Genetics, Vol. 153, 763-771, October 1999, Copyright © 1999

Genetic Analysis of rolled, Which Encodes a Drosophila Mitogen-Activated Protein Kinase

Young-Mi Lima,b, Kimiko Nishizawac, Yoshimi Nishic, Leo Tsudae, Yoshihiro H. Inoued, and Yasuyoshi Nishidaa
a Laboratory of Developmental Biology, Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan,
b Laboratory of Cell Regulation, Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan,
c Laboratory of Experimental Radiology, Aichi Cancer Center Research Institute, Chikusa-ku, Nagoya 464-8681, Japan
d Laboratory of Cell Biology, Aichi Cancer Center Research Institute, Chikusa-ku, Nagoya 464-8681, Japan
e Department of Biological Chemistry, MacDonald Medical Research Laboratories, Howard Hughes Medical Institute, University of California, Los Angeles, California 90095-1662

Corresponding author: Yasuyoshi Nishida, Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan., nishida{at}bio.nagoya-u.ac.jp (E-mail)

Communicating editor: N. TAKAHATA

Genetic and molecular characterization of the dominant suppressors of D-rafC110 on the second chromosome identified two gain-of-function alleles of rolled (rl), which encodes a mitogen-activated protein (MAP) kinase in Drosophila. One of the alleles, rlSu23, was found to bear the same molecular lesion as rlSem, which has been reported to be dominant female sterile. However, rlSu23 and the current stock of rlSem showed only a weak dominant female sterility. Detailed analyses of the rl mutations demonstrated moderate dominant activities of these alleles in the Torso (Tor) signaling pathway, which explains the weak dominant female sterility observed in this study. The dominant rl mutations failed to suppress the terminal class maternal-effect mutations, suggesting that activation of Rl is essential, but not sufficient, for Tor signaling. Involvement of rl in cell proliferation was also demonstrated by clonal analysis. Branching and integration of signals in the MAP kinase cascade is discussed.





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