FlyBase Allele Report: Dmel\hop[2]

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.

(Bertet et al., 2009)

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.

(Josten et al., 2004)

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.

(Chen et al., 2003)

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.

(Johansen et al., 2003)

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.

(Li et al., 2003)

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.

(Xi et al., 2003)

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.

(Beccari et al., 2002)

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.

(Chen et al., 2002)

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.

(McGregor et al., 2002)

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.

(Silver and Montell, 2001)

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

(Tulina and Matunis, 2001)

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.

(Luo et al., 1999)

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.

(Zeidler et al., 1999)

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.

(Harrison et al., 1998)

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.

(Hou et al., 1996)

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.

(Binari and Perrimon, 1994)

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.

(Perrimon and Mahowald, 1986)

larval/pupal lethal

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

hop²/hop[+] is an enhancer of increased cell death | adult stage phenotype of Hsap\MAPT^UAS.cWa, Scer\GAL4^repo.PU, Scer\GAL80^ts.αTub84B

(Colodner and Feany, 2010)

hop²/hop[+] is an enhancer of visible phenotype of Scer\GAL4^en-e16E, Socs44A^UAS.cRa

(Rawlings et al., 2004)

hop²/hop[+] is an enhancer of visible phenotype of Scer\GAL4^en-e16E, Socs36E^UASp.cCa

(Callus and Mathey-Prevot, 2002)

NOT Enhancer of

Statement

Reference

hop²/hop[+] is a non-enhancer of visible | adult stage phenotype of HPV18\E6^UAS.Tag:MYC, Hsap\UBE3A^UAS.cRa, Scer\GAL4^GMR.PU

(Padash Barmchi et al., 2016)

Suppressor of

Statement

Reference

hop² is a suppressor of melanotic mass phenotype | heat sensitive phenotype of Scer\GAL4^srp.D.cCa, Scer\GAL80^ts.αTub84B, gcm^DN.UAS

(Jacques et al., 2009)

hop²/hop[+] is a suppressor of visible phenotype of Scer\GAL4^GMR.PF, upd1^UAS.cCa

(Chen et al., 2002)

Phenotype Manifest In

Suppressed by

Statement

Reference

hop² has abdominal 4 ventral denticle belt | germline clone | maternal effect phenotype, suppressible by CycE^hs.PO

(Chen et al., 2003)

hop² has abdominal 5 ventral denticle belt | germline clone | maternal effect phenotype, suppressible by Cdk4^hs.PC

(Chen et al., 2003)

hop² has abdominal 5 ventral denticle belt | germline clone | maternal effect phenotype, suppressible by CycE^hs.PO

(Chen et al., 2003)

hop² has abdominal 4 ventral denticle belt | germline clone | maternal effect phenotype, suppressible by Cdk4^hs.PC

(Chen et al., 2003)

Enhancer of

Statement

Reference

hop²/hop[+] is an enhancer of adult brain phenotype of Hsap\MAPT^UAS.cWa, Scer\GAL4^repo.PU, Scer\GAL80^ts.αTub84B

(Colodner and Feany, 2010)

hop²/hop[+] is an enhancer of wing vein | ectopic phenotype of Scer\GAL4^en-e16E, Socs44A^UAS.cRa

(Rawlings et al., 2004)

hop²/hop[+] is an enhancer of wing vein L3 phenotype of Scer\GAL4^en-e16E, Socs44A^UAS.cRa

(Rawlings et al., 2004)

hop²/hop[+] is an enhancer of wing phenotype of Scer\GAL4^en-e16E, Socs36E^UASp.cCa

(Callus and Mathey-Prevot, 2002)

NOT Enhancer of

Statement

Reference

hop²/hop[+] is a non-enhancer of eye phenotype of HPV18\E6^UAS.Tag:MYC, Hsap\UBE3A^UAS.cRa, Scer\GAL4^GMR.PU

(Padash Barmchi et al., 2016)

Suppressor of

Statement

Reference

hop² is a suppressor of melanotic mass | heat sensitive phenotype of Scer\GAL4^srp.D.cCa, Scer\GAL80^ts.αTub84B, gcm^DN.UAS

(Jacques et al., 2009)

hop²/hop[+] is a suppressor of eye phenotype of Scer\GAL4^GMR.PF, upd1^UAS.cCa

(Chen et al., 2002)

hop²/hop[+] is a suppressor of ommatidium | increased number phenotype of Scer\GAL4^GMR.PF, upd1^UAS.cCa

(Chen et al., 2002)

NOT Suppressor of

Statement

Reference

hop²/hop² is a non-suppressor of ventral denticle belt | maternal effect phenotype of tor^12D

