NO synthase-generated NO acts downstream of auxin in regulating Fe-deficiency-induced root branching that enhances Fe-deficiency tolerance in tomato plants.
NO synthase-generated NO acts downstream of auxin in regulating Fe-deficiency-induced root branching that enhances Fe-deficiency tolerance in tomato plants.
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NO 合成酶产生的 NO 作用于生长素下游，调节缺铁诱导的根分枝，从而增强番茄植株的缺铁耐受性
DOI：
10.1093/jxb/err078
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发表时间：
2011-07
影响因子：
6.9
通讯作者：
Lin XY
中科院分区：
文献类型：
--
作者：
Jin CW;Du ST;Shamsi IH;Luo BF;Lin XY
在响应铁缺乏，各种双子叶植物增加其根分枝，这有助于提高铁螯合还原酶活性。缺铁诱导的这一反应是否最终增强了植物对缺铁的耐受能力，目前尚不清楚，触发这一反应的信号也缺乏证据。在缺铁条件下，番茄品系line 227/1和Roza及其正反交F1代的根系分枝与铁胁迫呈正相关。这表明缺铁诱导的根分枝是植物耐缺铁的关键。在另一个番茄系中，Micro-Tom，在缺铁植物中增加的根分枝伴随着内源生长素和一氧化氮（NO）水平的升高，并且被生长素转运抑制剂NPA和TIBA或NO清除剂cPTIO抑制。另一方面，在铁充足的植物诱导根分枝生长素类似物NAA和2，4-D或NO供体NONOate或SNP。此外，在铁缺乏的植物，NONOate恢复NPA终止的根分枝，但NAA不影响cPTIO终止的根分枝。缺铁诱导的根分枝被一氧化氮合酶（NOS）抑制剂L-NAME抑制，但不受硝酸还原酶（NR）抑制剂NH 4+，钨酸盐或甘氨酸。综上所述，本文提出了一种新的缺铁诱导的根分枝的功能和信号途径，其中一氧化氮生成的NO作用于生长素的下游，而非NR生成的NO作用于生长素的下游，调节缺铁诱导的反应，从而增强植物对缺铁的耐受性。
In response to Fe-deficiency, various dicots increase their root branching which contributes to the enhancement of ferric-chelate reductase activity. Whether this Fe-deficiency-induced response eventually enhances the ability of the plant to tolerate Fe-deficiency or not is still unclear and evidence is also scarce about the signals triggering it. In this study, it was found that the SPAD-chlorophyll meter values of newly developed leaves of four tomato (Solanum lycocarpum) lines, namely line227/1 and Roza and their two reciprocal F1 hybrid lines, were positively correlated with their root branching under Fe-deficient conditions. It indicates that Fe-deficiency-induced root branching is critical for plant tolerance to Fe-deficiency. In another tomato line, Micro-Tom, the increased root branching in Fe-deficient plants was accompanied by the elevation of endogenous auxin and nitric oxide (NO) levels, and was suppressed either by the auxin transport inhibitors NPA and TIBA or the NO scavenger cPTIO. On the other hand, root branching in Fe-sufficient plants was induced either by the auxin analogues NAA and 2,4-D or the NO donors NONOate or SNP. Further, in Fe-deficient plants, NONOate restored the NPA-terminated root branching, but NAA did not affect the cPTIO-terminated root branching. Fe-deficiency-induced root branching was inhibited by the NO-synthase (NOS) inhibitor L-NAME, but was not affected by the nitrate reductase (NR) inhibitor NH4+, tungstate or glycine. Taking all of these findings together, a novel function and signalling pathway of Fe-deficiency-induced root branching is presented where NOS-generated rather than NR-generated NO acts downstream of auxin in regulating this Fe-deficiency-induced response, which enhances the plant tolerance to Fe-deficiency.
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影响因子：
11.4
作者：
Jin, Chong-Wei;Chen, Wei-Wei;Zheng, Shao-Jian
通讯作者：
Zheng, Shao-Jian
影响因子：
7.4
作者：
Flores, Teresita;Todd, Christopher D.;Polacco, Joe C.
通讯作者：
Polacco, Joe C.
影响因子：
4.9
作者：
Dasgan, HY;Römheld, V;Abak, K
通讯作者：
Abak, K
影响因子：
4.3
作者：
MOOG, PR;VANDERKOOIJ, TAW;KUIPER, PJC
通讯作者：
KUIPER, PJC
影响因子：
4.3
作者：
Correa-Aragunde, N;Graziano, M;Lamattina, L
通讯作者：
Lamattina, L