Worm Breeder's Gazette 13(2): 32 (February 1, 1994)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
D sor1 ,a MAPKK of Drosophila, has been shown to function downstream of D raf1 (Drosophila Raf ) in signal transduction pathways mediated by a receptor tyrosine kinase. Taking evolutionary conservation of kinase cascades in signal transduction pathways into account, a MAPKK should exist downstream of Let-23 receptor tyrosine kinase in the vulval induction pathway of C. elegans. To test this idea, D sor1 cDNAs (wild type and su1 gain of function mutant ) under the control of hsp16 -41promoter of pPD49 .83vector were introduced into let-23 ( sy97 )vulvaless mutant as extrachromosomal arrays with rol-6 (d)marker gene. Heat shock treatment of the transformant lines induced a normal vulva in many individuals (Table 1 ). These results strongly suggest that a C. elegans MAPKK is involved in the vulval induction pathway downstream of the Let-23 .But, unexpectedly overexpression of a Drosophila MAPKK did not cause Muv in contrast to the overexpression of let-60 ras or lin-3 which causes Muv. We have an idea to explain these observations shown below. According to this idea, there is a difference between the middle three VPCs (P5.-P7.p) and the other VPCs in the ability to respond to MAPKK activation or overexpression, but not to those of let-60 ras or lin-3 .It is also expected that hs-D sor1 will cause Muv when it is introduced into a vulvaless double mutant with a let-23 mutation and another recessive Muv mutation ( lin-13 ,36, 8, 9, or 15 etc.). These experiments to test our idea are in progress, and we also plan to screen for mutants in which MAPKK activation causes Muv.