(Li et al., 2002)

Other

Statement

Reference

Scer\GAL4^en-e16E, Socs36E^UASp.cCa, hop²/hop[+] has wing vein | ectopic phenotype

(Callus and Mathey-Prevot, 2002)

Scer\GAL4^en-e16E, Socs36E^UASp.cCa, hop² has wing vein | ectopic phenotype

(Callus and Mathey-Prevot, 2002)

da², hop²/hop[+] has follicle cell phenotype

(Smith et al., 2002)

da², hop² has follicle cell phenotype

(Smith et al., 2002)

Additional Comments

Genetic Interactions

Statement

Reference

The melanotic tumour phenotype caused by expression of gcm^{DN.Scer\UAS.T:en-Rep} under the control of Scer\GAL4^srp.D.cCa (the animals also carry Scer\GAL80^ts.αTub84B which has been inactivated by shifting to the restrictive temperature) is completely suppressed in a hop²/Y background.

(Jacques et al., 2009)

The ectopic wing vein and arching of wing vein L3 phenotypes caused by expression of Socs44A^Scer\UAS.cRa under the control of Scer\GAL4^en-e16E are enhanced by hop²/+.

(Rawlings et al., 2004)

The enlarged eye phenotype seen in flies carrying one copy of upd1^GMR.PB is moderately suppressed by one copy of hop².

(Bach et al., 2003)

The loss of denticle belt A5 and gap in denticle belt A4 seen in hop² germ-line clone embryos is suppressed by Cdk4^hs.PC, or CycE^hs.PO, although in both cases the two rescued denticle belts tend to fuse with each other laterally.

(Chen et al., 2003)

Expression of Socs36E^{Act5C.T:Ivir\HA1} under the control of Scer\GAL4^en-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.

(Callus and Mathey-Prevot, 2002)

The extra number of ommatidia caused by expression of upd1^Scer\UAS.cCa under the control of Scer\GAL4^GMR.PF is partially suppressed by hop²/+; the flies have an average of 854 +/- 9 ommatidia.

The extra number of ommatidia caused by expression of os^Scer\UAS.cCa under the control of Scer\GAL4^GMR.PF is partially suppressed by hop²/+; the flies have an average of 854 +/- 9 ommatidia.

(Chen et al., 2002)

Xenogenetic Interactions

Statement

Reference

Heterozygosity for hop² does not modify the fully penetrant rough eye phenotype resulting from the co-expression of HPV18\E6^{Scer\UAS.T:Hsap\MYC} and Hsap\UBE3A^Scer\UAS.cRa under the control of Scer\GAL4^GMR.PU, leading to severe eye necrosis.

(Padash Barmchi et al., 2016)

The increased number of apoptotic cells in the brain of adult flies expressing Hsap\MAPT^Scer\UAS.cWa under the control of Scer\GAL4^repo.PU (using tub-Gal80[ts] to minimize the transgene expression during development) is increased further by combination with a single copy of hop².

(Colodner and Feany, 2010)

Complementation and Rescue Data

Rescued by

hop² is rescued by hop^UAS.cHa/Scer\GAL4^{VP16.mat.αTub67C}

(Bertet et al., 2009)

hop² is rescued by hop^T-r7.Act5C

(Luo et al., 1995)

Comments

Expression of hop^Scer\UAS.cHa under the control of Scer\GAL4^{mat.αTub67C.T:Hsim\VP16} rescues the germ-band extension and apical cell shape defects observed in hop² germ-line clones.

(Bertet et al., 2009)

Images (0)

Mutant

Wild-type

Stocks (2)

6032

108563

Notes on Origin

Discoverer

Lefevre.

G. Lefevre.

(Binari and Perrimon, 1994)

Comments

Fail to complement hop²⁵.

(Perrimon and Mahowald, 1986)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

C111

(Chen et al., 2002)

hop²

(Lai et al., 2023, Xu et al., 2019, Fregoso Lomas et al., 2016, Padash Barmchi et al., 2016, Santabárbara-Ruiz et al., 2015, Stratoulias and Heino, 2015, Colodner and Feany, 2010, Popodi et al., 2010-, Jacques et al., 2009)

hop^CIII

(Luo et al., 1995)

hop^c111

(Almudi et al., 2009, Rawlings et al., 2004, Xi et al., 2003, McGregor et al., 2002, Rennebeck et al., 2002, Silver and Montell, 2001, Harrison et al., 1998)

l(1)C111

l(1)hop^C111

(Perrimon and Mahowald, 1986)

Name Synonyms

Secondary FlyBase IDs

References (45)

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