Identification of a mechanism of photoprotective energy dissipation in higher plants

Under conditions of excess sunlight the efficient light-harvesting antenna found in the chloroplast membranes of plants is rapidly and reversibly switched into a photoprotected quenched state in which potentially harmful absorbed energy is dissipated as heat, a process measured as the non-photochemical quenching of chlorophyll fluorescence or qE. Although the biological significance of qE is established, the molecular mechanisms involved are not. LHCII, the main light-harvesting complex, has an inbuilt capability to undergo transformation into a dissipative state by conformational change and it was suggested that this provides a molecular basis for qE, but it is not known if such events occur in vivo or how energy is dissipated in this state. The transition into the dissipative state is associated with a twist in the configuration of the LHCII-bound carotenoid neoxanthin, identified using resonance Raman spectroscopy. Applying this technique to study isolated chloroplasts and whole leaves, we show here that the same change in neoxanthin configuration occurs in vivo, to an extent consistent with the magnitude of energy dissipation. Femtosecond transient absorption spectroscopy, performed on purified LHCII in the dissipative state, shows that energy is transferred from chlorophyll a to a low-lying carotenoid excited state, identified as one of the two luteins (lutein 1) in LHCII. Hence, it is experimentally demonstrated that a change in conformation of LHCII occurs in vivo, which opens a channel for energy dissipation by transfer to a bound carotenoid. We suggest that this is the principal mechanism of photoprotection.     

The von Neumann relation generalized to coarsening of three-dimensional microstructures

Cellular structures or tessellations are ubiquitous in nature. Metals and ceramics commonly consist of space-filling arrays of single-crystal grains separated by a network of grain boundaries, and foams (froths) are networks of gas-filled bubbles separated by liquid walls. Cellular structures also occur in biological tissue, and in magnetic, ferroelectric and complex fluid contexts. In many situations, the cell/grain/bubble walls move under the influence of their surface tension (capillarity), with a velocity proportional to their mean curvature. As a result, the cells evolve and the structure coarsens. Over 50 years ago, von Neumann derived an exact formula for the growth rate of a cell in a two-dimensional cellular structure (using the relation between wall velocity and mean curvature, the fact that three domain walls meet at 120 degrees and basic topology). This forms the basis of modern grain growth theory. Here we present an exact and much-sought extension of this result into three (and higher) dimensions. The present results may lead to the development of predictive models for capillarity-driven microstructure evolution in a wide range of industrial and commercial processing scenarios--such as the heat treatment of metals, or even controlling the 'head' on a pint of beer.     

A recurrent mutation in PALB2 in Finnish cancer families

BRCA1, BRCA2 and other known susceptibility genes account for less than half of the detectable hereditary predisposition to breast cancer. Other relevant genes therefore remain to be discovered. Recently a new BRCA2-binding protein, PALB2, was identified. The BRCA2-PALB2 interaction is crucial for certain key BRCA2 DNA damage response functions as well as its tumour suppression activity. Here we show, by screening for PALB2 mutations in Finland that a frameshift mutation, c.1592delT, is present at significantly elevated frequency in familial breast cancer cases compared with ancestry-matched population controls. The truncated PALB2 protein caused by this mutation retained little BRCA2-binding capacity and was deficient in homologous recombination and crosslink repair. Further screening of c.1592delT in unselected breast cancer individuals revealed a roughly fourfold enrichment of this mutation in patients compared with controls. Most of the mutation-positive unselected cases had a familial pattern of disease development. In addition, one multigenerational prostate cancer family that segregated the c.1592delT truncation allele was observed. These results indicate that PALB2 is a breast cancer susceptibility gene that, in a suitably mutant form, may also contribute to familial prostate cancer development.     

Skew of mantle upwelling beneath the East Pacific Rise governs segmentation

Mantle upwelling is essential to the generation of new oceanic crust at mid-ocean ridges, and it is generally assumed that such upwelling is symmetric beneath active ridges. Here, however, we use seismic imaging to show that the isotropic and anisotropic structure of the mantle is rotated beneath the East Pacific Rise. The isotropic structure defines the pattern of magma delivery from the mantle to the crust. We find that the segmentation of the rise crest between transform faults correlates well with the distribution of mantle melt. The azimuth of seismic anisotropy constrains the direction of mantle flow, which is rotated nearly 10 degrees anticlockwise from the plate-spreading direction. The mismatch between the locus of mantle melt delivery and the morphologic ridge axis results in systematic differences between areas of on-axis and off-axis melt supply. We conclude that the skew of asthenospheric upwelling and transport governs segmentation of the East Pacific Rise and variations in the intensity of ridge crest processes.     

Engraftment of connexin 43-expressing cells prevents post-infarct arrhythmia

Ventricular tachyarrhythmias are the main cause of sudden death in patients after myocardial infarction. Here we show that transplantation of embryonic cardiomyocytes (eCMs) in myocardial infarcts protects against the induction of ventricular tachycardia (VT) in mice. Engraftment of eCMs, but not skeletal myoblasts (SMs), bone marrow cells or cardiac myofibroblasts, markedly decreased the incidence of VT induced by in vivo pacing. eCM engraftment results in improved electrical coupling between the surrounding myocardium and the infarct region, and Ca2+ signals from engrafted eCMs expressing a genetically encoded Ca2+ indicator could be entrained during sinoatrial cardiac activation in vivo. eCM grafts also increased conduction velocity and decreased the incidence of conduction block within the infarct. VT protection is critically dependent on expression of the gap-junction protein connexin 43 (Cx43; also known as Gja1): SMs genetically engineered to express Cx43 conferred a similar protection to that of eCMs against induced VT. Thus, engraftment of Cx43-expressing myocytes has the potential to reduce life-threatening post-infarct arrhythmias through the augmentation of intercellular coupling, suggesting autologous strategies for cardiac cell-based therapy.