Both AtrbohD and AtrbohF are essential for mediating responses to oxygen deficiency in Arabidopsis

作者：Liu B, Sun LR, Ma LY, Hao FS.

刊名：Plant Cell Reports；

年卷页码：DOI: Volume 36, Issue 6, pp 947–957；

网联：https://link.springer.com/article/10.1007%2Fs00299-017-2128-x

Abstract

NADPH oxidase AtrbohD and AtrbohF cooperatively play key roles in regulation of growth and stress signaling in Arabidopsis. However, reports on AtrbohD and AtrbohF functioning together in hypoxia signaling are scarce, and the underlying mechanisms remain elusive. Here, we show that the double null mutant atrbohD/F is more sensitive to oxygen deprivation compared with wild type (WT) and the single mutant atrbohD and atrbohF. Under oxygen deficiency, enhancements of the transcripts of alcohol dehydrogenase 1 (ADH1) and pyruvate decarboxylase 1 (PDC1) and the activities of ADH, PDC and lactate dehydrogenase in WT are clearly reduced in the single mutants, and more strongly reduced in the double mutant. Moreover, increases in the production of ATP, H2O2 and Ca2+ in WT are significantly arrested in atrbohD, atrbohF, and especially in atrbohD/F. Hypoxia-promoted rise in the expression of some hypoxic responsive genes is also inhibited in atrbohD/F relative to WT, atrbohD andatrbohF. These genes include ethylene response factor 73, lactate dehydrogenase, MYB transcription factor 2, sucrose synthase 1 (SUS1), SUS4, heat stress transcription factor A2and heat-shock protein 18.2. These results suggest that both AtrbohD and AtrbohF are essential for mediating hypoxia signaling. H2O2 derived from AtrbohD and AtrbohF triggers the Ca2+increase and induces the expression of multiple hypoxia response genes, thus improvingArabidopsis tolerance to low-oxygen stress. These findings provide new insights into the mechanisms of AtrbohF in regulating the responses to oxygen deprivation in Arabidopsis.