A theoretical study on the dynamics of light harvesting in the dimeric photosystem II core complex: regulation and robustness of energy transfer pathways.

Here we present our theoretical investigations into the light reaction in the dimeric photosystem II (PSII) core complex. An effective model for excitation energy transfer (EET) and primary charge separation (CS) in the PSII core complex was developed, with model parameters constructed based on molecular dynamics (MD) simulation data. Compared to experimental results, we demonstrated that this model faithfully reproduces the absorption spectra of the RC and core light-harvesting complexes (CP43 and CP47) as well as the full EET dynamics among the chromophores in the PSII core complex. We then applied master equation simulations and network analysis to investigate detailed EET plus CS dynamics in the system, allowing us to identify key EET pathways and produce a coarse-grained cluster model for the light reaction in the dimeric PSII core complex. We show that non-equilibrium energy transfer channels play important roles in the efficient light harvesting process and that multiple EET pathways exist between subunits of PSII to ensure the robustness of light harvesting in the system. Furthermore, we revealed that inter-monomer energy transfer dominated by the coupling between the two CLA625 molecules enables efficient energy exchange between two CP47s in the dimeric PSII core complex, which leads to significant energy pooling in the CP47 domain during the light reaction. Our study provides a blueprint for the design of light harvesting in the PSII core and show that a structure-based approach using molecular dynamics simulations and quantum chemistry calculations can be effectively utilized to elucidate the dynamics of light harvesting in complex photosynthetic systems.

Liver-adipose tissue crosstalk: A key player in the pathogenesis of glucolipid metabolic disease.

Glucolipid metabolic disease (GLMD), a complex of interrelated disorders in glucose and lipid metabolism, has become one of the leading chronic diseases causing public and clinical problem worldwide. As the metabolism of lipid and glucose is a highly coordinated process under both physiological and diseased conditions, the impairment in the signals corresponding to the metabolism of either lipid or glucose represents the common mechanism underlying the pathogenesis of GLMD. The liver and adipose tissue are the major metabolic organs responsible for energy utilization and storage, respectively. This review article aims to summarize the current advances in the investigation of the functional roles and the underling mechanisms of the interplay between the liver and adipose tissue in the modulation of GLMD development. Fibroblast growth factor 21 (FGF21) and adiponectin represent the two major hormones secreted from the liver and adipose tissues, respectively. FGF21 exerts pleiotropic effects on regulating glucose and lipid homeostasis majorly through inducing the expression and secretion of adiponectin. Therefore, FGF21-adiponectin axis functions as the key mediator for the crosstalk between the liver and adipose tissue to exert the beneficial effects on the maintenance of the homeostasis of energy consumption. The liver- and adipose tissue-derived factors with pleiotropic effects on regulating of lipid and glucose metabolism function as the key mediator for the crosstalk between these two highly active metabolic organs, thereby coordinating the initiation and development of GLMD.

Toll-like receptor-4 signalling in the progression of non-alcoholic fatty liver disease induced by high-fat and high-fructose diet in mice.

The aim of the present study was to investigate Toll-like receptor-4 (TLR4) signalling at different stages of non-alcoholic fatty liver disease (NAFLD) induced by a high-fat, high-fructose (HFHFr) diet in mice. Both TLR4 wild-type (WT) and mutant (TLR4(mut) ) mice were fed either standard chow (SC) or the HFHFr diet for different periods of time from 4 to 16 weeks. Pathological characteristics and function of the liver were assessed. Simple steatosis, steatohepatitis and hepatic fibrosis occurred sequentially in Week 4, 8 and 16 in WT mice fed with the HFHFr. Expression of TLR4, myeloid differentiation factor 88 (MyD88), interferon regulatory factor (IRF) 3 and IRF7 started to increase at Week 4, peaked at Week 8 and then declined to basal levels at Week 16. This pattern was consistent with changes in inflammation in the liver revealed by haematoxylin and eosin staining. However, lipid accumulation, inflammation and fibrosis in livers of TLR4(mut) mice fed the HFHFr diet were significantly alleviated. In addition, the expression of activin A in WT mice fed the HFHFr diet increased at Week 16. The data suggest that TLR4 signalling mediates non-alcoholic steatohepatitis before fibrosis and that activin A is subsequently involved in NAFLD.