FlyBase Allele Report: Dmel\hop[25]

hop³²/hop²⁵ mutant flies die more rapidly than do wild-type controls following Drosophila C virus (DCV) infection, and contain about 10-fold more virus.

Compared with wild-type, hop³²/hop²⁵ mutant flies show decreased survival and contain significantly more virus particles when injected with Cricket Paralysis Virus (CrPV).

(Kemp et al., 2013)

Approximately 68% of adult hemizygous male escapers lose locomotor activity rhythms under constant darkness conditions

(Luo and Sehgal, 2012)

Stalks form in early hop³/hop²⁵ egg chambers and the oocyte moves to the posterior of the egg chamber as in wild type. However, the stalk cells fail to intercalate and the stalk consists of two rows of cells linked by adherens junctions. At later stages, the stalks collapse and fusions between egg chambers are seen.

(Assa-Kunik et al., 2007)

hop³²/hop²⁵ flies infected with Drosophila C virus have increased levels of viral RNA and viral capsid proteins than infected wild-type flies. hop³²/hop²⁵ flies show reduced survival compared to wild-type flies when injected with a low dose (1 x 10² LD₅₀) of Drosophila C virus.

(Dostert et al., 2005)

hop²⁵/hop³² animals have an ectopic vein near the posterior crossvein of the wing.

(Rawlings et al., 2004)

The mean ln (natural logarithm) circulating hemocyte concentration (CHC) value of hemizygous larvae is significantly higher than that of control siblings. The ability of hemizygous larvae to encapsulate L.boulardi eggs is significantly reduced compared to that of control larvae.

(Sorrentino et al., 2004)

There is no nuclear translocation of Stat92E protein into the nuclei of cells in the fat body in response to challenge with bacteria in hop²⁵/hop³² mutant adult flies.

(Agaisse et al., 2003)

Embryos derived from mothers carrying hop²⁵ germ-line clones have weak segmentation defects, visible as gaps and malformations of abdominal ventral denticle belts, particularly A4, A5 and A7. Many of these embryos hatch.

(Chen et al., 2003)

hop²⁵/hop² egg chambers lack border follicle cells and have reduced numbers of stretched (nurse) follicle cells and posterior follicle cells, but increased numbers of main body (oocyte) follicle cells. Nurse follicle cell and centripetally migrating follicle cell domains are shifted posteriorly.

(Xi et al., 2003)

hop²⁵/hop³ mutant females have reduced fertility and fused egg chamber phenotype.

(Baksa et al., 2002)

hop²⁵/hop³ ovaries often have compound egg chambers. The chambers contain multiple germline cysts each with its own oocyte and the chambers contain a multiple of 15 ring canals per chamber, indicating that these compound chambers are due to fusion or improper incapsulation of germline cysts rather than extra rounds of germline proliferation. hop²⁵/hop³ egg chambers have extra polar follicle cells. hop²⁵/hop³² females show extensive fusion of egg chambers and stalk cells are rare or absent. hop²⁵/hop³³ non-fused egg chambers often have extra polar follicle cells (having 3 or 4 cells rather than the normal number of 2 polar cells at both the anterior and posterior ends of the egg chamber). At stage 8/9, 93% of egg chambers have extra polar cells at the anterior end and 67% of egg chambers have extra polar cells at the posterior end. The number of interfollicular cells is reduced. The extra polar cells do not appear to be due to continued proliferation of the polar cell population. hop²⁵/hop²⁷ non-fused egg chambers sometimes have extra polar follicle cells (generally having 3 rather than the normal number of 2 polar cells at both the anterior and posterior ends of the egg chamber). At stage 8/9, 13% of egg chambers have extra polar cells at the anterior end and 36% of egg chambers have extra polar cells at the posterior end. The extra polar cells do not appear to be due to continued proliferation of the polar cell population. 5% of hop²⁵/hop²⁷ egg chambers are fused.

(McGregor et al., 2002)

Adult mutant males lack renewing germ line. The testes are shorter than normal and contain several bundles of elongated spermatids but completely lack early germ cell stages. Mutant embryonic gonads contain the normal number of primordial germ cells. Loss of stem cells is seen in mutant testes by the first larval instar, becoming more apparent in the second larval instar. Single germ cells are not detected at the apical tip of mutant first and second larval instar testes (in contrast to wild type), instead, the testes contain only a few clusters of differentiating germ cells, which resemble spermatogonia or early spermatocytes. 35% of mutant third larval instar testes have no somatic cyst progenitor cells (CPCs). The number of early cyst cells is dramatically reduced in the remaining 65% of testes. Somatic apical hub cells appear normal.

(Kiger et al., 2001)

Mutant adult testes contain hub cells but lack stem cells and spermatogonia.

