TY - JOUR
T1 - Frizzled and frizzled 2 play a partially redundant role in Wingless signaling and have similar requirements to wingless in neurogenesis
AU - Bhat, Krishna Moorthi
N1 - Funding Information:
Various fly stocks were thankfully received from Eric Wieschaus [fz 1 , Tp (3;2) N2-27/fz K21 and fz R52 , Tp (3;2) N2-27/fz R52 ], Paul Adler (fz mutants), R. Wides (Pc deficiencies), Kathy Matthews (various fly stocks), Ken Cadigan (UAS-ΔDfz2 and UAS-Δfz2 lines), and Rich Carthew (UAS-fz). The generous gifts of Eve antibody by Manfred Frasch and Gsb antibody by Bob Holmgren are appreciated. Thanks to Michael Boutros, Marek Mlodzik, and Kaoru Saigo for communicating their results prior to publication. I thank Eric Wieschaus and Paul Adler for discussion, suggestions, sharing their unpublished results, and comments on the work. I also thank Adam Berger for technical assistance. Comments from Barry Shur, Kevin Moses, and members of the Bhat and Moses labs were very much appreciated. This work is supported in part by a grant from NIH (R01GM58237).
PY - 1998/12/23
Y1 - 1998/12/23
N2 - The Drosophila Frizzled (Fz) and Frizzled2 (DFz2) proteins function as receptors for Wingless (Wg) in tissue culture cells. While previous results indicate that loss of function for fz has tissue polarity defects, loss-of- function effects of Dfz2 are not known. Here, we have examined the requirements of fz and Dfz2 during neurogenesis. Our results indicate that both Fz and DFz2 function in Wg signaling, and loss of either of the two affects the same subset of neuroblasts as those affected by loss of wg. While these defects are partially penetrant in embryos lacking either fz or Dfz2, the penetrance is significantly enhanced in embryos lacking both. Since the penetrance of the CNS phenotypes is not complete in double mutants, additional components that allow some degree of Wg signaling must exist in vivo.
AB - The Drosophila Frizzled (Fz) and Frizzled2 (DFz2) proteins function as receptors for Wingless (Wg) in tissue culture cells. While previous results indicate that loss of function for fz has tissue polarity defects, loss-of- function effects of Dfz2 are not known. Here, we have examined the requirements of fz and Dfz2 during neurogenesis. Our results indicate that both Fz and DFz2 function in Wg signaling, and loss of either of the two affects the same subset of neuroblasts as those affected by loss of wg. While these defects are partially penetrant in embryos lacking either fz or Dfz2, the penetrance is significantly enhanced in embryos lacking both. Since the penetrance of the CNS phenotypes is not complete in double mutants, additional components that allow some degree of Wg signaling must exist in vivo.
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U2 - 10.1016/S0092-8674(00)81726-2
DO - 10.1016/S0092-8674(00)81726-2
M3 - Article
C2 - 9875856
AN - SCOPUS:0032434512
SN - 0092-8674
VL - 95
SP - 1027
EP - 1036
JO - Cell
JF - Cell
IS - 7
ER -