Acclimation of photosynthesis and respiration is asynchronous in response to changes in temperature regardless of plant functional group

Gas exchange, fluorescence, western blot and chemical composition analyses were combined to assess if three functional groups (forbs, grasses and evergreen trees/shrubs) differed in acclimation of leaf respiration (R) and photosynthesis (A) to a range of growth temperatures (7, 14, 21 and 28 degrees C). When measured at a common temperature, acclimation was greater for R than for A and differed between leaves experiencing a 10-d change in growth temperature (PE) and leaves newly developed at each temperature (ND). As a result, the R : A ratio was temperature dependent, increasing in cold-acclimated plants. The balance was largely restored in ND leaves. Acclimation responses were similar among functional groups. Across the functional groups, cold acclimation was associated with increases in nonstructural carbohydrates and nitrogen. Cold acclimation of R was associated with an increase in abundance of alternative and/or cytochrome oxidases in a species-dependent manner. Cold acclimation of A was consistent with an initial decrease and subsequent recovery of thylakoid membrane proteins and increased abundance of proteins involved in the Calvin cycle. Overall, the results point to striking similarities in the extent and the biochemical underpinning of acclimation of R and A among contrasting functional groups differing in overall rates of metabolism, chemical composition and leaf structure.     

The pathologies associated with functional titration of phosphatidylinositol transfer protein alpha activity in mice

Phosphatidylinositol transfer proteins (PITPs) bind phosphatidylinositol (PtdIns) and phosphatidylcholine and play diverse roles in coordinating lipid metabolism/signaling with intracellular functions. The underlying mechanisms remain unclear. Genetic ablation of PITPalpha in mice results in neonatal lethality characterized by intestinal and hepatic steatosis, spinocerebellar neurodegeneration, and glucose homeostatic defects. We report that mice expressing a PITPalpha selectively ablated for PtdIns binding activity (Pitpalpha(T59D)), as the sole source of PITPalpha, exhibit phenotypes that recapitulate those of authentic PITPalpha nullizygotes. Analyses of mice with graded reductions in PITPalpha activity reveal proportionately graded reductions in lifespan, demonstrate that intestinal steatosis and hypoglycemia are apparent only when PITPalpha protein levels are strongly reduced (>or=90%), and correlate steatotic and glucose homeostatic defects with cerebellar inflammatory disease. Finally, reconstitution of PITPalpha expression in the small intestine substantially corrects the chylomicron retention disease and cerebellar inflammation of Pitpalpha(0/0) neonates, but does not rescue neonatal lethality in these animals. These data demonstrate that PtdIns binding is an essential functional property of PITPalpha in vivo, and suggest a causal linkage between defects in lipid transport and glucose homeostasis and cerebellar inflammatory disease. Finally, the data also demonstrate intrinsic neuronal deficits in PITPalpha-deficient mice that are independent of intestinal lipid transport defects and hypoglycemia.     

Astrovirus increases epithelial barrier permeability independently of viral replication

Astrovirus infection in a variety of species results in an age-dependent diarrhea; however, the means by which astroviruses cause diarrhea remain unknown. Studies of astrovirus-infected humans and turkeys have demonstrated few histological changes and little inflammation during infection, suggesting that intestinal damage or an overzealous immune response is not the primary mediator of astrovirus diarrhea. An alternative contributor to diarrhea is increased intestinal barrier permeability. Here, we demonstrate that astrovirus increases barrier permeability in a Caco-2 cell culture model system following apical infection. Increased permeability correlated with disruption of the tight-junction protein occludin and decreased the number of actin stress fibers in the absence of cell death. Additionally, permeability was increased when monolayers were treated with UV-inactivated virus or purified recombinant human astrovirus serotype 1 capsid in the form of virus-like particles. Together, these results demonstrate that astrovirus-induced permeability occurs independently of viral replication and is modulated by the capsid protein, a property apparently unique to astroviruses. Based on these data, we propose that the capsid contributes to diarrhea in vivo.     

