TY - JOUR
T1 - Drosophila homeodomain protein dHb9 directs neuronal fate via crossrepressive and cell-nonautonomous mechanisms
AU - Broihier, Heather T.
AU - Skeath, James B.
N1 - Funding Information:
We thank A. Brand, A. Chiba, A. DiAntonio, M. Fujioka, C. Goodman, R. Saint, S. Thor, and the Bloomington Stock Center for reagents; and K. O'Connor-Giles and A. DiAntonio for critical reading of the manuscript. We are also indebted to C. Kadavi and Y. Zhu for invaluable technical assistance. We are particularly grateful to an anonymous reviewer for suggestions that greatly improved this manuscript. This work was supported by an NRSA NIH postdoctoral fellowship (H.T.B.) and by an NINDS grant (R01-NS-36570) (J.B.S.).
PY - 2002/7/3
Y1 - 2002/7/3
N2 - Here we present the identification and characterization of dHb9, the Drosophila homolog of vertebrate Hb9, which encodes a factor central to motorneuron (MN) development. We show that dHb9 regulates neuronal fate by restricting expression of Lim3 and Even-skipped (Eve), two homeodomain (HD) proteins required for development of distinct neuronal classes. Also, dHb9 and Lim3 are activated independently of each other in a virtually identical population of ventrally and laterally projecting MNs. Surprisingly, dHb9 represses Lim3 cell nonautonomously in a subset of dorsally projecting MNs, revealing a novel role for intercellular signaling in the establishment of neuronal fate in Drosophila. Lastly, we provide evidence that dHb9 and Eve regulate each other's expression through Groucho-dependent crossrepression. This mutually antagonistic relationship bears similarity to the crossrepressive relationships between pairs of HD proteins that pattern the vertebrate neural tube.
AB - Here we present the identification and characterization of dHb9, the Drosophila homolog of vertebrate Hb9, which encodes a factor central to motorneuron (MN) development. We show that dHb9 regulates neuronal fate by restricting expression of Lim3 and Even-skipped (Eve), two homeodomain (HD) proteins required for development of distinct neuronal classes. Also, dHb9 and Lim3 are activated independently of each other in a virtually identical population of ventrally and laterally projecting MNs. Surprisingly, dHb9 represses Lim3 cell nonautonomously in a subset of dorsally projecting MNs, revealing a novel role for intercellular signaling in the establishment of neuronal fate in Drosophila. Lastly, we provide evidence that dHb9 and Eve regulate each other's expression through Groucho-dependent crossrepression. This mutually antagonistic relationship bears similarity to the crossrepressive relationships between pairs of HD proteins that pattern the vertebrate neural tube.
UR - http://www.scopus.com/inward/record.url?scp=0037014449&partnerID=8YFLogxK
U2 - 10.1016/S0896-6273(02)00743-2
DO - 10.1016/S0896-6273(02)00743-2
M3 - Article
C2 - 12123607
AN - SCOPUS:0037014449
SN - 0896-6273
VL - 35
SP - 39
EP - 50
JO - Neuron
JF - Neuron
IS - 1
ER -