Allele Dmel\dve⁰¹⁷³⁸

General Information
Symbol	Dmel\dve⁰¹⁷³⁸	Species	D. melanogaster
Name		FlyBase ID	FBal0060453
Feature type	allele	Associated gene	Dmel\dve
Also Known As	dve¹, dve^P1738

Map ( GBrowse )	Untitled Document
Allele class	hypomorphic allele - genetic evidence
Mutagen	P-element activity
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class	hypomorphic allele - genetic evidence (Nakagoshi et al., 1998, Fuss and Hoch, 1998)
Mutagen	P-element activity
Mutations Mapped to the Genome

Type Location Additional Notes References transposable element insertion site 2R:18,158,428..18,158,435 2R:18,158,421..18,158,421 (BDGP Project Members, 1994-1999, Carr et al., 2005, Fuss and Hoch, 1998, Nakagoshi et al., 1998, Spradling et al., 1999, Nakagawa et al., 2011)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference P{PZ} insertion in intron 1. (Carr et al., 2005) P{PZ} insertion in the second intron. (Fuss and Hoch, 1998) Insertion of a P{PZ} element in the second intron. (Nakagoshi et al., 1998)
Caused by insertion	P{PZ}dve⁰¹⁷³⁸ (BDGP Project Members, 1994-1999, Carr et al., 2005, Fuss and Hoch, 1998, Nakagoshi et al., 1998, Spradling et al., 1999, Nakagawa et al., 2011)
Cytology
Phenotypic Data
Phenotypic Class
	lethal (Carr et al., 2005) lethal (with Df(2R)X58-5) (Kolzer et al., 2003) lethal (with dve^BG02382) (Kolzer et al., 2003) lethal \| larval stage \| recessive (Nakagoshi et al., 1998, Fuss and Hoch, 1998, Nakagoshi et al., 1997) lethal \| recessive (Spradling et al., 1999) visible (Kolzer et al., 2003) visible \| recessive \| somatic clone (Nakagoshi et al., 2002)
Phenotype Manifest In
	cuprophilic cell (Nakagoshi et al., 1998) embryonic/larval proventriculus \| embryonic stage (Nakagoshi et al., 1998, Nakagoshi et al., 1997) joint \| ectopic \| somatic clone (Ciechanska et al., 2007) midgut (Nakagawa et al., 2011) midgut (with dve^E181) (Nakagawa et al., 2011) midgut (with dve^NP3060) (Nakagawa et al., 2011) 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 dve[01738]/dve[NP3060] trans-heterozygotes show normal morphology and function. dve[01738]/dve[E181] and dve[01738]/Df(2R)01D01W-L186 trans-heterozygotes exhibit substantially impaired proventriculus function. dve[01738] homozygotes exhibit a reduction in copper absorption and acid secretion in the midgut. dve[01738]/dve[E181] trans-heterozygotes exhibit a milder phenotype, with dve[01738]/dve[NP3060] trans-heterozygotes milder still, while dve[01738] heterozygotes exhibit a mild reduction in copper absorption and acid secretion compared to wild-type. (Nakagawa et al., 2011) dve[01738] 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement Reference dve⁰¹⁷³⁸/dve[+] is a suppressor of visible \| heat sensitive phenotype of peb¹ (Wilk et al., 2004) dve⁰¹⁷³⁸ is a suppressor of visible phenotype of H^Scer\UAS.cMa/H^Scer\UAS.cMa, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Mueller et al., 2005)
Phenotype Manifest In
Suppressor of
Statement Reference dve⁰¹⁷³⁸/dve[+] is a suppressor of eye \| heat sensitive phenotype of peb¹ (Wilk et al., 2004) dve⁰¹⁷³⁸ is a suppressor of eye phenotype of H^Scer\UAS.cMa/H^Scer\UAS.cMa, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Mueller et al., 2005)
Additional Comments
Genetic Interactions
Statement Reference
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Complements	dve⁰¹⁸²⁹ (BDGP Project Members, 1994-1999)
Fails to complement	dve⁰¹⁴⁹³ (BDGP Project Members, 1994-1999) dve⁰¹⁷⁰⁴ (BDGP Project Members, 1994-1999) dve⁰¹⁸²⁹ (Fuss and Hoch, 1998) dve⁰⁵⁰⁸⁴ (Fuss and Hoch, 1998, BDGP Project Members, 1994-1999) dve⁰⁶⁴³² (Fuss and Hoch, 1998, BDGP Project Members, 1994-1999) dve^k06515 (BDGP Project Members, 1994-1999)
Rescued by	dve⁰¹⁷³⁸ is rescued by dve^5.0.Scer\UAS/Scer\GAL4^fkh.14-3 (Fuss and Hoch, 1998)
Partially rescued by	dve⁰¹⁷³⁸/dve^BG02382 is partially rescued by dve^5.0.Scer\UAS/Scer\GAL4^dve-BG02382 (Kolzer et al., 2003)
Comments
Stocks ( 1 )
Bloomington	11073 cn¹ P{PZ}dve⁰¹⁷³⁸/CyO; ry⁵⁰⁶
Notes on Origin
Discoverer	A. Spradling.

