Plant cryptochromes undergo blue light-dependent phosphorylation to regulate their activity and abundance, but the protein kinases that phosphorylate plant cryptochromes have remained unclear. Here we show that photoexcited Arabidopsis cryptochrome 2 (CRY2) is phosphorylated in vivo on as many as 24 different residues, including 7 major phosphoserines. We demonstrate that four closely related Photoregulatory Protein Kinases (previously referred to as MUT9-like kinases) interact with and phosphorylate photoexcited CRY2. Analyses of the ppk123 and ppk124 triple mutants and amiR4k artificial microRNA-expressing lines demonstrate that PPKs catalyse blue light-dependent CRY2 phosphorylation to both activate and destabilize the photoreceptor. Phenotypic analyses of these mutant lines indicate that PPKs may have additional substrates, including those involved in the phytochrome signal transduction pathway. These results reveal a mechanism underlying the co-action of cryptochromes and phytochromes to coordinate plant growth and development in response to different wavelengths of solar radiation in nature.
Background Lack of time for exercise is common among office workers given their busy lives. Because of occupational restrictions and difficulty in taking time off, it is necessary to suggest effective ways for workers to exercise regularly. Sustaining lifestyle habits that increase nonexercise activity in daily life can solve the issue of lack of exercise time. Healthy Lifestyle Coaching Chatbot is a messenger app based on the habit formation model that can be used as a tool to provide a health behavior intervention that emphasizes the importance of sustainability and involvement. Objective This study aimed to assess the efficacy of the Healthy Lifestyle Coaching Chatbot intervention presented via a messenger app aimed at stair-climbing habit formation for office workers. Methods From February 1, 2018, to April 30, 2018, a total of 106 people participated in the trial after online recruitment. Participants were randomly assigned to the intervention group (n=57) or the control group (n=49). The intervention group received cues and intrinsic and extrinsic rewards for the entire 12 weeks. However, the control group did not receive intrinsic rewards for the first 4 weeks and only received all rewards as in the intervention group from the fifth to twelfth week. The Self-Report Habit Index (SRHI) of participants was evaluated every week, and the level of physical activity was measured at the beginning and end of the trial. SPSS Statistics version 21 (IBM Corp) was used for statistical analysis. Results After 4 weeks of intervention without providing the intrinsic rewards in the control group, the change in SRHI scores was 13.54 (SD 14.99) in the intervention group and 6.42 (SD 9.42) in the control group, indicating a significant difference between the groups (P=.04). When all rewards were given to both groups, from the fifth to twelfth week, the change in SRHI scores of the intervention and control groups was comparable at 12.08 (SD 10.87) and 15.88 (SD 13.29), respectively (P=.21). However, the level of physical activity showed a significant difference between the groups after 12 weeks of intervention (P=.045). Conclusions This study provides evidence that intrinsic rewards are important to enhance the sustainability and effectiveness of an intervention. The Healthy Lifestyle Coaching Chatbot program can be a cost-effective method for healthy habit formation. Trial Registration Clinical Research Information Service KCT0004009; https://tinyurl.com/w4oo7md
Necroptosis is a type of programmed necrosis regulated by receptor interacting protein kinase 1 (RIP1) and RIP3. Necroptosis is found to be accompanied by an overproduction of reactive oxygen species (ROS), but the role of ROS in regulation of necroptosis remains elusive. In this study, we investigated how shikonin, a necroptosis inducer for cancer cells, regulated the signaling leading to necroptosis in glinoma cells in vitro. Treatment with shikonin (2-10 μmol/L) dose-dependently triggered necrosis and induced overproduction of intracellular ROS in rat C6 and human SHG-44, U87 and U251 glioma cell lines. Moreover, shikonin treatment dose-dependently upregulated the levels of RIP1 and RIP3 and reinforced their interaction in the glioma cells. Pretreatment with the specific RIP1 inhibitor Nec-1 (100 μmol/L) or the specific RIP3 inhibitor GSK-872 (5 μmol/L) not only prevented shikonin-induced glioma cell necrosis but also significantly mitigated the levels of intracellular ROS and mitochondrial superoxide. Mitigation of ROS with MnTBAP (40 μmol/L), which was a cleaner of mitochondrial superoxide, attenuated shikonin-induced glioma cell necrosis, whereas increasing ROS levels with rotenone, which improved the mitochondrial generation of superoxide, significantly augmented shikonin-caused glioma cell necrosis. Furthermore, pretreatment with MnTBAP prevented the shikonin-induced upregulation of RIP1 and RIP3 expression and their interaction while pretreatment with rotenone reinforced these effects. These findings suggest that ROS is not only an executioner of shikonin-induced glioma cell necrosis but also a regulator of RIP1 and RIP3 expression and necrosome assembly.
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