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44 Takashi HIRAYAMA and Tsutomu UGAJIN perception. The ran1 mutants show the ethylene phenotype in response to treatment with transcyclooctene, a potent ethylene binding inhibitor, which normally inhibits the ethylene response. The ran1 mutants seem to have a relaxed ligand-specificity since they respond normally to ethylene. The RAN1 gene has been identified by map based cloning and shown to encode a P-type copper transporter similar to human Menkes or Wilson disease protein, or yeast Ccc2p. These proteins have been demonstrated to deliver copper ions to the post Golgi compartment where copper requiring proteins are modified and sorted subsequently to the plasma membrane or outside of the cell, etc. These finding lead us the idea that RAN1 delivers copper ions to ethylene receptors. Several RAN1 co-suppressed transgenic lines and the null-type ran1 mutant (ran1-3) exhibit strong ethylene constitutive responding phenotypes (HIRAYAMA et al. 1999; WOESTE and KIEBER 2000). In the ran1-3 mutant, ethylene receptors are expressed at the same level as wild type (ZHAO et al. 2002). These results strongly suggest that ethylene receptors cannot function without copper delivery. However, this conclusion seems inconsistent with the etr1-1 phenotype. As discussed above the conversion Cys65 to Tyr confers an ethylene insensitive phenotype, while the defect in RAN1 results in the constitutive activation of the ethylene response. One possible and plausible explanation for this discrepancy is that Cys65 is required not only for copper coordination but also for the proper conformation of ethylene receptor. Presumably, ethylene receptor is locked at active state without Cys65. Since both of the ran1-1 and ran1-2 mutations are missense mutations, these mutated genes presumably express mutated copper transporters. These mutations cause the conversion of important amino acid residue for copper transporting activity to another residue, indicating the mutated copper transporters have reduced activities. Actually a recombinant ran1-1 protein has a reduced copper transporting activity in the yeast cells (HIRAYAMA et al. 1999). If one copper ion is incorporated in a functional ethylene receptor as Bleecker’s group proposed, the ran1-1 or ran1-2 plant would have just two types of ethylene receptors, receptor with copper or without copper. However, having these two types of ethylene receptors cannot explain the relaxed ligand specificity of the ran1-1 and ran1-2 mutants. Determination of the fine structure of ethylene recognition domain is necessary. Although all the ethylene receptors have a His-kinase like domain, the amino acid sequences are different among them. ETR1 and ERS1 have all the motifs that are required for His-kinase activity, namely H, N, G1, F and G2 motifs. By contrast, ETR2, EIN4 and ERS2 lack some or all of them, indicating these His-kinase like domains do not have His-kinase activity. Recently, Wang et al. reported that the physiological roles of His-kinase accompanied receptors, ETR1, ERS1, are different from those of ETR2, EIN4 and ERS2, and that their His-kinase activities are not required for the ethylene response (WANG et al. 2003). Furthermore, NTHK1, a tobacco ethylene receptor, was shown to have Ser/Thr kinase activity (XIE et al. 2003). Based on these reports, it is more unlikely that the ethylene-signaling pathway belongs to His-Asp phospho-relay signaling pathway.