Comments
	Excision of the P{PZ} element results in viable, fertile flies indicating that the phenotype is caused by the P{PZ} insertion. (Fuss and Hoch, 1998) Excision of the P{PZ} element reverts the lethal phenotype. (Nakagoshi et al., 1998) Complements: ari-2⁰⁷⁷⁶⁸. Complements: l(2)k09801^k09801. (BDGP Project Members, 1994-1999)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 7 )
Reported As
Symbol Synonym	dep¹ (Nakagoshi et al., 1997) dve¹ (Nakagoshi et al., 2002, Nakagoshi et al., 1998, Nakagawa et al., 2011) dve⁰¹⁷³⁸ (Christensen et al., 2008.4.15, Christensen et al., 2008.9.3, Huet et al., 2002, Ciechanska et al., 2007) dve^P1738 (Kolzer et al., 2003, Fuss and Hoch, 1998) l(2)01738 (Spradling et al., 1999) l(2)01738⁰¹⁷³⁸ line 11073 (Carr et al., 2005)
Name Synonym
Secondary FlyBase IDs
	FBal0007982
References ( 17 )
Research paper	Nakagawa et al., 2011, Mech. Dev. 128(5-6): 258--267 Spatial and temporal requirement of Defective proventriculus activity during Drosophila midgut development. [FBrf0214038] Ciechanska et al., 2007, Genome 50(8): 693--705 dAP-2 and defective proventriculus regulate Serrate and Delta expression in the tarsus of Drosophila melanogaster. [FBrf0201939] Carr et al., 2005, Dev. Genes Evol. 215(8): 402--409 Expression of defective proventriculus during head capsule development is conserved in Drosophila and stalk-eyed flies (Diopsidae). [FBrf0187434] Mueller et al., 2005, Genetics 171(3): 1137--1152 Genetic modifier screens on hairless gain-of function phenotypes reveal genes involved in cell differentiation, cell growth and apoptosis in Drosophila melanogaster. [FBrf0190751] Wilk et al., 2004, Genetics 168(1): 281--300 Dose-sensitive autosomal modifiers identify candidate genes for tissue autonomous and tissue nonautonomous regulation by the Drosophila nuclear zinc-finger protein, hindsight. [FBrf0180294] Kolzer et al., 2003, Development 130(17): 4135--4147 defective proventriculus is required for pattern formation along the proximodistal axis, cell proliferation and formation of veins in the Drosophila wing. [FBrf0160689] Huet et al., 2002, Proc. Natl. Acad. Sci. U.S.A. 99(15): 9948--9953 A deletion-generator compound element allows deletion saturation analysis for genomewide phenotypic annotation. [FBrf0151478] Nakagoshi et al., 2002, Dev. Biol. 249(1): 44--56 Refinement of Wingless expression by a Wingless- and Notch-responsive homeodomain protein, defective proventriculus. [FBrf0151715] Spradling et al., 1999, Genetics 153(1): 135--177 The Berkeley Drosophila genome project gene disruption project. Single P-element insertions mutating 25% of vital Drosophila genes. [FBrf0111489] Fuss and Hoch, 1998, Mech. Dev. 79(1-2): 83--97 Drosophila endoderm development requires a novel homeobox gene which is a target of Wingless and Dpp signalling. [FBrf0108180] Nakagoshi et al., 1998, Genes Dev. 12(17): 2724--2734 A novel homeobox gene mediates the dpp signal to establish functional specificity within target cells. [FBrf0104547]
Personal communication to FlyBase	Christensen et al., 2008.4.15, Isolation and characterization of Df(2R)BSC424. Isolation and characterization of Df(2R)BSC424. [FBrf0204560] Christensen et al., 2008.9.3, Isolation and characterization of Df(2R)BSC597. Isolation and characterization of Df(2R)BSC597. [FBrf0205641] Beaton, 1999.12.12, Alleles of the lines in the P-element paper. Alleles of the lines in the P-element paper. [FBrf0125032] Meister and Braun, 1995.10, lacZ expression patterns for P{} insertions at Bloomington. lacZ expression patterns for P{} insertions at Bloomington. [FBrf0083714] BDGP Project Members, 1994-1999, BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file) BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file) [FBrf0067338]
Abstract	Nakagoshi et al., 1997, A. Dros. Res. Conf. 38: 230B defective proventriculus encodes a homeodomain protein required for midgut development. [FBrf0092263]

Allele Dmel\dve01738

Allele Dmel\dve⁰¹⁷³⁸