No.42 - è¾²æ¥çç©è³æºç 究æ
No.42 - è¾²æ¥çç©è³æºç 究æ
No.42 - è¾²æ¥çç©è³æºç 究æ
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60<br />
Takeshi NAKANO, Shigeo YOSHIDA and Tadao ASAMI<br />
mutant can be rescued by less stressful conditions, which may relate to the cross-talk between<br />
brassinosteroids and ABA. The bil5 mutation maps to the lower arm of chromosome I. Isolation<br />
of the bil5 mutant gene, by sequencing and complementation, is in progress.<br />
To screen for more bil mutants, we are starting from an activation-tagged line, in collaboration<br />
with the groups of Dr. Shinozaki and Dr. Matsui. The genes identified by analysis of these mutants<br />
may also be members of the brassinosteroid signaling cascade.<br />
Additional new players for brassinosteroid signaling<br />
brs1 and bak1 were identified as bri1-5 dwarf suppressor mutants by activation tagging.<br />
BRS1 encodes a carboxypeptidase, and its role in BR signalling has not been defined (Li et al.,<br />
2001) (Fig. 7). BAK1, however, encodes a leucine-rich-repeat type receptor-like kinase that could<br />
interact directly with BRI1 (Li et al., 2002, Nam and Li, 2002) (Fig. 7). On the basis of their<br />
phenotypes, bak1-1D and brs1-1D mutants could potentially be Brz-insensitive mutants. Several<br />
Fig. 7 Current key players on brassinosteroid signaling.<br />
BIL1: Brz-insensitive-long hypocotyl, BRI1: brassinosteroid insentive1, BAK1:bri1<br />
associated kinase, BIN: brassinosteorid insenstive, BRS1: bri1 suppressor. Brz:<br />
Brassinosteroid biosynthesis inhibitor.