TY - JOUR
T1 - huckebein specifies aspects of CNS precursor identity required for motoneuron axon pathfinding
AU - Chu-LaGraff, Q.
AU - Schmid, A.
AU - Leidel, J.
AU - Brönner, G.
AU - Jäckle, H.
AU - Doe, C. Q.
N1 - Funding Information:
We thank K. Schuske and M. P. Scott for providing the 5953 line; T. Bossing for instruction in Dil labeling; K. Troka for performing the genomic plasmid rescues; E. Christ-Harned for the chromosome in situ hybridization; and I. Duncan, M. Frasch, C. S. Goodman, N. H. Patel, and S. Poole for antibodies. We especially thank Jim Skeath and Eric Spana for comments on the manuscript. This work was supported by a Proctor and Gambte Predoctoral Fellowship (Q. C. -L.); by the Sonderforschungsbereich 271 of the Deutsche Forschungs-gemeinschaft (H. J.); and by the National Institutes of Health (HD 27056), the National Science Foundation (Presidential Young Investigator), and the Human Frontier Science Program (C. Q. D.). C. Q. D. is an assistant investigator of the Howard Hughes Medical Institute.
PY - 1995/11
Y1 - 1995/11
N2 - huckebein encodes a putative zinc finger protein expressed in a subset of Drosophila CNS precursors, including the NB 4-2/GMC 4-2a/RP2 cell lineage. Inhuckebein mutant embryos, GMC 4-2a does not express the cell fate marker EVEN-SKIPPED; conversely,huckebein overexpression produces a duplicate EVEN-SKIPPED-positive GMC 4-2a. We use Dil to trace the entire NB 4-2 lineage in wild-type andhuckebein mutant embryos. Loss ofhuckebein does not affect the number, position, or type of neurons in the NB 4-2 lineage; however, all motoneurons show axon pathfinding defects and never terminate at the correct muscle. Thus,huckebein regulates aspects of GMC and neuronal identity required for proper motoneuron axon pathfinding in the NB 4-2 lineage.
AB - huckebein encodes a putative zinc finger protein expressed in a subset of Drosophila CNS precursors, including the NB 4-2/GMC 4-2a/RP2 cell lineage. Inhuckebein mutant embryos, GMC 4-2a does not express the cell fate marker EVEN-SKIPPED; conversely,huckebein overexpression produces a duplicate EVEN-SKIPPED-positive GMC 4-2a. We use Dil to trace the entire NB 4-2 lineage in wild-type andhuckebein mutant embryos. Loss ofhuckebein does not affect the number, position, or type of neurons in the NB 4-2 lineage; however, all motoneurons show axon pathfinding defects and never terminate at the correct muscle. Thus,huckebein regulates aspects of GMC and neuronal identity required for proper motoneuron axon pathfinding in the NB 4-2 lineage.
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U2 - 10.1016/0896-6273(95)90093-4
DO - 10.1016/0896-6273(95)90093-4
M3 - Article
C2 - 7576648
AN - SCOPUS:0028973248
SN - 0896-6273
VL - 15
SP - 1041
EP - 1051
JO - Neuron
JF - Neuron
IS - 5
ER -