DLA-DRB1, DQA1, and DQB1 alleles and haplotypes in North American Gray Wolves

The canine major histocompatibility complex contains highly polymorphic genes, many of which are critical in regulating immune response. Since domestic dogs evolved from Gray Wolves (Canis lupus), common DLA class II alleles should exist. Sequencing was used to characterize 175 Gray Wolves for DLA class II alleles, and data from 1856 dogs, covering 85 different breeds of mostly European origin, were available for comparison. Within wolves, 28 new alleles were identified, all occurring in at least 2 individuals. Three DLA-DRB1, 8 DLA-DQA1, and 6 DLA-DQB1 alleles also identified in dogs were present. Twenty-eight haplotypes were identified, of which 2 three-locus haplotypes, and many DLA-DQA1/DQB1 haplotypes, are also found in dogs. The wolves studied had relatively few dog DLA alleles and may therefore represent a remnant population descended from Asian wolves. The single European wolf included carried a haplotype found in both these North American wolves and in many dog breeds. Furthermore, one wolf DQB1 allele has been found in Shih Tzu, a breed of Asian origin. These data suggest that the wolf ancestors of Asian and European dogs may have had different gene pools, currently reflected in the DLA alleles present in dog breeds.     

Cation control of dimensionality in isothiocyanate coordination polymers constructed from conformationally flexible 3,3′-bipyridine tethers

Two isothiocyanate coordination polymers constructed from the conformationally flexible tethering ligand 3,3′-bipyridine (3,3′-bpy) and divalent metal cations have been prepared and characterized via single crystal X-ray diffraction, infrared spectroscopy and elemental analysis. [Co(NCS)₂(3,3′-bpy)₂] (1), wherein the isothiocyanate ligands are coordinated in a trans fashion, manifests stacked two-dimensional (2-D) rhomboid grid layered motifs. In contrast, [Ni(NCS)₂(3,3′-bpy)₂] (2) possesses a doubly interpenetrated adamantoid three-dimensional (3-D) network despite the presence of trans isothiocyanate ligands. Thus, a metal cation-based control of coordination polymer dimensionality has been revealed in this system, reflective of different donor dispositions allowed by the conformational flexibility of the exobidentate 3,3′-bpy ligand. The 3-D framework of 2 decomposes at a temperature ∼40 °C higher than the 2-D network of 1.     

Mast cells promote atherosclerosis by releasing proinflammatory cytokines

Mast cells contribute importantly to allergic and innate immune responses by releasing various preformed and newly synthesized mediators. Previous studies have shown mast cell accumulation in human atherosclerotic lesions. This report establishes the direct participation of mast cells in atherogenesis in low-density lipoprotein receptor-deficient (Ldlr(-/-)) mice. Atheromata from compound mutant Ldlr(-/-) Kit(W-sh)(/W-sh) mice showed decreased lesion size, lipid deposition, T-cell and macrophage numbers, cell proliferation and apoptosis, but increased collagen content and fibrous cap development. In vivo, adoptive transfer of syngeneic wild-type or tumor necrosis factor (TNF)-alpha-deficient mast cells restored atherogenesis to Ldlr(-/-)Kit(W-sh/W-sh) mice. Notably, neither interleukin (IL)-6- nor interferon (IFN)-gamma-deficient mast cells did so, indicating that the inhibition of atherogenesis in Ldlr(-/-)Kit(W-sh/W-sh) mice resulted from the absence of mast cells and mast cell-derived IL-6 and IFN-gamma. Compared with wild-type or TNF-alpha-deficient mast cells, those lacking IL-6 or IFN-gamma did not induce expression of proatherogenic cysteine proteinase cathepsins from vascular cells in vitro or affect cathepsin and matrix metalloproteinase activities in atherosclerotic lesions, implying that mast cell-derived IL-6 and IFN-gamma promote atherogenesis by augmenting the expression of matrix-degrading proteases. These observations establish direct participation of mast cells and mast cell-derived IL-6 and IFN-gamma in mouse atherogenesis and provide new mechanistic insight into the pathogenesis of this common disease.     

Metabolic rates of a widely distributed crayfish shift along a latitudinal gradient

Hydrobiologia - Species are often exposed to novel thermal regimes as a result of anthropogenic activities. Understanding the extent to which populations are locally adapted to the thermal regime...