FlyBase Allele Report: Dmel\dve[01738]

(Sugimori et al., 2016, Nakagawa et al., 2011, Carr et al., 2005, Spradling et al., 1999, Fuss and Hoch, 1998, Nakagoshi et al., 1998, BDGP Project Members, 1994-1999)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

copper cell

(Nakagoshi et al., 1998)

embryonic/larval proventriculus | embryonic stage

(Nakagoshi et al., 1998, Nakagoshi et al., 1997)

eye | somatic clone

(Puli et al., 2024)

eye disc | larval stage | somatic clone

(Puli et al., 2024)

leg joint | ectopic | somatic clone

(Ciechanska et al., 2007)

male accessory gland, with Scer\GAL4^dve.13, dve^KK115422

(Minami et al., 2012)

male accessory gland secondary cell | somatic clone

(Minami et al., 2012)

midgut

(Nakagawa et al., 2011)

midgut (with dve^E181)

(Nakagawa et al., 2011)

midgut (with dve^NP3060)

(Nakagawa et al., 2011)

ocellus | absent

(Puli et al., 2024)

proventriculus (with Df(2R)01D01W-L186)

(Nakagawa et al., 2011)

proventriculus (with dve^E181)

(Nakagawa et al., 2011)

proventriculus inner layer

(Fuss and Hoch, 1998)

proventriculus outer layer

(Fuss and Hoch, 1998)

tarsal segment | somatic clone

(Ciechanska et al., 2007)

wing

(Kolzer et al., 2003)

wing | proximal

(Kolzer et al., 2003)

wing | somatic clone

(Nakagoshi et al., 2002)

wing disc

(Kolzer et al., 2003)

wing disc | somatic clone

(Kolzer et al., 2003)

wing margin bristle | ectopic | somatic clone

(Nakagoshi et al., 2002)

wing vein L2 | proximal

(Kolzer et al., 2003)

wing vein L5 | distal

(Kolzer et al., 2003)

Detailed Description

Statement

Reference

The ratio of the cross-section areas of the accessory gland/ejaculatory bulb is significantly reduced compared to wild type in males expressing dve^KK115422 under the control of Scer\GAL4^dve.13 in a dve⁰¹⁷³⁸/+ background. Binucleation of main type cells is relatively normal in the mutant accessory glands.

The number of eggs laid per day by females mated to males expressing dve^KK115422 under the control of Scer\GAL4^dve.13 in a dve⁰¹⁷³⁸/+ background is reduced and these females show high re-mating activity (comparable to those of virgin female controls) at 48 hours after the first mating.

Homozygous clones in the male accessory gland do not contain cells with secondary morphology.

(Minami et al., 2012)

dve⁰¹⁷³⁸/dve^NP3060 trans-heterozygotes show normal morphology and function.

dve⁰¹⁷³⁸/dve^E181 and dve⁰¹⁷³⁸/Df(2R)01D01W-L186 trans-heterozygotes exhibit substantially impaired proventriculus function.

dve⁰¹⁷³⁸ homozygotes exhibit a reduction in copper absorption and acid secretion in the midgut. dve⁰¹⁷³⁸/dve^E181 trans-heterozygotes exhibit a milder phenotype, with dve⁰¹⁷³⁸/dve^NP3060 trans-heterozygotes milder still, while dve⁰¹⁷³⁸ heterozygotes exhibit a mild reduction in copper absorption and acid secretion compared to wild-type.

(Nakagawa et al., 2011)

dve⁰¹⁷³⁸ clones in the leg are frequently associated with ectopic joint structures in the tarsal segments, whereas clones in the femur or tibia are not associated with ectopic joints. Clones encompassing multiple tarsal segments induce extra joints in each segment, though clones spanning the joint have no effect on endogenous joint morphology. Clones spanning several joints induce only one ectopic partial joint per segment, which tends to appear in the middle of the segment. The curvature of the ectopic joints is reversed relative to the endogenous joints. No obvious effects on bristle polarity are observed.

(Ciechanska et al., 2007)

Wings of mutant flies are smaller and shorter than normal. The wings lack a region that encompasses most of the distal costa and a small part of the adjacent wing blade. The mutant wings are also reduced in size along the anterior-posterior axis. Wing vein 2 is interrupted in the proximal part and the distal part of wing vein 5 is missing. The size of the area of the wing outlined by wing veins 3 and 4, and the anterior crossvein and wing margin is similar in size in mutant and wild-type animals. The cell density in the area of the wing outlined by wing veins 3 and 4 is very similar in mutant and wild-type animals. The distance between wing vein 3 and 4, measured by the numbers of cells between them, is the same in mutant and wild-type animals. The cell density in the region anterior to wing vein 3 is similar in mutant and wild-type animals, but the distance between wing vein 3 and the anterior margin is reduced in mutant animals, indicating that this area consists of fewer cells in the mutant. The distance from vein 4 to the posterior wing margin is reduced in mutant animals compared to wild type, and cell density in this region is also lower than wild-type in the mutant animals, indicating that this region consists of fewer, larger cells in mutant animals compared to wild type. Mutant third larval instar wing discs are abnormal; the anlage of the dorsal part of the wing pouch is shorter than normal. In early pupae, the wing pouch is smaller than normal and has a small indentation at the anterior wing margin. The fold adjacent to the wing blade appears to be reduced in mutant wing discs. Homozygous clones induced in the wing disc are smaller than their wild-type twin clones. Clones in the regions of the disc extending from the anterior wing margin to vein 3 and from vein 4 to the posterior margin are about half the size of their wild-type counterparts. In addition, nearly half the wild-type clones in these regions do not have a mutant counterpart (suggesting that the mutant cells have died). Clones in the region from wing vein 3 to 4 are about two-thirds the size of their wild-type counterparts.

(Kolzer et al., 2003)

Homozygous clones in the wing result in ectopic margin bristles (which can be derived from mutant or wild-type tissue) and wing margin notches.

(Nakagoshi et al., 2002)

Homozygotes die as first instar larvae. Passage of food is blocked at the proventriculus in these larvae. The specification of the proventriculus primordium occurs normally in homozygous embryos. At stage 17, the endoderm outer wall structure of the proventriculus shows a collapsed phenotype and the ingrowth of the ectodermal valve cells into the endoderm fails. The number of outer wall cells is wild-type and no cell death occurs in the defective outer wall.

(Fuss and Hoch, 1998)

Homozygous larvae show normal locomotion behaviour immediately after hatching, however they develop into small larvae and die within a day of hatching. Food accumulates in the proventriculus, in contrast to control larvae where it is present throughout the length of the gut. The proventriculus is not correctly formed; cell migration of the foregut epithelium into the anteriormost midgut is greatly delayed and the internalisation is only temporary. Constriction of the midgut normally occurs in the midgut of homozygous embryos and the arrangement of the stage 17 midgut appears normal. The arrangement of copper cells appears disorganised in hemizygous larvae.

(Nakagoshi et al., 1998)

Larvae have a nonfunctional proventriculus, leading to lethality at the first instar stage.

(Nakagoshi et al., 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

dve⁰¹⁷³⁸ has visible | adult stage | somatic clone phenotype, enhanceable by pan^ΔN.UAS/Scer\GAL4^unspecified