The changes in external K^＋ concentration affect plant root growth. However, the molecular mechanism for perceiving a K^＋ signal to modulate root growth remains unknown. It is hypothesized that the K^＋ channel AKTI...The changes in external K^＋ concentration affect plant root growth. However, the molecular mechanism for perceiving a K^＋ signal to modulate root growth remains unknown. It is hypothesized that the K^＋ channel AKTI is involved in low K^＋ sensing in the Arabidopsis root and subsequent regulation of root growth. Along with the decline of external K^＋ concentration, the primary root growth of wild-type plants was gradually inhibited. However, the primary root of the akt1 mutant could still grow under low K^＋（LK） conditions. Application of NAA inhibited akt1 root growth, but promoted wild-type root growth under LK conditions. By using the ProDR5：GFP and ProPIN1：PIN1-GFP lines, we found that LK treatment reduced auxin accumulation in wild-type root tips by degrading PIN1 proteins, which did not occur in the akt1 mutant. The LK-induced PIN1 degradation may be due to the inhibition of vesicle trafficking of PIN1 proteins. In conclusion, our findings indicate that AKT1 is required for an Arabidopsis response to changes in external K^＋, and subsequent regulation of K^＋-dependent root growth by modulating PINt degradation and auxin redistribution in the root.展开更多
基金supported by grants from the National Natural Science Foundation of China(31570243No.31622008No.31421062)
文摘The changes in external K^＋ concentration affect plant root growth. However, the molecular mechanism for perceiving a K^＋ signal to modulate root growth remains unknown. It is hypothesized that the K^＋ channel AKTI is involved in low K^＋ sensing in the Arabidopsis root and subsequent regulation of root growth. Along with the decline of external K^＋ concentration, the primary root growth of wild-type plants was gradually inhibited. However, the primary root of the akt1 mutant could still grow under low K^＋（LK） conditions. Application of NAA inhibited akt1 root growth, but promoted wild-type root growth under LK conditions. By using the ProDR5：GFP and ProPIN1：PIN1-GFP lines, we found that LK treatment reduced auxin accumulation in wild-type root tips by degrading PIN1 proteins, which did not occur in the akt1 mutant. The LK-induced PIN1 degradation may be due to the inhibition of vesicle trafficking of PIN1 proteins. In conclusion, our findings indicate that AKT1 is required for an Arabidopsis response to changes in external K^＋, and subsequent regulation of K^＋-dependent root growth by modulating PINt degradation and auxin redistribution in the root.
