FlyBase Allele Report: Dmel\hh[8]

The eyes of hh⁸/hh^bar3 flies are smaller than wild-type and are slightly rough, due to some disorganisation of ommatidial and inter-ommatidial structure.

(D'Costa et al., 2006)

Heterozygotes have wild-type eyes.

hh^bar3/hh⁸ flies have a slight rough eye phenotype.

(Jones et al., 2006)

Homozygous hh⁸ mutants are zygotic lethal and exhibit strong cuticle phenotypes.

hh⁸ heterozygotes are not significantly different from wild-type.

(Rogers et al., 2005)

Mutant embryos have a reduced number of visceral mesoderm parasegmental cells. The gastric caecum is virtually abolished in these embryos. When hh⁴/hh⁸ embryos are shifted from permissive to non-permissive temperatures for three hours during mid-stage 11 to stage 12, the majority have a short gastric caecum phenotype. While in about 10% one or few gastric caeca are lost and the size of those remaining is considerably reduced.

(Hosono et al., 2003)

Most mutant embryos show a reduction (approximately 50%) in the number of cells in tracheal pit 3. 71% of embryos show a reduction of tracheal cell number in pits 2, 4, 8 or 9. A small number of tracheal cells fail to invaginate at stage 11 and remain on the ectoderm. In the tracheal cells that do invaginate, there is a distinct failure of migration of all tracheal branches at stage 12. This phenotype is penetrant in all mutant embryos. The dorsal and visceral branches are never formed, while the dorsal trunk cells migrate partially, especially in the posterior segments. A reduced number of cells is allocated to the lateral trunk anterior branch. The correct cell number is allocated to the lateral trunk posterior in most segments. Minimal tracheal cell migration is seen beyond the residual migration seen at stage 12 (in contrast to wild type where pronounced tracheal cell migration is seen between stages 12 to 14), with the majority of the tracheal cells remaining in the transverse connective.

(Glazer and Shilo, 2001)

Bolwig's organ neurons are missing in mutant embryos.

(Suzuki and Saigo, 2000)

Denticle belts are made up of mostly type 5 denticles.

(Gritzan et al., 1999)

Homozygous embryos have severe head defects. The antennal sense organ is frequently duplicated.

(Gallitano-Mendel and Finkelstein, 1998)

Denticle belts are completely eliminated and the ventral surface of the cuticle is covered in a continuous lawn of denticles of similar size and random polarity.

(Quirk et al., 1997)

The hh⁴/hh⁸ combination istemperature sensitive: loss of hh function 6hrs AEL leads to loss of 1^o, 2^o and 3^o but not 4^o fates. Loss of hh function 7hrs AEL leads to loss of 1^o, 2^o but not 3^o and 4^o fates. In double mutants with ptc⁹, 1^o and 2^o cell types are restored.

(Bokor and DiNardo, 1996)

Most of the heart cells are missing in homozygous embryos. hh⁴/hh⁸ embryos raised at 29^oC throughout development exhibit a severely reduced heart, at 18^oC the number of heart cells is normal. Temperature shift experiments show heart formation is most sensitive between 3.5 and 4.5 hours of development. hh⁸, P{HS-wg} embryos kept at 25^oC exhibit lack of heart formation, 30 minutes of heat shock between 3 and 4 hours of development significantly restores heart development. hh⁸, P{HShh.I} embryos that are heat shocked between 3 and 4 hours of development exhibit rescue (and hypertrophy) of heart precursors.

(Park et al., 1996)

Naked cuticle and polarity of the embryo is lost.

(van den Heuvel and Ingham, 1996)

Embryos exhibit a ventral cuticle phenotype.

(Porter et al., 1995)

hh^bar3/hh⁶ produces an intermediate reduced eye phenotype.

(Chiang and Beachy, 1994)

Mutant embryos have exclusively row-5-type denticles arranged in a disorganized pattern of ventral midline whorls, with no naked cuticle.

(Bejsovec and Wieschaus, 1993)

Lethal when in homozygous or heterozygous combination with hh^A, hh^AC, hh^AE or hh^AM.

(Lee et al., 1992)

Severe disruptions in the neuron pattern occur during germ-band shortening, may be due to widespread cell death in the CNS.

(Patel et al., 1989)

40% length of wild type larvae and exhibit a ventral lawn of denticles associated with the loss of naked cuticle from the ventral surface. No obvious segmentation.

(Mohler, 1988)

Strong phenotype. Mutant embryos show no obvious segmentation, and are 40% the length of wild type; denticles form a lawn arranged in a number of whorls on the ventral surface as a result of loss of naked cuticle.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

hh^bar3/hh⁸ has visible phenotype, enhanceable by snama^PX1/mnm[+]

(Jones et al., 2006)

hh^bar3/hh⁸ has visible phenotype, enhanceable by l(2)rQ313[+]/snama^rQ313

(Jones et al., 2006)

hh^bar3/hh⁸ has visible phenotype, enhanceable by snama¹/mnm[+]

(Jones et al., 2006)

Suppressed by

Statement

Reference

hh^bar3/hh⁸ has visible phenotype, suppressible by BRWD3^ram1

(D'Costa et al., 2006)

NOT suppressed by

Statement

Reference

hh^bar3/hh⁸ has visible phenotype, non-suppressible by BRWD3^s5349/BRWD3[+]

