Iron uptake system mediates nitrate-facilitated cadmium accumulation in tomato (Solanum lycopersicum) plants.

Nitrogen (N) management is a promising agronomic strategy to minimize cadmium (Cd) contamination in crops. However, it is unclear how N affects Cd uptake by plants. Wild-type and iron uptake-inefficient tomato (Solanum lycopersicum) mutant (T3238fer) plants were grown in pH-buffered hydroponic culture to investigate the direct effect of N-form on Cd uptake. Wild-type plants fed NO3⁻ accumulated more Cd than plants fed NH4⁺. Iron uptake and LeIRT1 expression in roots were also greater in plants fed NO3⁻. However, in mutant T3238fer which loses FER function, LeIRT1 expression in roots was almost completely terminated, and the difference between NO3⁻ and NH4⁺ treatments vanished. As a result, the N-form had no effect on Cd uptake in this mutant. Furthermore, suppression of LeIRT1 expression by NO synthesis inhibition with either tungstate or L-NAME, also substantially inhibited Cd uptake in roots, and the difference between N-form treatments was diminished. Considering all of these findings, it was concluded that the up-regulation of the Fe uptake system was responsible for NO3⁻-facilitated Cd accumulation in plants.

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

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 F(1) 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 NH(4)(+), 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.