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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Deletion of about 300bp of genomic DNA.

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 ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

hop2 heterozygote flies do not show any significant increase in the number of apoptotic cells in the adult brain compared to controls.

40% of embryos from hop2 germ line clones show germ-band extension defects.

Hemizygous hop2 mutant germ-band epithelial cells are normal in the head and dorsal-most regions of the embryo, however intercalating (ventrolateral) cells show a smaller apical cell surface.

The proventriculus development is normal in early stages of proventriculus development in mutants. However in the keyhole stage, the anterior boundary cells fail to move inward into the endodermal keyhole domain and arrest anterior to the proventricular endoderm until late stages of embryonic development. Furthermore, the endodermal cell layer of the keyhole is disorganised and the proventriculus is collapsed.

Paternally rescued hop2 germ-line clone embryos are missing denticle belt A5 and part of A4. In the absence of paternal rescue, more severe segmentation defects are seen. Paternally rescued hop2 germ-line clone embryos have defective tracheal systems, generally having several disruptions in the main trunk and several branches.

Homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic hop function) have incompletely elongated hindguts which are wider than normal. There are a greater number of cells in the circumference of the mutant hindgut than in wild type. The total number of hindgut epithelial cells is 89% of wild type.

The number of pole cells in embryos derived from hop2 female germ line clones is not different to the number in wild-type embryos. However, in late stage embryos these pole cells fail to coalesce and/or form gonads.

hop25/hop2 egg chambers lack border follicle cells and have reduced numbers of stretched (nurse) follicle cells and posterior polar follicle cells, but increased numbers of main body (oocyte) follicle cells. Nurse follicle cell and centripetally migrating follicle cell domains are shifted posteriorly. When presumptive border cells are mutant for hop2 they fail to express markers of differentiation, and are delayed in migration. When follicle cells overlying the nurse cells are mutant for hop2 they fail to stretch at stage 9 as wild-type nurse follicle cells do, or to express nurse follicle cell markers.

Homozygous mutant border cells, made as somatic clones, fail to migrate. Occasionally a mutant border cell cluster is displaced quite far from the anterior tip of the egg chamber and is associated with abnormally shaped mutant stretch cells.

Paternally rescued embryos derived from females containing homozygous germ-line clones lack abdominal segment 5 and part of abdominal segment 4. These embryos form a defective tracheal system with several disruptions in the main trunk and many branches.

Mosaic egg chambers which are homozygous for hop2 in the germline (but not in the soma) are not fused and all contain 15 nurse cells and one oocyte.

When homozygous somatic clones are made in the egg chamber, defects in border cell migration are seen. Whenever the polar cells are mutant, a complete failure in border cell migration is seen. However, in egg chambers in which the germ-line is mutant, no migration defect is seen. Nor are border cell defects seen when large clones are made in the rest of the follicle cell epithelium. In mutant egg chambers outer border cell clusters consist of an average of 2.1 cells, as compared to 6 in wild-type.

Mutant adult testes contain hub cells but lack stem cells and spermatogonia. A few spermatocytes and terminal epithelial cells remain.

hop2 somatic clones in the eye are rare and have a cell autonomous growth disadvantage when compared to their wildtype twins. They occasionally have missing photoreceptor cells and polarity defects. In the rare larger clones a striking cell non-autonomous effect is seen. Ommatidia at the polar margin of the clones reverse their polarity such that the ommatidia point away rather than toward the equator, thus creating an ectopic equator. When a clone is observed very close to the dorso-ventral midline, the equator was deflected away and formed along the border of the clone. Most of the ommatidia with reversed polarity were composed entirely of wild-type photoreceptor cells. This effect was seen in both dorsal and ventral halves of the eye.

