DFL1, an auxin-responsive GH3 gene homologue, negatively regulates shoot cell elongation and lateral root formation, and positively regulates the light response of hypocotyl length.

M. Nakazawa, N. Yabe, T. Ichikawa, Yoshiharu Y. Yamamoto, T. Yoshizumi, Kohji Hasunuma, M. Matsui
{"title":"DFL1, an auxin-responsive GH3 gene homologue, negatively regulates shoot cell elongation and lateral root formation, and positively regulates the light response of hypocotyl length.","authors":"M. Nakazawa, N. Yabe, T. Ichikawa, Yoshiharu Y. Yamamoto, T. Yoshizumi, Kohji Hasunuma, M. Matsui","doi":"10.1046/J.1365-313X.2001.00957.X","DOIUrl":null,"url":null,"abstract":"A novel dominant mutant designated 'dwarf in light 1' (dfl1-D) was isolated from screening around 1200 Arabidopsis activation-tagged lines. dfl1-D has a shorter hypocotyl under blue, red and far-red light, but not in darkness. Inhibition of cell elongation in shoots caused an exaggerated dwarf phenotype in the adult plant. The lateral root growth of dfl1-D was inhibited without any reduction of primary root length. The genomic DNA adjacent to the right border of T-DNA was cloned by plasmid rescue. The rescued genomic DNA contained a gene encoding a GH3 homologue. The transcript was highly accumulated in the dfl1-D. The dfl1-D phenotype was confirmed by over-expression of the gene in the wild-type plant. The dfl1-D showed resistance to exogenous auxin treatment. Moreover, over-expression of antisense DFL1 resulted in larger shoots and an increase in the number of lateral roots. These results indicate that the gene product of DFL1 is involved in auxin signal transduction, and inhibits shoot and hypocotyl cell elongation and lateral root cell differentiation in light.","PeriodicalId":142476,"journal":{"name":"The Plant journal : for cell and molecular biology","volume":"29 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2008-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"295","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Plant journal : for cell and molecular biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1046/J.1365-313X.2001.00957.X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 295

Abstract

A novel dominant mutant designated 'dwarf in light 1' (dfl1-D) was isolated from screening around 1200 Arabidopsis activation-tagged lines. dfl1-D has a shorter hypocotyl under blue, red and far-red light, but not in darkness. Inhibition of cell elongation in shoots caused an exaggerated dwarf phenotype in the adult plant. The lateral root growth of dfl1-D was inhibited without any reduction of primary root length. The genomic DNA adjacent to the right border of T-DNA was cloned by plasmid rescue. The rescued genomic DNA contained a gene encoding a GH3 homologue. The transcript was highly accumulated in the dfl1-D. The dfl1-D phenotype was confirmed by over-expression of the gene in the wild-type plant. The dfl1-D showed resistance to exogenous auxin treatment. Moreover, over-expression of antisense DFL1 resulted in larger shoots and an increase in the number of lateral roots. These results indicate that the gene product of DFL1 is involved in auxin signal transduction, and inhibits shoot and hypocotyl cell elongation and lateral root cell differentiation in light.
DFL1是生长素响应型GH3基因的同源物,负调控茎部细胞伸长和侧根形成,正调控下胚轴长度的光响应。
从筛选的1200个拟南芥激活标记系中分离到一个新的显性突变体'dwarf in light 1' (dfl1-D)。dfl1-D在蓝光、红光和远红光下的下胚轴较短,而在黑暗中则不然。抑制芽部细胞伸长导致成株矮化表型过度。dfl1-D的侧根生长受到抑制,但主根长度没有减少。利用质粒拯救法克隆了T-DNA右缘附近的基因组DNA。获救的基因组DNA包含一个编码GH3同源物的基因。转录本在dfl1-D中高度积累。dfl1-D基因在野生型植物中的过表达证实了其表型。dfl1-D对外源生长素处理表现出抗性。此外,过表达反义DFL1导致芽变大,侧根数量增加。这些结果表明,DFL1基因产物参与生长素信号转导,并在光照下抑制茎、下胚轴细胞伸长和侧根细胞分化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信