(D'Costa et al., 2006)

Suppressor of

Statement

Reference

hh[+]/hh⁸ is a suppressor of visible phenotype of ro^DOM

(Chanut et al., 2000)

Phenotype Manifest In

Enhanced by

Statement

Reference

hh^bar3/hh⁸ has eye phenotype, enhanceable by snama^PX1/mnm[+]

(Jones et al., 2006)

hh^bar3/hh⁸ has ommatidium phenotype, enhanceable by snama^PX1/mnm[+]

(Jones et al., 2006)

hh^bar3/hh⁸ has eye phenotype, enhanceable by l(2)rQ313[+]/snama^rQ313

(Jones et al., 2006)

hh^bar3/hh⁸ has ommatidium phenotype, enhanceable by l(2)rQ313[+]/snama^rQ313

(Jones et al., 2006)

hh^bar3/hh⁸ has eye phenotype, enhanceable by snama¹/mnm[+]

(Jones et al., 2006)

hh^bar3/hh⁸ has ommatidium phenotype, enhanceable by snama¹/mnm[+]

(Jones et al., 2006)

Suppressed by

Statement

Reference

hh^bar3/hh⁸ has eye phenotype, suppressible by BRWD3^ram1

(D'Costa et al., 2006)

hh^bar3/hh⁸ has ommatidium phenotype, suppressible by BRWD3^ram1

(D'Costa et al., 2006)

Suppressor of

Statement

Reference

hh^AC/hh⁸ is a suppressor of abdominal ventral acute muscle 1 founder cell | increased number phenotype of Scer\GAL4^Mef2.PR, wg^UAS.cGa

(Cox and Baylies, 2005)

hh^AC/hh⁸ is a suppressor of abdominal ventral acute muscle 2 founder cell | increased number phenotype of Scer\GAL4^Mef2.PR, wg^UAS.cGa

(Cox and Baylies, 2005)

hh^AC/hh⁸ is a suppressor of abdominal ventral acute muscle 3 founder cell | increased number phenotype of Scer\GAL4^Mef2.PR, wg^UAS.cGa

(Cox and Baylies, 2005)

hh[+]/hh⁸ is a suppressor of ommatidium phenotype of amos^Roi-1

(Chanut et al., 2002)

hh[+]/hh⁸ is a suppressor of eye phenotype of ro^DOM

(Chanut et al., 2000)

Other

Statement

Reference

BRWD3^s5349/BRWD3[+], hh^bar3/hh⁸ has rhabdomere phenotype

(D'Costa et al., 2006)

hh⁸, trr¹ has eye phenotype

(Sedkov et al., 2003)

Additional Comments

Genetic Interactions

Statement

Reference

The presense of BRWD3^s5349/+ does not significantly affect the size or roughness of eye in hh⁸/hh^bar3 flies. However, retinal sections reveal the presence of small rhabdomeres in these eyes, which are not present in the eyes of hh⁸/hh^bar3 animals in the absence of BRWD3^s5349/+.

(D'Costa et al., 2006)

hh⁸ dominantly suppresses the amos^Roi-1/+ phenotype; at least 50% of the ommatidia have normal structure and orientation in double heterozygotes.

(Chanut et al., 2002)

Has no effect on the eye phenotype produced by activated arm constructs. (either arm^S44Y.GMR or arm^S56F.GMR).

(Freeman and Bienz, 2001)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially rescued by

hh⁸ is partially rescued by Scer\GAL4^btl.PS/hh^UAS.cIa

(Glazer and Shilo, 2001)

hh⁸ is partially rescued by hh^UAS.cKa/Scer\GAL4^da.G32

(Suzuki and Saigo, 2000)

hh⁸ is partially rescued by hh^UAS.cKa/Scer\GAL4^h-1J3

(Suzuki and Saigo, 2000)

Comments

hh^Scer\UAS.cIa partially rescues the hh⁸ tracheal defects when expressed under the control of Scer\GAL4^btl.PS. In particular, rescue of the dorsal trunk, visceral branches and some lateral trunk anterior branches is seen. The ectodermal defects are not rescued in these embryos.

(Glazer and Shilo, 2001)

The lack of Bolwig's organ neurons seen in hh⁸ embryos is partially rescued by hh^Scer\UAS.cKa expressed under the control of either Scer\GAL4^h-1J3 or Scer\GAL4^da.G32.

(Suzuki and Saigo, 2000)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

Allelic series in terms of phenotype severity: hh³ > hh⁸ > hh⁴.

(Glazer and Shilo, 2001)

Strong allele of hh.

(Mohler, 1988)

Mutations in hh enhance the wg phenotype.

(Bejsovec and Wieschaus, 1993)

Strong hh allele, strength based on severity of ventral cuticle phenotype.

(Porter et al., 1995)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

hh^13C26

(Patel et al., 1989)

hh^13C29

(Lee and Frasch, 2000, Azpiazu et al., 1996, D'Alessio and Frasch, 1996, Motzny and Holmgren, 1995, Bejsovec and Wieschaus, 1993)

hh^13c

(Biehs et al., 2010, Chanut et al., 2002, Suzuki and Saigo, 2000)

hh⁸

(Jones et al., 2006, Rogers et al., 2005)

Name Synonyms

Secondary FlyBase IDs

References (43)

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