ETHYLENE-SIGNALING PATHWAY 45 The fact that the ethylene-signaling pathway does not require the His-kinase activity of ethylene receptors raises another question why ETR1 and ERS1 possess His-kinase activity. It is possible that the His-kinase activities of those ethylene receptors are required for functions other than the ethylene-signaling pathway. Arabidopsis has several His-kinases although their physiological roles are not fully elucidated. A cytokinin receptor, CRE1, is one of the histidine kinase signal transducers whose physiological functions have been assigned. Recent studies have demonstrated that the cytokinin signal was transduced from CRE1 to nucleus by phospho-relay components (SAKAI et al. 2001). Some of those components have the ability to interact with ETR1 (URAO et al. 2000). It might be possible that the His-kinase activity of ETR1 or ERS1 is involved in the crosstalk between the signal transduction pathways for ethylene and other stimuli or plant hormones such as cytokinin. Since ethylene molecules can pass freely through the lipid bilayer membrane, ethylene receptors do not need to localize to the plasma membrane. Schaller’s group showed that ethylene receptors localized to the membrane of endoplasmic reticulum (CHEN et al. 2002). By contrast, Xie et al. demonstrated that a tobacco ethylene receptor, NTHK1, fused to green fluorescent protein localized to the plasma membrane (XIE et al. 2003). Further analysis is required for the determination of the subcellular localization of ethylene receptors. Signaling components from receptor to nucleus How do the ethylene receptors transduce the signal downstream? The genetically identified component is CTR1, a Raf-type Ser/Thr kinase. Loss-of-function mutations of CTR1 cause recessive ethylene constitutive response phenotypes, suggesting CTR1 functions as a negative regulator like ethylene receptors. Thus ethylene receptors presumably activate CTR1. Two-hybrid analysis using budding yeast revealed that CTR1 interacted with ETR1 and ERS1 (CLARK et al. 1998). Recently, one of the mutant alleles, ctr1-8, turned out to be defective in the association with ETR1, providing in vivo evidence for the requirement of physical interaction between them for the CTR1 function (HUANG et al. 2003). Furthermore, a recent study showed that ETR1 and CTR1 colocalized to ER membrane, supporting this idea (GAO et al. 2003). Raf-1 in mammal cells functions as a MAP-kinase-kinase-kinase. It has been postulated that CTR1 is one of the components of a MAP kinase cascade that is responsible for the ethylenesignaling pathway. Ouaked et al. reported that a sort of MAP-Kinase-kinase and MAP-kinase were activated upon ethylene treatment in a CTR1-dependent manner (OUAKED et al. 2003). The authors reported overexpression of this MAPKK induced the triple response phenotype in the absence of ethylene. These kinases might constitute a MAP kinase cascade with CTR1. However these kinases are activated by ethylene while CTR1 is inactivated. Such a regulation has not been reported in other MAP kinase systems so far. Although the ctr1 mutants exhibit constitutive ethylene phenotypes, treatment with ethylene
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ISSN 0435-1096 Gamma Field Symposia
Page 3 and 4: The lecturers and the members of th
Page 5 and 6: KANEKO, T. KARITA, E. KASHIMA, M. K
Page 7 and 8: TANO, S. TSUCHIDA, Y. TSUTSUMI, N.
Page 9 and 10: The Symposium Committee Shigeki NAG
Page 11 and 12: CONTENTS Y. KAMIYA Biosyntheses and
Page 13 and 14: 2 Yuji KAMIYA Fig. 1. Gibberellin b
Page 15 and 16: 4 Yuji KAMIYA using the receptor pr
Page 17 and 18: 6 Yuji KAMIYA Fig. 3. Origin of sid
Page 19 and 20: 8 Yuji KAMIYA References AKIYOSHI,
Page 21 and 22: 10 Yuji KAMIYA SHINOMURA, T. (1997)
Page 23 and 24: 12 Yuji KAMIYA 8’ 8’ 273
Page 25 and 26: 14 Motoyuki ASHIKARI, Hironori ITOH
Page 37 and 38: 26 Atsuhiro OKA and how their signa
Page 39 and 40: 28 Atsuhiro OKA At almost the same
Page 41 and 42: 30 Atsuhiro OKA division for xylem
Page 43 and 44: 32 Atsuhiro OKA the RR domain in th
Page 45 and 46: 34 Atsuhiro OKA Fig. 4. Cross-talk
Page 47 and 48: 36 Atsuhiro OKA OKA, A., SAKAI, H.
Page 49 and 50: 38 Atsuhiro OKA ARR4 PHYB PHYBP
Page 51 and 52: Gamma Field Symposia, No. 42, 2003
Page 53: ETHYLENE-SIGNALING PATHWAY 43 signa
Page 57 and 58: ETHYLENE-SIGNALING PATHWAY 47 Snf3p
Page 59 and 60: ETHYLENE-SIGNALING PATHWAY 49 In sp
Page 61 and 62: ETHYLENE-SIGNALING PATHWAY 51
Page 63 and 64: Gamma Field Symposia, No. 42, 2003
Page 65 and 66: MECHANISM OF BRASSINOSTEROID SIGNAL
Page 77 and 78: 68 Yoshikatsu MATSUBAYASHI are grow
Page 79 and 80: 70 Yoshikatsu MATSUBAYASHI Fig. 3.
Page 85 and 86: 76 Yoshikatsu MATSUBAYASHI 33. Yang
Page 87 and 88: 78 Yoshikatsu MATSUBAYASHI GUS
Page 89 and 90: 80 BRI1
Page 91 and 92: 82 BRI 10
Page 93 and 94: 84 100
Page 95 and 96: 86 PSK 23 BIL1/CFP
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