele is not considered as a strong allele, as was previously published (Bang et al., Development 111:89-104 ).

Bristle double socket phenotype.

Recessive phenotypic effects. Bristle loss on head and notum and double socket phenotype.

Haplo-insufficient.

Terminal gaps in LIV and LV and occasionally short terminal gaps in LII and LIII.

Causes reduction of neural hyperplasia due to homozygosity for neur- and mam- alleles.

Bristle effect more extreme than in H1 and more easily separated from wild type. Venation effect slighter than in H1.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

H2 has visible | adult stage phenotype, enhanceable by Sirt1[+]/Sirt12A-7-11

H2 has abnormal size phenotype, enhanceable by Df(3R)Exel9019/+

H2 has abnormal size phenotype, enhanceable by +/Df(3L)Exel9001

NOT Enhanced by
Statement
Reference

H2 has abnormal size phenotype, non-enhanceable by Df(2L)BSC251/+

H2 has abnormal size phenotype, non-enhanceable by Df(2R)BSC651/+

H2 has abnormal size phenotype, non-enhanceable by Df(2R)BSC274/+

H2 has abnormal size phenotype, non-enhanceable by Df(2L)Exel6005/+

H2 has abnormal size phenotype, non-enhanceable by Df(2L)BSC255/+

H2 has abnormal size phenotype, non-enhanceable by Df(2L)BSC184/+

H2 has abnormal size phenotype, non-enhanceable by Df(2L)Exel8034/+

H2 has abnormal size phenotype, non-enhanceable by Df(2R)BSC337/+

H2 has abnormal size phenotype, non-enhanceable by Df(3R)Exel6179/+

H2 has abnormal size phenotype, non-enhanceable by Df(2R)BSC660/+

H2 has abnormal size phenotype, non-enhanceable by Df(2R)BSC668/+

H2 has abnormal size phenotype, non-enhanceable by Df(2R)ED2076/+

H2 has abnormal size phenotype, non-enhanceable by Df(3L)BSC773/+

H2 has abnormal size phenotype, non-enhanceable by Df(2L)BSC226/+

H2 has abnormal size phenotype, non-enhanceable by Df(1)BSC535/+

H2 has abnormal size phenotype, non-enhanceable by Df(3R)Exel6212/+

H2 has abnormal size phenotype, non-enhanceable by +/Df(2R)Exel7123

H2 has abnormal size phenotype, non-enhanceable by Df(2L)Exel6028/+

Suppressed by
Statement
Reference

H2 has abnormal size phenotype, suppressible by Df(2L)BSC200/+

H2 has abnormal size phenotype, suppressible by Df(1)Exel6233/+

H2 has abnormal size phenotype, suppressible by Df(1)Exel6251/+

H2 has abnormal size phenotype, suppressible by Df(1)BSC352/+

H2 has abnormal size phenotype, suppressible by Df(1)BSC870/+

H2 has visible | dominant phenotype, suppressible by dx24

H2 has visible phenotype, suppressible by kuzk01405

NOT suppressed by
Statement
Reference

H2 has abnormal size phenotype, non-suppressible by Df(2R)BSC337/+

H2 has abnormal size phenotype, non-suppressible by Df(3R)Exel6179/+

H2 has abnormal size phenotype, non-suppressible by Df(2R)BSC660/+

H2 has abnormal size phenotype, non-suppressible by Df(2R)BSC668/+

H2 has abnormal size phenotype, non-suppressible by Df(2R)ED2076/+

H2 has abnormal size phenotype, non-suppressible by Df(3L)BSC773/+

H2 has abnormal size phenotype, non-suppressible by Df(2L)BSC226/+

H2 has abnormal size phenotype, non-suppressible by Df(1)BSC535/+

H2 has abnormal size phenotype, non-suppressible by Df(3R)Exel6212/+

H2 has abnormal size phenotype, non-suppressible by +/Df(2R)Exel7123

H2 has abnormal size phenotype, non-suppressible by Df(2L)Exel6028/+

H2 has abnormal size phenotype, non-suppressible by Df(2L)BSC251/+

H2 has abnormal size phenotype, non-suppressible by Df(2R)BSC651/+

H2 has abnormal size phenotype, non-suppressible by Df(2R)BSC274/+

H2 has abnormal size phenotype, non-suppressible by Df(2L)Exel6005/+

H2 has abnormal size phenotype, non-suppressible by Df(2L)BSC255/+

H2 has abnormal size phenotype, non-suppressible by Df(2L)BSC184/+

H2 has abnormal size phenotype, non-suppressible by Df(2L)Exel8034/+

NOT Enhancer of
Statement
Reference

H2 is a non-enhancer of visible phenotype of upd1GMR.PB

Suppressor of
Statement
Reference

H2/H[+] is a suppressor | partially of visible phenotype of edslH8/ed1X5

H2/H[+] is a suppressor of visible | dominant phenotype of amosTft

H2/H[+] is a suppressor of visible | dominant phenotype of dx24

H2 is a suppressor of visible phenotype of Scer\GAL4455.2, l(1)scUAS.cHa

H2 is a suppressor of visible | recessive phenotype of kuzk01405

NOT Suppressor of
Statement
Reference

H2 is a non-suppressor of visible phenotype of upd1GMR.PB

Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference

H2 has wing vein L2 phenotype, suppressible by Past1[+]/Past160-4

H2 has wing vein L4 phenotype, suppressible by Past1[+]/Past160-4

H2 has wing vein L4 phenotype, suppressible by Snr1E1

H2 has wing vein phenotype, suppressible by dx24

H2 has sense organ phenotype, suppressible by kuzk01405

H2 has phenotype, suppressible by Su(H)8

H2 has phenotype, suppressible by EgfrE3/Egfr[+]

