Vein

Vein

Add Correction Suggestion

Symbol: AKA: Vn{Links}	Flybase ID: {Flybase_ID}
Synonyms: {Name}	{GadFly}
Function: {Short_Function}	{LocusLink}
Keywords: {Keywords}	{Interactive_Fly}

a secreted neuregulin-like molecule that activates EGFR signaling and is a candidate moledule for establishing the notum

Function/Pathway

a secreted neuregulin-like molecule that activates EGFR signaling and is a candidate moledule for establishing the notum

Genetic interactions

In wg mutants there is a dramatic and early expansion of vn expression to include distal cells (Fig 1I), presaging the development of these cells as an extra notum. However, vn mutants did not lead to expansion of wg expression (Wang, 2000)
vn is a target of EGFR signaling in the embryo (Golembo et al. 1999; Wessells et al. 1999)
Vn/EGFR signaling regulates Ap expression in a cell autonomous fashion only early in wing development
- ap expression partially overlaps that of vn in the second instar (Fig 4I) (Wang, 2000)
- ap can be induced ectopically in ventral clones misexpressing an activated form of the receptor, EGFR^lambdatop4.2 (Fig. 4J) (Wang, 2000)
- Egfr^tsla mutant clones generated in the first instar show autonomous loss of ap expression (Fig. 4K), whereas clones generated in the second instar express ap normally (data not shown) (Wang, 2000)
- loss of EGFR activity in whole discs from mid-first to mid-second instar (with a temperature-sensitive allele) results in complete loss of ap expression, whereas ap is still expressed in discs from larvae given a temperature shift slightly later during the second instar (Fig. 4L–N). (Wang, 2000)

Physical interactions

{Physical interactions}

Transcriptional Regulation

vn is a target of EGFR signaling in the embryo (Golembo et al. 1999; Wessells et al. 1999)

Structure

{Structure}

Location (protein and transcript)

vn is expressed in the presumptive notum in second instar wing discs (Simcox, 1996)

Protein Modifications and Regulation

{Modifications}

Related to

{Related to}

Mutations

hypomorphic vn mutants lack the notum (Simcox, 1996)
wing primordium fails to grow in vn null alleles and in some Egfr alleles (Clifford, 1989; Simcox, 1996)
Inactivating Vn/EGFR activity (with temp sensitive alleles; Egfr^ts1a, vn^tsWB240) during the second instar (a 24 hr period) caused loss of the notum (Fig. 1 E,F) (Wang, 2000). The wing developed but showed pattern abnormalities characteristic of vn hypomorphs (Fig 1E) (Wang, 2000). Later shifts during the third instar did not cause loss of the notum (data not shown) (Wang, 2000). This demonstrates Vn/EGFR activity is required for notum development in the second instar when wg is required to specify the wing (Ng, 1996).
EGFR signaling is needed from mid-first to mid-second instar for wing development. This was analysised by using a temperature-sensitive allele Egfr^ts1a (Wang, 2000)
In vn null mutants, the initiation of wg expression is normal and the expression of its target gene optomotor-blind (omb) (Grimm and Pflugfelder 1996; (Wang, 2000: Fig 1). Later in second instar, wg expression normally expands to fill the growing wing pouch, however vn mutants wg expression failed to undergo this expansion (Fig. 4D) (Wang, 2000). A similar defect in wg expression is seen in ap mutants (Ng et al. 1996) consistent with Ap function being impaired in vn mutants.
Ap expression is completely absent in second instar vn muant discs (Fig. 4E&F) (Wang, 2000). This is probably why there is no wing in vn mutants. This is supported by the demonstration that ectopic ap was capable of rescuing wing development in vn mutants (Fig. 4G,H). (Wang, 2000)
In vn mutants, expression of Caup/Ara is lost (Fig. 2E) and loss of EGFR signaling, in EGFR^ts clones, in the medial notum resulted in a loss of Caup/Ara expression (Fig. 2G). However, clones in the lateral notum continued to express Caup/Ara (Fig. 2G), suggesting other factors regulate Iro-C gene expression in these cells at this stage (Wang, 2000)
Expression of vn-lacZ is lost in a vn^L6/rF264 early third instar mutant wing disc (Wang, 2000)
when Vn/EGFR signaling is inhibited in the notum by expressing a ligand antagonist (Vn::Aos–EGF) (Schnepp et al. 1998) under the control of ptc–Gal4, ectopic wings were induced in ~10% of the flies (Fig. 3G,H). This result demonstrates that presumptive notal tissue can be transformed to wing by reducing EGFR signaling. However, the transformation occurred only when EGFR signaling was reduced in a subset of cells, rather than all cells in the notum (as in a vn mutant) (Wang, 2000)
- this may reflect an indirect requirement for EGFR activity to also promote wing development (Wang, 2000)

Overexpression / Ectopic expression

{Overexpression}

Reagents

{Reagents}