Nitric Oxide Plays a Role in Stem Cell Niche Homeostasis through Its Interaction with Auxin1[W][OPEN]

被引:74
作者
Sanz, Luis [1 ]
Fernandez-Marcos, Maria [1 ]
Modrego, Abelardo [1 ]
Lewis, Daniel R. [2 ,3 ]
Muday, Gloria K. [2 ,3 ]
Pollmann, Stephan [4 ]
Duenas, Montserrat [5 ]
Santos-Buelga, Celestino [5 ]
Lorenzo, Oscar [1 ]
机构
[1] Univ Salamanca, Fac Biol, Inst Hispano Luso Invest Agr, Dept Fisiol Vegetal, Salamanca 37185, Spain
[2] Wake Forest Univ, Dept Biol, Winston Salem, NC 27109 USA
[3] Wake Forest Univ, Ctr Mol Commun & Signaling, Winston Salem, NC 27109 USA
[4] Univ Madrid, Ctr Biotecnol & Genom Plantas, Inst Nacl Invest & Tecnol Agr & Alimentaria, Madrid 3, Spain
[5] Univ Salamanca, Unidad Nutr & Bromatol, Grp Invest Polifenoles, Salamanca 37007, Spain
基金
美国国家科学基金会;
关键词
AUXIN TRANSPORT; ARABIDOPSIS-THALIANA; ROOT DEVELOPMENT; GENE-EXPRESSION; CYCLIC-GMP; IN-VIVO; GROWTH; BIOSYNTHESIS; DIFFERENTIATION; PROLIFERATION;
D O I
10.1104/pp.114.247445
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Nitric oxide (NO) is a unique reactive nitrogen molecule with an array of signaling functions that modulates plant developmental processes and stress responses. To explore the mechanisms by which NO modulates root development, we used a pharmacological approach and NO-deficient mutants to unravel the role of NO in establishing auxin distribution patterns necessary for stem cell niche homeostasis. Using the NO synthase inhibitor and Arabidopsis (Arabidopsis thaliana) NO biosynthesis mutants (nitric oxide-associated1 [noa1], nitrate reductase1 [nia1] and nia2, and nia1 nia2 noa1), we show that depletion of NO in noa1 reduces primary root elongation and increases flavonol accumulation consistent with elevated reactive oxygen species levels. The elevated flavonols are required for the growth effect, because the transparent testa4 mutation reverses the noa1 mutant root elongation phenotype. In addition, noa1 and nia1 nia2 noa1 NO-deficient mutant roots display small root meristems with abnormal divisions. Concomitantly, auxin biosynthesis, transport, and signaling are perturbed. We further show that NO accumulates in cortex/ endodermis stem cells and their precursor cells. In endodermal and cortical cells, the noa1 mutant acts synergistically to the effect of the wuschel-related homeobox5 mutation on the proximal meristem, suggesting that NO could play an important role in regulating stem cell decisions, which has been reported in animals.
引用
收藏
页码:1972 / U1195
页数:28
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