NOT suppressed by
Statement
Reference

H2 has wing vein phenotype, non-suppressible by kuzk01405

Enhancer of
Statement
Reference

H2/H[+] is an enhancer of phenotype of Egfrt1/Egfrf11

NOT Enhancer of
Statement
Reference

H2 is a non-enhancer of eye phenotype of upd1GMR.PB

Suppressor of
Statement
Reference

H2/H[+] is a suppressor of macrochaeta | ectopic phenotype of edslH8/ed1X5

H2/H[+] is a suppressor of macrochaeta | ectopic phenotype of amosTft

H2/H[+] is a suppressor of wing vein phenotype of dx24

H2/H[+] is a suppressor of wing phenotype of dx24

H2/H[+] is a suppressor of phenotype of Hsc70-4195

H2 is a suppressor of wing phenotype of kuzk01405

H2/H[+] is a suppressor of phenotype of EgfrE3

H2 is a suppressor of eye | somatic clone phenotype of Delta9P

H2 is a suppressor of eye | somatic clone phenotype of neur11

NOT Suppressor of
Statement
Reference

H2 is a non-suppressor of eye phenotype of upd1GMR.PB

H2/H[+] is a non-suppressor of microchaeta phenotype of edslH8/ed1X5

H2/H[+] is a non-suppressor of wing phenotype of dx24

Other
Additional Comments
Genetic Interactions
Statement
Reference

H2 heterozygous adults also expressing Rbfox1dsRNA.Scer\UAS under the control of Scer\GAL4sca-109-68 exhibit an enhanced loss of thoracic sensory bristles and exhibit a significant amount of sockets instead of bristles, as compared to H2 heterozygotes.

The shortening of the wing vein L5 observed H2 heterozygous adults is partially rescued by combination with one or (more strongly) two copies of Sirt12A-7-11.

Only 6% of H2, Past160-4 double heterozygous mutant flies show defects in wing veins, much reduced compared to single H2 mutant flies.

Only 6% of H2, Past1110-1 double heterozygous mutant flies show defects in wing veins, much reduced compared to single H2 mutant flies.

A Eps-152/Eps-15EP2513 transheterozygous background significantly enhances the hair loss phenotype observed in H2 heterozygotes. This enhancement is gene dosage dependent with loss of both copies of Eps-15 increasing the hair loss to 46%, accompanied by increases of nearly four-fold in the number of double sockets and nearly two-fold in the number of areas with no external sensory organs.

Su(H)1 heterozygosity suppresses the hair loss phenotype found in Eps-152/Eps-15EP2513; H2/+ mutants.

The incomplete L4 wing vein phenotype seen in H2 mutants is suppressed by Snr1E1.

H2/+ almost completely eliminates the extra macrochaetae seen on the notum of ed1X5/edslH8 animals, although the increased density of microchaetae seen in ed1X5/edslH8 flies is not reduced by H2/+.

The average number of ectopic macrochaetae per heminotum in amosTft/+ flies is reduced to 19 +/- 2 if they are also carrying H2/+.

Effects on wing development by dx24/Y and H2/+ are mutually levelled. dx24/Y wing phenotypes, both regarding vein broadening and spread out wings, as well as haploinsufficient vein shortening in H2 mutants are largely restored in dx24/Y, H2/+ flies. Yet the fragile wing texture typical of dx mutants remains.

The presence of H2 suppresses the supernumerary phenotype seen in flies with m4Scer\UAS.cAa driven by Scer\GAL4ptc-559.1.

Mutation suppresses the ectopic scutellar bristle phenotype seen from Scer\GAL4455.2-mediated expression of l(1)scScer\UAS.cHa.

The sensory organ but not the wing vein phenotypes of H2 are suppressed by kuzk01405. The neurogenic phenotype and reduced wing size of kuzk01405 homozygotes is suppressed by H2.

Phenotype can be suppressed by Su(H)8, alleviated by introduction of P{Su(H)+6.0} into H2 Su(H)8 flies and enhanced by a copy of P{Su(H)+6.0} introduced into heterozygotes.

Egfrt1/Egfrf11 H2/+ double mutants have a superadditive phenotype. EgfrE3/+ shows a negative interaction in combination with H2/+.

H2 reduces the central nervous system hypertrophy seen in Dl9P homozygous embryos. Double homozygous Dl9P H2 clones in the eye are viable, and are sometimes indistinguishable from wild-type. H2 reduces the severity of the phenotype of neur11 clones in the eye.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (7)
Notes on Origin
Discoverer

Sturtevant.

Comments
Comments

Strong H allele.

Heteroallelic combinations with other alleles can allow development of pharate adults, therefore this allele is not considered as a strong allele, as was previously published (Bang et al., Development 111:89-104 ). Phenotypic series of H alleles, progressing from strongest (amorphic) to weakest mutant phenotype: HB79 = H81 >> H1 = H99 > Hbob > H94a > H88d > HB8 > H2 >= H3 > HA120.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (45)