ROS and Ethylene

ROS have been shown to accumulate in a discrete region of roots active in K+ uptake and they are translocated during low K+ stress (Shin and Schachtman 2004). Knock-out of an NADPH oxidase (rhd2 plants) prevented upregulation of genes that are normally induced by K+ starvation, such as AtHAK5, but the high-affinity K+ uptake remained unchanged. Application of H2O2 restored the expression of those genes induced by K+ deficiency in rhd2 plants. Both ethylene production and the transcription of genes involved in ethylene biosynthesis also increased when plants were deprived of K+ (Jung et al. 2009; Shin and Schachtman 2004). However, in the ethylene insensitive2-1 (ein2-1) mutant, the ethylene-mediated low K+ responses were not completely eliminated, suggesting that some K+ deprivation-induced responses are either ethylene independent or EIN2 independent. Ethylene signaling stimulated the production of ROS and thereby it seems to constitute an earlier step in low K+ response. Nevertheless, elements acting upstream ethylene signaling in the onset of low K+ responses are still unknown. These results suggested that K+-dependent regulation of AtHAK5 mRNA levels relied, at least to some extent, on this ethylene-ROS pathway.

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