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Chen, Y.-l.

Publications and source records attributed to Chen, Y.-l..

2 recordsLinked to original sources

OsUVR8b, rather than OsUVR8a, plays a predominant role in rice UVR8-mediated UV-B response.

UV RESISTANCE LOCUS 8 (UVR8) has been identified in Arabidopsis thaliana as the receptor for UV-B radiation mediating photomorphogenic responses and acclimation to UV-B radiation. However, UVR8-mediated UV-B signaling pathways in rice, that has two proteins (UVR8a and UVR8b) with homology to AtUVR8, remain largely unknown. In this study, UVR8a and UVR8b were found to be expressed mainly in rice leaves and leaf sheaths, while the level of UVR8b was higher than that of UVR8a. In agreement with prior studies on AtUVR8, uvr8b and uvr8a uvr8b rice mutants exposed to UV-B showed reduced UVB-induced growth inhibition and upregulation of CHS and HY5 transcripts along with acclimation to UV-B, overexpressing UVR8a or UVR8b enhanced UV-B-induced growth inhibition and acclimation to UV-B, compared to wild-type plants. UV-B was able to enhance the interaction between CONSTITUTIVE PHOTOMORPHOGENESIS1 (COP1) with UVR8a/UVR8b, whereas the interaction intensity of REPRESSOR OF UV-B PHOTOMORPHOGENESIS2 (RUP2) with UVR8a was significantly higher than that with UVR8b. In addition, UVR8a and UVR8b were also found in the nucleus and cytoplasm, but OsUVR8 proteins were localized in nucleus in the absence of UV-B. The level of OsUVR8 monomer showed an invisible change in the leaves of rice seedlings transferred from white light to white light supplemented with UV-B, even UV-B can weaken the interactions of UVR8a or/and UVR8b. Therefore, both UVR8a and UVR8b, that have different location and response modes with Arabidopsis UVR8, function in the response of rice to UV-B radiation, whereas UVR8b plays a predominant role in this process.

plant biology↗

Muscle FOXO-specific overexpression and endurance exercise protects skeletal muscle and heart from defects caused by a high-fat diet in young Drosophila

Obesity appears to significantly reduce physical activity, but it remains unclear whether this is related to obesity-induced damage to skeletal muscle(SM) and heart muscle(HM). Endurance exercise(EE) reduces obesity-induced defects in SM and HM, but its molecular mechanism is poorly understood. The results showed that the structure and function of SM and HM were impaired by a high-fat diet(HFD) and muscle-FOXO-specific RNAi(MFSR), including reduced climbing speed and climbing endurance, reduced fractional shortening of the heart, damaged myofibrils, and reduced mitochondria in HM. Besides, a HFD and MFSR increased triglyceride level and MDA level, decreased the Sirt1 and FOXO protein level, and reduced CPT1, SOD, and CAT activity level, and they dow-regulated FOXO and bmm expression level in SM and HM. On the contrary, both muscle FOXO-specific overexpression(MFSO) and EE prevented abnormal changes of SM and HM in function, structure, or physiology caused by HFD and MFSR. Besides, EE also prevented defects of SM and HM induced by MFSR. Therefore, Current findings confirmed that MFSO and EE protected SM and heart from defects caused by a HFD via enhancing FOXO-realated antioxidant pathways and lipid catabolism. FOXO played a vital role in regulating HFD-induced defects in SM and HM, but FOXO was not a key regulatory gene of EE against damages in SM and HM. The mechanism was related to activity of Sirt1/FOXO/ SOD, CAT pathways and lipid catabolism in SM and HM.

physiology↗