(Tulina and Matunis, 2001)

hop²⁵/hop³ females show a mild reduction in eye size and show roughness in the equatorial region, within which ommatidial fusion and duplicated bristles can be seen. hop²⁵/hop³² females can have eyes that are smaller in the dorso-ventral axis with significantly fewer ommatidia compared to wild-type. Ommatidia are arranged irregularly and duplicated bristles are seen. hop²⁵/hop³² females with an eyeless phenotype with a concomitant duplication of the antenna can also be seen. In hop²⁵ homozygotes misrotation and chirality change is seen in the ommatidia. In hop²⁵/hop³ females a loss of photoreceptor cells is seen, misrotations and loss of ommatidial chirality is seen.

(Luo et al., 1999)

Homozygotes show 25% viability. 100% viable in transheterozygous combination with hop²⁷, hop¹⁴, hop³ or hop¹². 70% viable in transheterozygous combination with hop³³, 50% viable in transheterozygous combination with hop³², 5% viable in transheterozygous combination with hop^M637 and 2% viable in transheterozygous combination with hop²⁹.

(Harrison et al., 1998)

Embryos derived from homozygous mothers show weak segmentation defects. This phenotype is exacerbated by reduction of Stat92E dosage.

(Hou et al., 1996)

Semilethal: 9% of viability.

(Zhimulev et al., 1987)

Homozygous females are less viable than hemizygous males. Hemizygous males have rudimentary testes that do not mature properly and hemizygous or homozygous females have atrophic gonads and no egg chambers are detectable. 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)

The viability and fertility of both male and female flies is adversely affected by this mutation. Hemizygous males have rudimentary testes, which either lack gametes, or contain gametes ranging from early stages to the spermatid stage. Spermatid maturation is abnormal and terminates at an early stage. Axonemes are incomplete or degenerate, and many mitochondrial derivatives are associated with membranes other than the axonemal sheath.

(Dybas et al., 1983)

Mutation blocks gene functions that are critical to the development of both reproductive and non-reproductive tissues. Testes devoid of gametes.

(Geer et al., 1983)

viability and fertility poor in males and females. Testes of hemizygous males are usually rudimentary and lack sperm; ovaries of homozygous and hemizygous females usually abnormal, lack egg chambers <up>believed to be somatic defect since eggs appear normal when allele is analyzed in germ-line clones (Perrimon and Mahowald, 1986a)</up>. hop²⁹/hop²⁵ 12% viable hop³/hop²⁵ 16% viable hop¹⁴/hop²⁵ 40% viable hop¹²/hop²⁵ 68% viable hop²⁷/hop²⁵ 100% viable hop³²/hop²⁵ 100% viable hop³³/hop²⁵ 100% viable

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

hop²⁵ has partially lethal - majority die | embryonic stage | maternal effect phenotype, enhanceable by Cdk4³/Cdk4[+]

(Chen et al., 2003)

hop²⁵/hop²⁹ has lethal phenotype, enhanceable by upd1^YM55

(Harrison et al., 1998)

hop³³/hop²⁵ has partially lethal phenotype, enhanceable by upd1^YM55

(Harrison et al., 1998)

hop³/hop²⁵ has partially lethal phenotype, enhanceable by upd1^YM55

(Harrison et al., 1998)

hop^M637/hop²⁵ has lethal phenotype, enhanceable by upd1^YM55

(Harrison et al., 1998)

hop³²/hop²⁵ has partially lethal phenotype, enhanceable by upd1^YM55

(Harrison et al., 1998)

Enhancer of

Statement

Reference

hop²⁵ is an enhancer of visible phenotype of Df(1)os¹

(Tsai and Sun, 2004)

Other

Statement

Reference

Scer\GAL4^en-e16E, Socs44A^UAS.cRa, hop³²/hop²⁵ has lethal phenotype

(Rawlings et al., 2004)

Scer\GAL4^en-e16E, Socs44A^UAS.cRa, hop³/hop²⁵ has lethal phenotype

(Rawlings et al., 2004)

Scer\GAL4^en-e16E, Socs44A^UAS.cRa, hop³³/hop²⁵ has lethal phenotype

(Rawlings et al., 2004)

hop²⁵, upd1^YM55 has lethal | recessive phenotype

(Harrison et al., 1998)

Phenotype Manifest In

Enhanced by

Statement

Reference

hop²⁵ has abdominal 4 ventral denticle belt | maternal effect | germline clone phenotype, enhanceable by Cdk4³/Cdk4[+]

(Chen et al., 2003)

hop²⁵ has abdominal 5 ventral denticle belt | maternal effect | germline clone phenotype, enhanceable by Cdk4³/Cdk4[+]

(Chen et al., 2003)

hop²⁵ has abdominal 7 ventral denticle belt | maternal effect | germline clone phenotype, enhanceable by Cdk4³/Cdk4[+]

(Chen et al., 2003)

hop²⁷/hop²⁵ has egg chamber phenotype, enhanceable by os[+]/upd1^YM55

(McGregor et al., 2002)

hop²⁷/hop²⁵ has polar follicle cell | increased number phenotype, enhanceable by os[+]/upd1^YM55

(McGregor et al., 2002)

hop²⁷/hop²⁵ has egg chamber phenotype, enhanceable by upd1^YC43/os[+]

