Target of rapamycin (TOR) kinase is a sensor and a central integrator of internal and external metabolic cues. However, in algae and in higher plants, the components of TOR kinase signaling are yet to be characterized. Here, we establish an assay system to study TOR kinase activity in Chlamydomonas reinhardtii using the phosphorylation status of its putative downstream target, CrS6K. Using this assay, we probe the modulation of cellular TOR kinase activity under various physiological states such as photoautotrophy, heterotrophy, mixotrophy, and nitrogen (N) starvation. Importantly, we uncover that excess acetate in the medium leads to high cellular reactive oxygen species levels, triggering autophagy and a concomitant drop in TOR kinase activity in a dose-dependent manner, thus leading to a N-starvationlike cellular phenotype, even when nitrogen is present.
Target Of Rapamycin (TOR) kinase is a sensor as well as a central integrator of internal and external metabolic cues. The upstream and downstream signals of this kinase are very well characterized in animals. However, in algae, higher plants and other photosynthetic organisms, the components of the TOR kinasesignaling are yet to be characterized. Here, we establish an assay system to study TOR kinase activity in C.reinhardtii using the phosphorylation status of its downstream target, CrS6K. We further use this assay to monitor TOR kinase activity under various physiological states such as photoautotrophy, heterotrophy, mixotrophy and nitrogen starvation. We observe that autotrophy in light (and not in dark) leads to TOR kinase attenuation during N starvation while the same is not observed in mixotrophy. Importantly, we show that the external carbon source glucose is sensed and uptaken by C.reinhardtii cells only in the presence of light and not in the dark. And such exogenously added glucose, as the photoassimilate carbon mimic, results in enhanced production of ROS, induction of autophagy and concomitant drop in TOR kinase activity, creating Nstarvation-like cellular state even in N+ conditions. Interestingly, dose dependent addition of glucose revealed TOR kinase activation in low glucose regime (ROS independent) followed by attenuation of TOR kinase (ROS dependent) at high glucose levels.
Nutrition plays a pivotal role in depression, but dietary interventions are usually not personalized and do not consider patients microbial and human molecular functions. This preliminary study evaluated the effectiveness of precision supplements (PS) on depression symptoms as part of a personalized nutrition subscription plan that accounts for the gene expression activity of the microbiome and the human host. People with depression, 86 taking PS and 45 controls responded to the patient health questionnaire-9 (PHQ-9) at two time points an average of ~6 months apart. Categorical changes were evaluated using the PHQ-9 score system, and clinically significant categorical differences were observed between the two groups (effect size = 0.48; p <0.001). The difference in differences was calculated using multiple group propensity score weighting adjusting for age, sex, BMI, and physical activity, and the PHQ-9 score decreased by ~4 points (~29%) for the intervention group (t0: 13.75+-3.80, t1: 9.78+-6.42) vs Controls (t0: 14.07+-3.64, t1: 13.59 +-6.65). Thus, precision supplement use over ~6 months significantly reduced depression symptoms, with 69.8% of the individuals in the intervention group improving their category to no/low depression vs. 15.6% in the control group.
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