Structure and Efficiency in Bacterial Photosynthetic Light Harvesting

Photosynthetic organisms use networks of chromophores to absorb sunlight and deliver the energy to reaction centres, where charge separation triggers a cascade of chemical steps to store the energy. We present a detailed model of the light-harvesting complexes in purple bacteria, including explicit interaction with sunlight; energy loss through radiative and non-radiative processes; and dephasing and thermalizing effects of coupling to a vibrational bath. An important feature of the model is that we capture the effect of slow vibrational modes by introducing time-dependent disorder. Our model describes the experimentally observed high efficiency of light harvesting, despite the absence of long-range quantum coherence. The one-exciton part of the quantum state fluctuates due to slow vibrational changes, but remains highly mixed at all times. This lack of long-range coherence suggests a relatively minor role for structure in determining the efficiency of bacterial light harvesting. To investigate this we built hypothetical models with randomly arranged chromophores, but still observed high efficiency when typical nearest-neighbour distances are comparable with those found in nature. This helps to explain the efficiency of energy transport in organisms whose chromophore networks differ widely in structure, while also suggesting new design criteria for efficient artificial light-harvesting devices

How Static Disorder Mimics Decoherence in Anisotropy Pump-Probe Experiments on Purple-Bacteria Light Harvesting Complexes

Anisotropy pump-probe experiments have provided insights into the character of excitons formed in photosynthetic complexes. Rapid decay in the observed anisotropy is cited as evidence of the strength of coupling of the excitonic degrees of freedom to their environment. Here we show that ensemble averaging over realistic model Hamiltonians leads to a rapid decay of anisotropy to a value close to the observed asymptote, and at a rate comparable to observed decay rates, even in the absence of coupling to the environment. While coupling to the environment will clearly play a role in the dynamics of such systems, our calculations suggest that caution is needed in deducing the strength of this coupling from anisotropy experiments. We also set out to clarify the nature quantum states and processes involved in the dynamics of such systems, and the associated terminology.status: publishe

Galectin-1 Regulates Tissue Exit of Specific Dendritic Cell Populations

During inflammation, dendritic cells emigrate from inflamed tissue across the lymphatic endothelium into the lymphatic vasculature and travel to regional lymph nodes to initiate immune responses. However, the processes that regulate dendritic cell tissue egress and migration across the lymphatic endothelium are not well defined. The mammalian lectin galectin-1 is highly expressed by vascular endothelial cells in inflamed tissue and has been shown to regulate immune cell tissue entry into inflamed tissue. Here, we show that galectin-1 is also highly expressed by human lymphatic endothelial cells, and deposition of galectin-1 in extracellular matrix selectively regulates migration of specific human dendritic cell subsets. The presence of galectin-1 inhibits migration of immunogenic dendritic cells through the extracellular matrix and across lymphatic endothelial cells, but it has no effect on migration of tolerogenic dendritic cells. The major galectin-1 counter-receptor on both dendritic cell populations is the cell surface mucin CD43; differential core 2 O-glycosylation of CD43 between immunogenic dendritic cells and tolerogenic dendritic cells appears to contribute to the differential effect of galectin-1 on migration. Binding of galectin-1 to immunogenic dendritic cells reduces phosphorylation and activity of the protein-tyrosine kinase Pyk2, an effect that may also contribute to reduced migration of this subset. In a murine lymphedema model, galectin-1(−/−) animals had increased numbers of migratory dendritic cells in draining lymph nodes, specifically dendritic cells with an immunogenic phenotype. These findings define a novel role for galectin-1 in inhibiting tissue emigration of immunogenic, but not tolerogenic, dendritic cells, providing an additional mechanism by which galectin-1 can dampen immune responses