FlyBase Allele Report: Dmel\dpp[H46]

Newly formed spectrosomes in primordial germ cells of stage 11-12 dpp^H46 embryos are similar in size and morphology to wild-type of the same age. In older embryos, differences are readily apparent and the spectrosomes in dpp^H46 primordial germ cells fall into three classes. Primordial germ cells in the first class (39%) resemble wild-type and have a single large spherical spectrosome. The second class (28%) display either small diffusely stained spectrosomes or several small fragmented spectrosomes. In the third and final class (33%), primordial germ cells have no spectrosome and can be deformed and irregular in appearance.

(Deshpande et al., 2014)

dpp^H46 mutant embryos occasionally show fusion of the embryonic denticle belts.

(Eivers et al., 2009)

dpp^H46 exhibit a phenotype in the development of the dorsal head. The dorso-median strip of epidermis that normally separates the placodes is absent and replaced by hyperplastic placodes in stage 12 embryos.

(de Velasco et al., 2007)

dpp^H46 clones generated in the wing at 22-26 hours after pupariation (AP), using the Minute technique, have no effect on venation when they are limited to one surface of the wing. When there is overlap between dpp^H46 clones on the dorsal and ventral surfaces, there is no consistent cell-autonomous disruption of the posterior crossvein (PCV) within regions of overlap. However, a slight disruption of the posterior end of the PCV, largely outside the region of the clone, has been observed in one case. When overlapping clones cover the region of the fourth longitudinal vein normally intersected by the PCV, the anterior of the PCV can be disrupted.

(Ralston and Blair, 2005)

The corpus cardiacum is normal in size in mutant embryos, but shows defects in migration.

(De Velasco et al., 2004)

In stage-15 dpp^H46 mutant embryos, the lymph gland, cardioblasts and pericardial nephrocytes fail to develop from the cardiogenic mesoderm.

(Mandal et al., 2004)

The average number of crystal cells per embryo is significantly reduced in homozygous stage 13-14 embryos compared to wild type.

(Milchanowski et al., 2004)

In dpp^H46 homozygotes cycle 14 mitotic domains 1 and 5 are fused across the midline, and domain 3 is absent.

(Sutherland et al., 2003)

Ventral denticle belts cover the whole epidermis in mutant embryos.

(Oh et al., 2002)

Head midline epidermis does not form in mutant embryos, with both midline and dorsolateral regions showing characteristics of lateral neuroectoderm. Optic lobe and Bolwig's organ are absent. The dorsal head ectoderm is "invaded" by protocerebral neuroblasts.

(Chang et al., 2001)

Homozygous clones in the wing have no effect on the posterior cross vein (PCV) unless both dorsal and ventral surfaces are homozygous ("double-sided" clones). Double-sided clones that cover half the PCV show loss of the vein in the mutant clone up to or within 2 to 3 cells of the clone boundary. Vein L4 can also be truncated in clones.

(Ray and Wharton, 2001)

The hindgut of mutant embryos is significantly shorter than that of wild-type embryos. Incorporation of BrdU in the large intestine is abolished in mutant embryos.

(Takashima and Murakami, 2001)

Gnathal morphology is severely disrupted in mutant embryos.

(Rusch and Kaufman, 2000)

The cuticle of homozygous embryos consists only of ventral epidermis. This phenotype is not altered if the embryos are derived from homozygous dl¹ females. brk^M68; dpp^H46 sna¹⁸ Df(2R)twi quadruple mutant embryos secrete cuticles showing partial transformation of ventral into dorsal epidermis.

(Jazwinska et al., 1999)

Gonadal mesoderm development is largely unaffected in mutants. Germ cells do not migrate from endoderm to mesoderm, presumably due to the gastrulation defects.

(Broihier et al., 1998)

Embryos are strongly ventralised and germ band extension is abnormal.

(Carmena et al., 1998)

Fat body precursor cells do develop in dpp^H46 embryos.

(Moore et al., 1998)

Homozygous clones induced in first instar larvae produce abnormalities in the dorsal side of the leg. Pattern elements from the dorsal side are missing. Occasional defects in the ventral side of the leg are also seen.

(Held and Heup, 1996)

Haploinsufficient.

(Frasch, 1995)

Suppresses the majority of pattern defects caused by Pka-C1^H2 clones in the wing, notum, halteres and antennae and partially suppresses defects in the ventral regions of the leg.

(Li et al., 1995)

Dominant lethality greater than 50%. Homozygous and transheterozygous embryos were examined with respect to 25 cuticular markers, results demonstrate a graded requirement for dpp along the dorso-ventral axis.

