8
R. Nusse et al.
1.8 Misexpression of Dfz2
To further examine the role of Dfz2 in vivo, we studied its expression
pattern in the developing wing and the consequences of misexpression
of the intact receptor. In the wing pouch, the region of the disc destined
to become wing blade, Dfz2 is expressed in an inverse concentration
gradient to that of W g, with the lowest levels found at the DN boundary
(Cadigan et al. 1998). This pattern is W g-dependent, since Dfz2 expression is elevated when Wg activity is inactivated. Conversely, expression
of an activated form of Arm throughout the wing pouch represses Dfz2
expression. Thus, W g signaling is responsible for the graded expression
of Dfz2.
To test whether the lowering of Dfz2 expression is important for
normal wing development, we misexpressed Dfz2 using UAS-Dfz2
lines crossed to various Gal4 drivers (Brand and Perrimon 1993). Surviving animals have ectopic bristles on their wing blades. These sensory
organs are normally found only at the wing margin, the adult structure
corresponding to the DN boundary, and depend on W g activity for their
formation (Couso et al. 1994; Phillips and Whittle 1993). The ectopic
bristles in the anterior compartment were almost always of the slender
or chemosensory type. The slender and chemosensory bristle cell fates
are determined during the 3rd larval instar by prone ural genes such as
ac, whose expression is Wg-dependent. ac is initially expressed at
mid-3rd instar in the anterior compartment in a stripe on each side of the
DN boundary. Consistent with the hairy wing phenotype, 113/Dfz2
discs have a dramatic increase in cells expressing high levels of Ac
(Cadigan et al. 1998). These cells are found at a greater distance from
the DN stripe than in controls and presumably cause the ectopic bristles
seen in adult wings.
Thus, misexpression of Dfz2 at high levels throughout the wing
pouch expands the domains of both short- and long-range Wg targets.
1.9 The Dfz2 Phenotype is W g-dependent
Increased activation of W g targets by misexpression of Dfz2 could be
due to an increased response of the cells to the W g signal, or a constitutive activation of the signaling pathway. To address this, we examined
R. Nusse et al.
1.8 Misexpression of Dfz2
To further examine the role of Dfz2 in vivo, we studied its expression
pattern in the developing wing and the consequences of misexpression
of the intact receptor. In the wing pouch, the region of the disc destined
to become wing blade, Dfz2 is expressed in an inverse concentration
gradient to that of W g, with the lowest levels found at the DN boundary
(Cadigan et al. 1998). This pattern is W g-dependent, since Dfz2 expression is elevated when Wg activity is inactivated. Conversely, expression
of an activated form of Arm throughout the wing pouch represses Dfz2
expression. Thus, W g signaling is responsible for the graded expression
of Dfz2.
To test whether the lowering of Dfz2 expression is important for
normal wing development, we misexpressed Dfz2 using UAS-Dfz2
lines crossed to various Gal4 drivers (Brand and Perrimon 1993). Surviving animals have ectopic bristles on their wing blades. These sensory
organs are normally found only at the wing margin, the adult structure
corresponding to the DN boundary, and depend on W g activity for their
formation (Couso et al. 1994; Phillips and Whittle 1993). The ectopic
bristles in the anterior compartment were almost always of the slender
or chemosensory type. The slender and chemosensory bristle cell fates
are determined during the 3rd larval instar by prone ural genes such as
ac, whose expression is Wg-dependent. ac is initially expressed at
mid-3rd instar in the anterior compartment in a stripe on each side of the
DN boundary. Consistent with the hairy wing phenotype, 113/Dfz2
discs have a dramatic increase in cells expressing high levels of Ac
(Cadigan et al. 1998). These cells are found at a greater distance from
the DN stripe than in controls and presumably cause the ectopic bristles
seen in adult wings.
Thus, misexpression of Dfz2 at high levels throughout the wing
pouch expands the domains of both short- and long-range Wg targets.
1.9 The Dfz2 Phenotype is W g-dependent
Increased activation of W g targets by misexpression of Dfz2 could be
due to an increased response of the cells to the W g signal, or a constitutive activation of the signaling pathway. To address this, we examined