Regulated Degradation of HFR1 Desensitizes Light Signaling in Arabidopsis

Arabidopsis seedlings undergo photomorphogenesis in the light and etiolation in the dark. HFR1, a bHLH transcription factor, is required for both phytochrome A (phyA)-mediated far-red and cryptochrome 1 (cry1)-mediated blue light signaling. We report that HFR1 is a short-lived protein in darkness and is degraded through a 26S proteasome-dependent pathway. Light, irrespective of its quality, enhances HFR1 protein accumulation via promoting its stabilization. We demonstrate that HFR1 physically interacts with COP1 and that COP1 exhibits ubiquitin ligase activity toward HFR1 in vitro. In addition, we show that COP1 is required for degradation of HFR1 in vivo. Furthermore, plants overexpressing a C-terminal 161 amino acid fragment of HFR1 (CT161) display enhanced photomorphogenesis, suggesting an autonomous function of CT161 in promoting light signaling. This truncated HFR1 gene product is more stable than the full-length HFR1 protein in darkness, indicating that the COP1-interacting N-terminal portion of HFR1 is essential for COP1-mediated destabilization of HFR1. These results suggest that light enhances HFR1 protein accumulation by abrogating COP1-mediated degradation of HFR1, which is necessary and sufficient for promoting light signaling. Additionally, our results substantiate the E3 ligase activity of COP1 and its critical role in desensitizing light signaling.

Radiation-induced 1/f noise degradation of bipolar linear voltage regulator

Radiation-induced 1/f noise degradation in the LM117 bipolar linear voltage regulator is studied. Based on the radiation-induced degradation mechanism of the output voltage, it is suggested that the band-gap reference subcircuit is the critical component which leads to the 1/f noise degradation of the LM117. The radiation makes the base surface current of the bipolar junction transistors of the band-gap reference subcircuit increase, which leads to an increase in the output 1/f noise of the LM117. Compared to the output voltage, the 1/f noise parameter is more sensitive, it may be used to evaluate the radiation resistance capability of LM117.

Optimization of the in vitro biodegradability,cytocompatibility,and wear resistance of the AZ31B alloy by micro-arc oxidation coatings doped with zinc phosphate

As implanted bone fixation materials,magnesium(Mg)alloys have significant advantages because the density and elastic modulus are closest to those of the human bone and they can bio-degrade in the physiological environment.However,Mg alloys degrade too rapidly and uncontrollably thus hampering clinical adoption.In this study,a highly corrosion-resistant zinc-phosphate-doped micro-arc oxidation(MAO)coating is prepared on the AZ31B alloy,and the degradation process is assessed in vitro.With increasing zinc phosphate concentrations,both the corrosion potentials and charge transfer resistance of the AZ31B alloy coated with MAO coatings increase gradually,while the corrosion current densities di-minish gradually.Immersion tests in the simulated body fluid(SBF)reveal that the increased zinc phos-phate concentration in MAO coating decreases the degradation rate,consequently reducing the release rates of Mg^(2+)and OH-in the physiological micro-environment,which obtains the lowest weight loss of only 5.22%after immersion for 56 days.Effective regulation of degradation provides a weak alkaline environment that is suitable for long-term cell growth and subsequent promotion of bone proliferation,differentiation,mineralization,and cytocompatibility.In addition,the zinc-phosphate-doped MAO coat-ings show an improved wear resistance as manifested by a wear rate of only 3.81 x 10^(-5) mm^(3) N^(-1) m^(-1).The results reveal a suitable strategy to improve the properties of biodegradable Mg alloys to balance tissue healing with mechanical degradation.