(McGregor et al., 2002)

Suppressed by

Statement

Reference

hop³²/hop²⁵ has wing vein | ectopic phenotype, suppressible | partially by +/Df(2R)CA53

(Rawlings et al., 2004)

hop³²/hop²⁵ has wing vein | ectopic phenotype, suppressible | partially by Df(2R)NCX10/+

(Rawlings et al., 2004)

NOT suppressed by

Statement

Reference

hop³²/hop²⁵ has wing vein | ectopic phenotype, non-suppressible by Df(2R)Drl^rv18/+

(Rawlings et al., 2004)

Enhancer of

Statement

Reference

hop²⁵ is an enhancer of eye phenotype of Df(1)os¹

(Tsai and Sun, 2004)

Suppressor of

Statement

Reference

hop[+]/hop²⁵ is a suppressor of eye phenotype of Scer\GAL4^ey.PH, Ser^UAS.cSa

(Reynolds-Kenneally and Mlodzik, 2005)

hop[+]/hop²⁵ is a suppressor of eye phenotype of Delta^UAS.cHa, Scer\GAL4^ey.PH

(Reynolds-Kenneally and Mlodzik, 2005)

hop²⁵ is a suppressor of testis phenotype of Scer\GAL4^{VP16.nanos.UTR}, upd1^UAS.cZa

(Kiger et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

Heterozygosity for hop²⁵ supresses the large eye phenotype of Scer\GAL4^ey.PH > Ser^Scer\UAS.cSa and Scer\GAL4^ey.PH > Dl^Scer\UAS.cHa flies.

(Reynolds-Kenneally and Mlodzik, 2005)

The penetrance of the ectopic wing vein phenotype seen in hop²⁵/hop³² animals (98%) is decreased by Df(2R)CA53/+ (46%) or Df(2R)NCX10/+ (58%), but is not significantly decreased by Df(2R)Drl^rv18/+ (87%).

(Rawlings et al., 2004)

Df(1)os¹, hop²⁵/Y males have no eyes.

(Tsai and Sun, 2004)

hop²⁵ does not modify the enlarged eye phenotype seen in flies carrying one copy of upd1^GMR.PB.

(Bach et al., 2003)

The weak segmentation defects of embryos derived from mothers carrying hop²⁵ germ-line clones are enhanced when these mothers are heterozygous for Cdk4³ : this is particularly noticeable for denticle belts A4 and A5 which are lost completely in such embryos. None of these embryos hatch.

(Chen et al., 2003)

75% of hop²⁵ upd1^YC43/hop²⁷ egg chambers are fused.

92% of hop²⁵ upd1^YM55/hop²⁷ egg chambers are fused and the number of extra polar cells is increased compared to hop²⁵/hop²⁷ single mutants.

(McGregor et al., 2002)

The viability of homozygotes or transheterozygotes with hop²⁷, hop¹⁴, hop³, hop¹², hop³³, hop³², hop^M637 or hop²⁹ is reduced in all cases if the flies also carry os^upd-4.

(Harrison et al., 1998)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

hop²⁵ is rescued by hop^T-r7.Act5C

(Kiger et al., 2001)

hop²⁵ is rescued by hop^T-r7.Act5C

(Luo et al., 1995)

Comments

Male hemizygous sterility can be rescued by one copy of P{Act/T-r7}.

(Luo et al., 1995)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Geer.

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (13)

Reported As

Symbol Synonym

MSV1

(Geer et al., 1983)

hop-msv1

(Kiger and Fuller, 1999)

hop²⁵

(Shen et al., 2022, Nagai et al., 2021, Xing and Li, 2015, Luo and Sehgal, 2012, Jiang et al., 2011, Popodi et al., 2010-)

hop^MSV1

(Luo and Dearolf, 2001)

hop^Msv1

(Oh et al., 2004)

hop^msv1

(Lamiable et al., 2016, Buchon et al., 2009, Brun et al., 2006, Dostert et al., 2005, Reynolds-Kenneally and Mlodzik, 2005, Agaisse and Perrimon, 2004, Sorrentino et al., 2004, Tsai and Sun, 2004, Agaisse et al., 2003, Bach et al., 2003, Chen et al., 2003, Baksa et al., 2002, Boutros et al., 2002, Luo et al., 1999, Hou and Perrimon, 1997, Hou et al., 1996, Zhimulev et al., 1987)

hop^msv

(Rawlings et al., 2004, Xi et al., 2003, McGregor et al., 2002, Devanaboyina and Harrison, 1998)

hop^msvi

(Assa-Kunik et al., 2007)

hop^msvl

(Harrison et al., 1998)

hop^mv1

(Assa-Kunik et al., 2007)

l(1)hop^msv1

(Perrimon and Mahowald, 1986)

ms(1)v1

(Dybas et al., 1983, Geer et al., 1983)

msv1

(Kemp et al., 2013, Kiger and Fuller, 1998, Luo et al., 1995)

Name Synonyms

Secondary FlyBase IDs

References (41)

Report Sections

Open Close