NO synthase-generated NO acts downstream of auxin in regulating Fe-deficiency-induced root branching that enhances Fe-deficiency tolerance in tomato plants

Abstract

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.

Increased Sucrose Accumulation Regulates Iron-Deficiency Responses by Promoting Auxin Signaling in Arabidopsis Plants

“…S8). The result is consistent with previous reports (Chen et al, 2010b;Jin et al, 2011). Application of 2 mM Suc further increased the GUS staining in roots of Fe-deficient plants.…”

“…Since previous studies have shown that auxins play a critical role in the regulation of Fe deficiency responses (Chen et al, 2010b;Jin et al, 2011;Wu et al, 2012b), it is therefore necessary to clarify whether auxins have an association with Suc in the regulation of Fe deficiency responses. As shown in Figure 9, in the presence of the auxin transport inhibitor NPA, the stimulating effect of Suc on root FCR activity and expression of IRT1, FRO2, and FIT in Fedeficient Col-0 plants were completely terminated.…”

“…In addition to the above transcription factors, we and others showed that the chemical molecules, auxins and nitric oxide (NO), both of which accumulate to higher levels in Fe-deficient plants, are also two general regulators controlling the initiation of adaptations to Fe deficiency in Strategy I plants (Graziano and Lamattina, 2007;Jin et al, 2009Jin et al, , 2011Chen et al, 2010b;Bacaicoa et al, 2011;Wu et al, 2012b). The NO acts upstream of FIT to trigger Fe deficiency responses through a mechanism of reducing the proteasomal degradation of FIT (Meiser et al, 2011), while the elevation of auxin levels is required for the regulation of increased synthesis of NO under Fe-deficient conditions (Chen et al, 2010b;Jin et al, 2011).…”

“…The NO acts upstream of FIT to trigger Fe deficiency responses through a mechanism of reducing the proteasomal degradation of FIT (Meiser et al, 2011), while the elevation of auxin levels is required for the regulation of increased synthesis of NO under Fe-deficient conditions (Chen et al, 2010b;Jin et al, 2011). Therefore, we previously suggested an auxin→NO→FIT signaling cascade in transmitting Fe deficiency information (Chen et al, 2010b), but the identity of the upstream signal of auxins remains unknown.…”

Cross–talk between nitric oxide and Ca2+in elevated CO2-induced lateral root formation

“…Many studies have investigated plant responses to elevated CO 2 on the ecosystem, community, population, physiological and molecular scales. [1][2][3][4] Based previous studies, we reported that elevated CO 2 promoted the development of LRs of tomato and NO was a signaling molecule that controls these processes. 5 Increased LRs could eliminate nutrient stress under elevated CO 2 , which play an important role in nutrient acquisition.…”