(Wharton et al., 1993)

Strong ventralised phenotype. Rings of ventral denticle belts differentiate around the entire dorsoventral axis, almost no dorsal hairs are seen and the antennal and maxillary sense organs are missing. Defective movements of the germ band: due to loss of the amnioserosa and because the dorsalmost cells have acquired the lateral fate of the dorsal ectoderm. Dorsal cell fates are deleted and ventrolateral mitotic domains are expanded.

(Arora and Nusslein-Volhard, 1992)

Ventralized embryos: rings or patches of ventral denticles along dorsoventral axis. Disruption of germ band extension that leads to the invagination of posterior segments into the interior of the embryo.

(Ray et al., 1991)

Fail to complete germ band extension, die with strong ventralized phenotype and no dorsal derived epidermis.

(St. Johnston et al., 1990)

Homozygotes have a ventralized embryonic phenotype: normally ventral epidermal pattern elements are present ventrally and dorsally.

(Irish and Gelbart, 1987)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

dpp^H46 has lethal | dominant phenotype, suppressible by Df(2L)Gpdh1-A/+

(Li et al., 2005)

dpp^H46 has lethal | dominant phenotype, suppressible by Su(dpp)YE10[+]/Su(dpp)YE10^YE10

(Li et al., 2005)

dpp^H46 has lethal | dominant phenotype, suppressible by Su(dpp)YE12[+]/Su(dpp)YE12^YE12

(Li et al., 2005)

dpp^H46 has lethal | dominant phenotype, suppressible by Su(dpp)YE28^YE28/Su(dpp)YE28[+]

(Li et al., 2005)

dpp^H46 has lethal | dominant phenotype, suppressible by Su(dpp)YE31^YE31/Su(dpp)YE31[+]

(Li et al., 2005)

dpp^H46 has lethal | dominant phenotype, suppressible by Su(dpp)YE5[+]/Su(dpp)YE5^YE5

(Li et al., 2005)

dpp^H46 has lethal | dominant phenotype, suppressible by Df(2L)Gpdh1-A/eIF4A^R321H.UAS/Scer\GAL4^{VP16.mat.αTub67C}

(Li et al., 2005)

dpp^H46 has lethal | dominant phenotype, suppressible by eIF-4a[+]/eIF4A^YE9

(Li et al., 2005)

dpp^H46 has lethal | dominant phenotype, suppressible by Su(dpp)YE2[+]/Su(dpp)YE2^YE2

(Li et al., 2005)

dpp^H46 has lethal | dominant phenotype, suppressible by Smurf^15C

(Podos et al., 2001)

NOT suppressed by

Statement

Reference

dpp^H46 has lethal phenotype, non-suppressible by Smurf^15C

(Podos et al., 2001)

Suppressor of

Statement

Reference

dpp^H46/dpp[+] is a suppressor of lethal | rescuable maternal effect phenotype of Smurf^15C

(Podos et al., 2001)

Phenotype Manifest In

Suppressed by

Statement

Reference

dpp^H46 has phenotype, suppressible by Su(dpp)39CDE[+]/Su(dpp)39CDE¹

(Murthy and Gelbart, 1999)

NOT suppressed by

Statement

Reference

dpp^H46 has cuticle phenotype, non-suppressible by Smurf^15C

(Podos et al., 2001)

Suppressor of

Statement

Reference

dpp^H46/dpp[+] is a suppressor of embryonic/first instar larval cuticle | maternal effect phenotype of tor^12D

(Li and Li, 2003)

dpp^H46/dpp[+] is a suppressor of embryonic/first instar larval cuticle | maternal effect phenotype of tor^13D

(Li and Li, 2003)

dpp^H46/dpp[+] is a suppressor of embryonic hindgut | rescuable maternal effect phenotype of Smurf^15C

(Podos et al., 2001)

dpp^H46 is a suppressor of somatic muscle cell | embryonic stage phenotype of Ras85D^G13Q.UAS, Scer\GAL4^unspecified

(Carmena et al., 1998)

dpp^H46 is a suppressor of wing | somatic clone phenotype of Pka-C1^H2

(Li et al., 1995)

dpp^H46 is a suppressor of scutum | somatic clone phenotype of Pka-C1^H2

(Li et al., 1995)

dpp^H46 is a suppressor of haltere | somatic clone phenotype of Pka-C1^H2

(Li et al., 1995)

dpp^H46 is a suppressor of antenna | somatic clone phenotype of Pka-C1^H2

(Li et al., 1995)

dpp^H46 is a suppressor of leg | somatic clone phenotype of Pka-C1^H2

(Li et al., 1995)

Additional Comments

Genetic Interactions

Statement

Reference

Maternal and zygotic homozygosity for lack^15C partially suppresses the dominant lethality of dpp^H46 (83% survival to adulthood), but has no effect on the lethality or cuticle phenotypes due to homozygosity for dpp^H46. Embryonic lethality due to maternal and zygotic homozygosity for lack^15C is partially suppressed (83% survival to adulthood) by heterozygosity for dpp^H46. The embryonic midgut phenotype of maternal and zygotic lack^15C/lack^15C embryos is fully suppressed by heterozygosity for dpp^H46.

