Activation-Tagged Suppressors of a Weak Brassinosteroid Receptor Mutant

Brassinosteroids (BRs) are important plant hormones that act synergistically with auxin to regulate a variety of plant developmental and physiological processes. In the past decade, genetic and biochemical studies have revealed a linear signaling pathway that relies on protein phosphorylation to tra...

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Veröffentlicht in:Molecular plant 2010-01, Vol.3 (1), p.260-268
Hauptverfasser: Kang, Bin, Wang, Hao, Nam, Kyoung Hee, Li, Jiayang, Li, Jianming
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Nam, Kyoung Hee
Li, Jiayang
Li, Jianming
description Brassinosteroids (BRs) are important plant hormones that act synergistically with auxin to regulate a variety of plant developmental and physiological processes. In the past decade, genetic and biochemical studies have revealed a linear signaling pathway that relies on protein phosphorylation to transmit the BR signal into the nucleus, altering ex- pression of hundreds of genes to promote plant growth. We conducted an activation-tagging based suppressor screen to look for Arabidopsis genes that, when overexpressed by inserted 35S enhancer elements, could suppress the dwarf phe- notype of a weak BR receptor mutant bril-301. This screen identified a total of six dominant activation-tagged bril sup- pressors (atbs-Ds). Using a plasmid rescue approach, we discovered that the bril-301 suppression effect in four atbs-D mutants (atbs3-D to atbs6-D) was caused by overexpression of a YUCCA gene thought to be involved in tryptophan- dependent auxin biosynthesis. Interestingly, the three activation-tagged YUCCA genes belong to the YUCCA IIA subfamily that includes two other members out of 11 known Arabidopsis YUCCA genes. In addition, our molecular studies revealed a T-DNA insertion near a basic helix-loop-helix gene in atbsl-D and a T-DNA insertion in a region carrying a BR biosynthetic gene in atbs2-D. Further studies of these atbs-D mutants could lead to better understanding of the BR signaling process and the BR-auxin interaction.
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In the past decade, genetic and biochemical studies have revealed a linear signaling pathway that relies on protein phosphorylation to transmit the BR signal into the nucleus, altering ex- pression of hundreds of genes to promote plant growth. We conducted an activation-tagging based suppressor screen to look for Arabidopsis genes that, when overexpressed by inserted 35S enhancer elements, could suppress the dwarf phe- notype of a weak BR receptor mutant bril-301. This screen identified a total of six dominant activation-tagged bril sup- pressors (atbs-Ds). Using a plasmid rescue approach, we discovered that the bril-301 suppression effect in four atbs-D mutants (atbs3-D to atbs6-D) was caused by overexpression of a YUCCA gene thought to be involved in tryptophan- dependent auxin biosynthesis. Interestingly, the three activation-tagged YUCCA genes belong to the YUCCA IIA subfamily that includes two other members out of 11 known Arabidopsis YUCCA genes. In addition, our molecular studies revealed a T-DNA insertion near a basic helix-loop-helix gene in atbsl-D and a T-DNA insertion in a region carrying a BR biosynthetic gene in atbs2-D. 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Further studies of these atbs-D mutants could lead to better understanding of the BR signaling process and the BR-auxin interaction.</description><subject>35S启动子</subject><subject>Arabidopsis - genetics</subject><subject>Arabidopsis - metabolism</subject><subject>Arabidopsis Proteins - genetics</subject><subject>Arabidopsis Proteins - metabolism</subject><subject>auxin</subject><subject>Brassinosteroid</subject><subject>BRI1</subject><subject>bri1-301</subject><subject>Gene Expression Regulation, Plant - genetics</subject><subject>Gene Expression Regulation, Plant - physiology</subject><subject>Molecular Sequence Data</subject><subject>Plants, Genetically Modified - genetics</subject><subject>Plants, Genetically Modified - metabolism</subject><subject>Steroids, Heterocyclic - metabolism</subject><subject>YUCCA</subject><subject>受体</subject><subject>基因过度表达</subject><subject>抑制因子</subject><subject>油菜素内酯</subject><subject>激活标签</subject><subject>生物圈保护区</subject><subject>突变体</subject><issn>1674-2052</issn><issn>1752-9867</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kF1rFTEQhhdRbKm98A_IIoJ4sTYfuyebG6EtWoWKoBUvwyQ7uw3dTdIke8B_b2QPfoB4NQPz5JnJW1VPKXlNieRnSzhLKRApH1THVHSskf1OPCz9TrQNIx07qk5TspowTinbkfZxdUSllJ1g9Li6OjfZ7iFb75obmCYc6i9rCBFT8jHVfqyh_oZwV19EKBbnU8bo7VB_RoMh-1h_XDO4_KR6NMKc8PRQT6qv797eXL5vrj9dfbg8v25MK9rc9CPVo-6hG6kAhlIKLpASQrBroaVUDx1QuqNCm15rzkrXAWqNDDoDBvhJ9WbzhlUvOBh0OcKsQrQLxO_Kg1V_T5y9VZPfK9YTIZkogpcHQfT3K6asFpsMzjM49GtSgresLVtpIV9tpIk-pYjjry2UqJ_RqyWoLfrCPvvzrN_kIegCvNgAv4b_eviGYclwbzGqZCw6g4ONaLIavP3nq-eHS2-9m-6tm5QGczfaGRXnjJe_c_4D_pursA</recordid><startdate>20100101</startdate><enddate>20100101</enddate><creator>Kang, Bin</creator><creator>Wang, Hao</creator><creator>Nam, Kyoung Hee</creator><creator>Li, Jiayang</creator><creator>Li, Jianming</creator><general>Elsevier Inc</general><general>Oxford University Press</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W94</scope><scope>WU4</scope><scope>~WA</scope><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100101</creationdate><title>Activation-Tagged Suppressors of a Weak Brassinosteroid Receptor Mutant</title><author>Kang, Bin ; 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subjects 35S启动子
Arabidopsis - genetics
Arabidopsis - metabolism
Arabidopsis Proteins - genetics
Arabidopsis Proteins - metabolism
auxin
Brassinosteroid
BRI1
bri1-301
Gene Expression Regulation, Plant - genetics
Gene Expression Regulation, Plant - physiology
Molecular Sequence Data
Plants, Genetically Modified - genetics
Plants, Genetically Modified - metabolism
Steroids, Heterocyclic - metabolism
YUCCA
受体
基因过度表达
抑制因子
油菜素内酯
激活标签
生物圈保护区
突变体
title Activation-Tagged Suppressors of a Weak Brassinosteroid Receptor Mutant
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