ABSTRACT

The siz1 mutants exhibit high SA accumulation and consequently severe dwarfism. Although siz1 mutants exhibit growth recovery upon exogenous ammonium supply, the underlying mechanism remains unknown. Here, we investigated the effect of ammonium on SA level and plant growth in SA-accumulating mutants. The growth of siz1-2 and siz1-3 mutants was recovered to wild-type (WT) levels upon exogenous ammonium supply, but that of siz1-3 ndr1 (non-race-specific disease resistance 1) and siz1-3 npr1 (non-expressor of pathogenesis related gene 1) double mutants was unaffected. The SA level was decreased by exogenous ammonium application in siz1-3 ndr1, siz1-3 npr1, and siz1-3 mutants. The level of nitrate reductase (NR) was almost the same in all genotypes (WT, siz1-3, ndr1, npr1, siz1-3 ndr1, and siz1-3 npr1), regardless of the ammonium treatment, suggesting that exogenous ammonium supply to ndr1 siz1-3 and npr1 siz1-3 double mutants does not have any effect on their growth and NR levels, but decreases the SA level. Taken together, these results indicate that ammonium acts as a signaling molecule to regulate the SA amount, and NDR1 and NPR1 play a positive role in the ammonium-mediated growth recovery of siz1 mutants.

 抽象的

siz1突变体表现出高SA积累并因此导致严重的侏儒症。尽管siz1突变体在外源铵供应下表现出生长恢复，但其潜在机制仍不清楚。在这里，我们研究了铵对 SA 积累突变体中 SA 水平和植物生长的影响。外源铵供应后， siz1-2和siz1-3突变体的生长恢复到野生型 (WT) 水平，但siz1-3 ndr1 （非种族特异性抗病性 1 ）和siz1-3 npr1 （非-发病机制相关基因1)双突变体的表达不受影响。在siz1-3 ndr1、siz1-3 npr1和siz1-3突变体中施用外源铵可降低 SA 水平。无论铵处理如何，所有基因型（WT、 siz1-3、ndr1、npr1、siz1-3 ndr1和siz1-3 npr1 ）的硝酸还原酶 (NR) 水平几乎相同，这表明外源铵供应ndr1 siz1-3和npr1 siz1-3双突变体对其生长和NR水平没有任何影响，但降低了SA水平。综上所述，这些结果表明铵作为信号分子来调节SA量，并且NDR1和NPR1在铵介导的siz1突变体的生长恢复中发挥积极作用。