(Podos et al., 2001)

The production of extra eve-positive mesodermal cells caused by expression of Ras85D^{G13Q.Scer\UAS} under the control of Scer\GAL4^unspecified is suppressed if the embryos are also carrying dpp^H46.

(Carmena et al., 1998)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

dpp^s6/dpp^H46 is rescued by dpp^Sal20

(Stultz et al., 2005)

Partially rescued by

dpp^H46/dpp^s11 is partially rescued by dpp^Sal20

(Stultz et al., 2005)

dpp^s20/dpp^H46 is partially rescued by dpp^Sal20

(Stultz et al., 2005)

dpp^s7/dpp^H46 is partially rescued by dpp^Sal20

(Stultz et al., 2005)

dpp^H46/dpp^s3 is partially rescued by dpp^Sal20

(Stultz et al., 2005)

dpp^s28/dpp^H46 is partially rescued by dpp^Sal20

(Stultz et al., 2005)

dpp^s26/dpp^H46 is partially rescued by dpp^Sal20

(Stultz et al., 2005)

Not rescued by

dpp^s6/dpp^H46 is not rescued by dpp^P15

(Stultz et al., 2005)

dpp^s7/dpp^H46 is not rescued by dpp^P15

(Stultz et al., 2005)

dpp^H46/dpp^s3 is not rescued by dpp^P15

(Stultz et al., 2005)

dpp^s26/dpp^H46 is not rescued by dpp^P15

(Stultz et al., 2005)

dpp^s13/dpp^H46 is not rescued by dpp^P15

(Stultz et al., 2005)

Comments

Mutant phenotype rescued by P element mediated transformation of a wild type copy of dpp.

(Hoffmann and Goodman, 1987)

Allele class: Hin

Images (0)

Mutant

Wild-type

Stocks (5)

Bloomington

604827

y^* w^*; dpp^H46, P{neoFRT}40A/CyO, P{dpp-P23}RP1

2061

dpp^H46 wg^Sp-1 cn¹ bw¹/CyO, P{dpp-P23}RP1

2060

Dp(2;1)G146, dpp⁺/+; dpp^H46 wg^Sp-1 cn¹ bw¹/CyO

Kyoto

108956

dpp^H46 wg^Sp-1 cn¹ bw¹/CyO, P{dpp-P23}RP1

106643

Dp(2;1)G146, dpp⁺/+; dpp^H46 wg^Sp-1 cn¹ bw¹/CyO

Notes on Origin

Discoverer

Blackman.

(Wharton et al., 1993)

Comments

Previously thought to delete whole of dpp and affect other genes (ie to be in Hin-Df class), hence Df synonyms.

Based on considerations of degree of dominant lethality, dpp alleles can be placed in an allelic series. Progressing from weakest to most severe the series is: dpp^e87 < dpp^e90 < dpp^hr56 < dpp^hr4 < dpp^hr92 < dpp^hr27 < dpp^hr93 < dpp^H94 < dpp^H95 < dpp^H96 = dpp^H91 = dpp^H46.

(Wharton et al., 1993)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

Df(2L)dpp-H46

Df(2L)dpp46

Hin46

(Stultz et al., 2005, Arora and Nusslein-Volhard, 1992, Gelbart, 1989)

dpp^H46

(Casas-Tintó and Ferrús, 2021, Hatori et al., 2021, Dominguez et al., 2016, Deshpande et al., 2014, Hodar et al., 2014, Liang et al., 2012, Knox et al., 2011, Eivers et al., 2009, Lin et al., 2006)

dpp^Hin46

(de Velasco et al., 2007, De Velasco et al., 2004, Chang et al., 2001, Mellerick and Nirenberg, 1995, St. Johnston et al., 1990, Hoffmann and Goodman, 1987, Irish and Gelbart, 1987)

dpp^h46

(Esteves et al., 2014, Hwang and Rulifson, 2011)

dppH46

(Grigorian et al., 2011, Oh et al., 2002)

Name Synonyms

Secondary FlyBase IDs

References (58)

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