α-Synuclein levels modulate Huntington's disease in mice.

α-Synuclein and mutant huntingtin are the major constituents of the intracellular aggregates that characterize the pathology of Parkinson's disease (PD) and Huntington's disease (HD), respectively. α-Synuclein is likely to be a major contributor to PD, since overexpression of this protein resulting from genetic triplication is sufficient to cause human forms of PD. We have previously demonstrated that wild-type α-synuclein overexpression impairs macroautophagy in mammalian cells and in transgenic mice. Overexpression of human wild-type α-synuclein in cells and Drosophila models of HD worsens the disease phenotype. Here, we examined whether α-synuclein overexpression also worsens the HD phenotype in a mammalian system using two widely used N-terminal HD mouse models (R6/1 and N171-82Q). We also tested the effects of α-synuclein deletion in the same N-terminal HD mouse models, as well as assessed the effects of α-synuclein deletion on macroautophagy in mouse brains. We show that overexpression of wild-type α-synuclein in both mouse models of HD enhances the onset of tremors and has some influence on the rate of weight loss. On the other hand, α-synuclein deletion in both HD models increases autophagosome numbers and this is associated with a delayed onset of tremors and weight loss, two of the most prominent endophenotypes of the HD-like disease in mice. We have therefore established a functional link between these two aggregate-prone proteins in mammals and provide further support for the model that wild-type α-synuclein negatively regulates autophagy even at physiological levels.

Seasonal response of photosynthetic electron transport and energy dissipation in the eighth year of exposure to elevated atmospheric CO2 (FACE) in Pinus taeda (loblolly pine).

To determine the effect of growth under elevated CO(2) partial pressures (pCO(2)) on photosynthetic electron transport and photoprotective energy dissipation, we examined light-saturated net photosynthetic CO(2) assimilation (A(sat)), the capacity for photosynthetic O(2) evolution, chlorophyll fluorescence emission and the pigment composition of upper-canopy loblolly pine needles in the eighth year of exposure to elevated pCO(2) (20 Pa above ambient) at the free-air CO(2) enrichment facility in the Duke Forest. During the summer growing season, A(sat) was 50% higher in current-year needles and 24% higher in year-old needles in elevated pCO(2) in comparison with needles of the same age cohort in ambient pCO(2). Thus, photosynthetic down-regulation at elevated pCO(2) was observed in the summer in year-old needles. In the winter, A(sat) was not significantly affected by growth pCO(2). Reductions in A(sat), the capacity for photosynthetic O(2) evolution and photosystem II (PSII) efficiency in the light-acclimated and fully-oxidized states were observed in the winter when compared to summer. Growth at elevated pCO(2) had no significant effect on the capacity for photosynthetic O(2) evolution, PSII efficiencies in the light-acclimated and fully-oxidized states, chlorophyll content or the size and conversion state of the xanthophyll cycle, regardless of season or needle age cohort. Therefore, we observed no evidence that photosynthetic electron transport or photoprotective energy dissipation responded to compensate for the effects of elevated pCO(2) on Calvin cycle activity.