GENETIC-ANALYSIS OF A DROSOPHILA NEURAL CELL-ADHESION MOLECULE - INTERACTION OF FASCICLIN-I AND ABELSON TYROSINE KINASE MUTATIONS

被引:326
作者
ELKINS, T
ZINN, K
MCALLISTER, L
HOFFMANN, FM
GOODMAN, CS
机构
[1] UNIV CALIF BERKELEY,HOWARD HUGHES MED INST,BERKELEY,CA 94720
[2] UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,BERKELEY,CA 94720
[3] UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706
关键词
D O I
10.1016/0092-8674(90)90660-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Drosophila fasciclin I is a homophilic cell adhesion molecule expressed in the developing embryo on the surface of a subset of fasciculating IONS axons, all PNS axons, and some nonneuronal cells. We have identified protein-null mutations in the fasciclin I (fas I) gene, and show that these mutants are viable and do not display gross defects in nervous system morphogenesis. The Drosophila Abelson (abo proto-oncogene homolog encodes a cytoplasmic tyrosine kinase that is expressed during embryogenesis primarily in developing CNS axons; abl mutants show no gross defects in CNS morphogenesis. However, embryos doubly mutant for fas 1 and abl display major defects in CNS axon pathways, particularly in the commissural tracts where expression of these two proteins normally overlaps. The double mutant shows a clear defect in growth cone guidance; for example, the RP1 growth cone (normally fas 1 positive) does not follow its normal path across the commissure. © 1990.
引用
收藏
页码:565 / 575
页数:11
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