Rhizosphere acidification is essential for iron （Fe） uptake into plant roots. Plasma membrane （PM） H＊-ATPases play key roles in rhizosphere acidification. However, it is not fully understood how PM H＋-ATPase act...Rhizosphere acidification is essential for iron （Fe） uptake into plant roots. Plasma membrane （PM） H＊-ATPases play key roles in rhizosphere acidification. However, it is not fully understood how PM H＋-ATPase activity is regulated to enhance root Fe uptake under Fe-deficient conditions. Here, we present evidence that cytochrome b5 reductase 1 （CBR1） increases the levels of unsaturated fatty acids, which stimulate PM H＋-ATPase activity and thus lead to rhizosphere acidification. CBRl-overexpressing （CBRI-OX） Arabidopsis thaliana plants had higher levels of unsaturated fatty acids （18：2 and 18：3）, higher PM H＊-ATPase activity, and lower rhizosphere pH than wild-type plants. By contrast, cbrl loss-of-function mutant plants showed lower levels of unsaturated fatty acids and lower PM H＊-ATPase activity but higher rhizosphere pH. Reduced PM H＊-ATPase activity in cbrl could be restored in vitro by addition of unsatu- rated fatty acids. Transcript levels of CBR1, fatty acids desaturase 2 （FAD2）, and fatty acids desaturase 3 （FAD3） were increased under Fe-deficient conditions. We propose that CBR1 has a crucial role in increasing the levels of unsaturated fatty acids, which activate the PM H＊-ATPase and thus reduce rhizosphere pH. This reaction cascade ultimately promotes root Fe uptake.展开更多
Many approaches to neurodegenerative diseases that focus on amyloid-βclearance and gene therapy have not been successful.Some therapeutic applications focus on enhancing neuronal cell survival during the pathogenesis...Many approaches to neurodegenerative diseases that focus on amyloid-βclearance and gene therapy have not been successful.Some therapeutic applications focus on enhancing neuronal cell survival during the pathogenesis of neurodegenerative diseases,including mitochondrial dysfunction.Plasma membrane(PM)redox enzymes are crucial in maintaining cellular physiology and redox homeostasis in response to mitochondrial dysfunction.Neurohormetic phytochemicals are known to induce the expression of detoxifying enzymes under stress conditions.In this study,mechanisms of neuroprotective effects of 4-hydroxycinnamic acid(HCA)were examined by analyzing cell survival,levels of abnormal proteins,and mitochondrial functions in two different neuronal cells.HCA protected two neuronal cells exhibited high expression of PM redox enzymes and the consequent increase in the NAD^(+)/NADH ratio.Cells cultured with HCA showed delayed apoptosis and decreased oxidative/nitrative damage accompanied by decreased ROS production in the mitochondria.HCA increased the mitochondrial complexes I and II activities and ATP production.Also,HCA increased mitochondrial fusion and decreased mitochondrial fission.Overall,HCA maintains redox homeostasis and energy metabolism under oxidative/metabolic stress conditions.These findings suggest that HCA could be a promising therapeutic approach for neurodegenerative diseases.展开更多
文摘Rhizosphere acidification is essential for iron （Fe） uptake into plant roots. Plasma membrane （PM） H＊-ATPases play key roles in rhizosphere acidification. However, it is not fully understood how PM H＋-ATPase activity is regulated to enhance root Fe uptake under Fe-deficient conditions. Here, we present evidence that cytochrome b5 reductase 1 （CBR1） increases the levels of unsaturated fatty acids, which stimulate PM H＋-ATPase activity and thus lead to rhizosphere acidification. CBRl-overexpressing （CBRI-OX） Arabidopsis thaliana plants had higher levels of unsaturated fatty acids （18：2 and 18：3）, higher PM H＊-ATPase activity, and lower rhizosphere pH than wild-type plants. By contrast, cbrl loss-of-function mutant plants showed lower levels of unsaturated fatty acids and lower PM H＊-ATPase activity but higher rhizosphere pH. Reduced PM H＊-ATPase activity in cbrl could be restored in vitro by addition of unsatu- rated fatty acids. Transcript levels of CBR1, fatty acids desaturase 2 （FAD2）, and fatty acids desaturase 3 （FAD3） were increased under Fe-deficient conditions. We propose that CBR1 has a crucial role in increasing the levels of unsaturated fatty acids, which activate the PM H＊-ATPase and thus reduce rhizosphere pH. This reaction cascade ultimately promotes root Fe uptake.
基金supported by the National Research Foundation of Korea(NRF)of the Korean Government(NRF-2021R1F1A1051212)by Logsynk Co.Ltd.(2-2021-1435-001).
文摘Many approaches to neurodegenerative diseases that focus on amyloid-βclearance and gene therapy have not been successful.Some therapeutic applications focus on enhancing neuronal cell survival during the pathogenesis of neurodegenerative diseases,including mitochondrial dysfunction.Plasma membrane(PM)redox enzymes are crucial in maintaining cellular physiology and redox homeostasis in response to mitochondrial dysfunction.Neurohormetic phytochemicals are known to induce the expression of detoxifying enzymes under stress conditions.In this study,mechanisms of neuroprotective effects of 4-hydroxycinnamic acid(HCA)were examined by analyzing cell survival,levels of abnormal proteins,and mitochondrial functions in two different neuronal cells.HCA protected two neuronal cells exhibited high expression of PM redox enzymes and the consequent increase in the NAD^(+)/NADH ratio.Cells cultured with HCA showed delayed apoptosis and decreased oxidative/nitrative damage accompanied by decreased ROS production in the mitochondria.HCA increased the mitochondrial complexes I and II activities and ATP production.Also,HCA increased mitochondrial fusion and decreased mitochondrial fission.Overall,HCA maintains redox homeostasis and energy metabolism under oxidative/metabolic stress conditions.These findings suggest that HCA could be a promising therapeutic approach for neurodegenerative diseases.