Homozygous clones in the eye show a regular array of ommatidia which contain the wild-type complement of correctly differentiated and positioned photoreceptor cells within the ommatidia. A large proportion of homozygous clones in the eye result in polarity defects in which ommatidia straddling the polar boundary of the clone show inverted dorsoventral polarity. The phenotype is strongest in larger clones and in clones in which the polar boundary runs parallel to the equator of the eye. Typically, one or two rows of ommatidia are inverted, with the strongest phenotype seen having about five inverted rows. Both totally mutant ommatidia adjacent to the polar boundary of the clone and mosaic ommatidia at the clonal border can assume an inverted fate, and occasionally, an ommatidial cluster immediately outside the clone in which all the photoreceptors are wild type is seen to have inverted polarity. Mutant ommatidia in the centre of the clone and on the equatorial margin of the clone show normal orientation. This phenotype is seen in both adults and third larval instar imaginal discs.

hop2 embryos derived from homozygous female germ line clones show loss of the fifth abdominal denticle band and the posterior mid-ventral portion of the fourth band. Variable reduction of the second thoracic and eighth abdominal denticle bands and variable fusion of the sixth and seventh denticle bands is seen.

Maternal effect segmentation phenotype is similar to that caused by loss of Stat92E activity during embryogenesis. Both paternally rescued and unrescued embryos show a consistent deletion of the fifth abdominal segment and the posterior midventral portion of the fourth abdominal segment. Additional defects are seen in the head and tail of the unrescued embryos.

Larval diploid imaginal tissues are reduced in size. Embryos derived from females lacking hop die with characteristic segmentation defects, deletion of the fifth abdominal denticle belt and posterior mid-ventral portion of the fourth abdominal denticle belt.

Paternal rescue of the maternal effect. Germline clone analysis demonstrates that embryos have one abdominal segment missing and A4 appears wider than wild type, and partial or complete fusion of T1 and T2.

larval/pupal lethal

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
NOT Enhancer of
Suppressor of

hop2/hop[+] is a suppressor | partially of visible phenotype of upd1GMR.PB

hop2/hop[+] is a suppressor | partially of abnormal size | adult stage phenotype of upd1GMR.PB

Phenotype Manifest In
Suppressed by
Enhancer of
NOT Enhancer of
Suppressor of

hop2/hop[+] is a suppressor | partially of eye phenotype of upd1GMR.PB

NOT Suppressor of

hop2/hop2 is a non-suppressor of denticle belt | maternal effect phenotype of tor12D

Additional Comments
Genetic Interactions

The melanotic tumour phenotype caused by expression of gcmDN.Scer\UAS.T:en-Rep under the control of Scer\GAL4srp.D.cCa (the animals also carry Scer\GAL80ts.αTub84B which has been inactivated by shifting to the restrictive temperature) is completely suppressed in a hop2/Y background.

The ectopic wing vein and arching of wing vein L3 phenotypes caused by expression of Socs44AScer\UAS.cRa under the control of Scer\GAL4en-e16E are enhanced by hop2/+.

The enlarged eye phenotype seen in flies carrying one copy of upd1GMR.PB is moderately suppressed by one copy of hop2.

The loss of denticle belt A5 and gap in denticle belt A4 seen in hop2 germ-line clone embryos is suppressed by Cdk4hs.PC, or CycEhs.PO, although in both cases the two rescued denticle belts tend to fuse with each other laterally.

Expression of Socs36EAct5C.T:Ivir\HA1 under the control of Scer\GAL4en-e16E in a hop2/+ background induces ectopic vein formation in 17-26% of wings and the size and penetrance of the humeral outgrowth phenotype is increased.

The extra number of ommatidia caused by expression of osScer\UAS.cCa under the control of Scer\GAL4GMR.PF is partially suppressed by hop2/+; the flies have an average of 854 +/- 9 ommatidia.

The extra number of ommatidia caused by expression of upd1Scer\UAS.cCa under the control of Scer\GAL4GMR.PF is partially suppressed by hop2/+; the flies have an average of 854 +/- 9 ommatidia.

Xenogenetic Interactions

Heterozygosity for hop2 does not modify the fully penetrant rough eye phenotype resulting from the co-expression of HPV18\E6Scer\UAS.T:Hsap\MYC and Hsap\UBE3AScer\UAS.cRa under the control of Scer\GAL4GMR.PU, leading to severe eye necrosis.

The increased number of apoptotic cells in the brain of adult flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4repo.PU (using tub-Gal80[ts] to minimize the transgene expression during development) is increased further by combination with a single copy of hop2.

Complementation and Rescue Data

Expression of hopScer\UAS.cHa under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 rescues the germ-band extension and apical cell shape defects observed in hop2 germ-line clones.

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Stocks (2)
Notes on Origin



Fail to complement hop25.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (44)