Correlates of survival in Swainson's hawks breeding in northern California

We used a 30-year study of breeding Swainson's hawks (Buteo swainsoni) in northern California to examine correlates of adult apparent survival using multistate models in Program MARK. Specifically, we examined age-related patterns in adult apparent survival and how adult survival was correlated with average annual nest productivity, annual reproductive output, western juniper (Juniperus occidentalis) density around nest sites, distance to agriculture, and amount of agriculture within a territory. Annual estimates of adult survival varied from 0.85 to 0.9 (SE = 0.02). There were no indications of senescence or other patterns of age-related changes in adult apparent survival. Adult survival was inversely correlated with average reproductive output, with individuals producing >2 offspring having decreased survival, reflecting a possible trade-off between reproduction and survival. Conversely, reproduction in any year was positively correlated with survival, providing evidence of individual quality influencing adult survival. The distance an individual had to travel to agriculture, where most individuals forage, was negatively related to survival. Primary productivity within the average Swainson's hawk territory was positively correlated with adult survival. Our results indicate that individuals may have higher survival and fitness in areas with high proportions of irrigated agriculture that provides high prey densities, particularly alfalfa. © 2011 The Wildlife Society.     

Lipids of the Spirochaetales: Comparison of the Lipids of Several Members of the Genera Spirochaeta, Treponema, and Leptospira

The lipid compositions of 17 spirochetes belonging to the genera Spirochaeta and Treponema were investigated and compared with data previously derived from 11 strains of Leptospira. The lipid compositions and lipid metabolism of any of these genera is sufficiently different to be characteristic of that genus and to differentiate it from the other two genera. Members of the genus Leptospira are characterized by their ability to beta-oxidize long chain fatty acids as their major carbon and energy source. With few exceptions, they are incapable of synthesizing fatty acids de novo. The major phospholipid found was phosphatidyl ethanolamine. No glycolipid or phosphatidyl choline was found in these organisms. Members of the genus Treponema studied were incapable of beta-oxidation as well as de novo synthesis of fatty acids. Phosphatidyl choline is the major phospholipid of this genus. The glycolipid, monogalactosyl diglyceride, is a major component of the Treponema. Members of the Spirochaeta did synthesize fatty acids de novo. Although these spirochetes contain a monoglycosyl diglyceride, the hexose content of the glycolipid varied from species to species. Neither phosphatidyl ethanolamine nor phosphatidyl choline was found in the Spirochaeta.     

Deoxycytidine triphosphate deaminase of Salmonella typhimurium. Purification and characterization.

Deoxycytidine triphosphate deaminase (EC 3.5.4., dCTP aminohydrolase) of Salmonella typhimurium LT2 has been pruified 500-fold. The reaction requires the presence of Mg-2plus, Mn-2plus, Ca-2lus, or Co-2plus. Kinetics of the reaction with varying Mg-2plus concentrations, keeping the concentration of dCTP constant, suggests that the true substrate of the reaction is MgdCTP. The dependence of the rate of reaction on dCTP concentration in the presnece of 5-fold excess of Mg-2plus is sigmoid, with a Hill coefficient of 1.7. The enzyme is specifically inhibited by dTTP and dUTP. In the presence of increasing dTTP concentrations the sigmoidicity of the substrate saturation curves increases. With 0.2 and 0.4 mM dTTP the Hill coefficients are 2.6 and 3.0, respectively. Despite several attempts no dissociation of the substrate site and the inhibitor site of the enzyme was achieved.     

Crystallization and X-ray analysis of a single fab binding domain from protein L of Peptostreptococcus magnus

Protein L is a multi domain cell wall constituent of certain strains of Peptostreptococcus magnus which binds to the variable domain of immunoglobulin κ-light chains. A single immunoglobulin-binding domain of M_r = 9000 from this protein has been isolated and crystallized. The crystals are of space group P4₂2₁2, with cell dimensions a = b = 66.9 Å, c = 68.3 Å, and diffract to at least 2.2 Å resolution. The asymmetric unit of the crystal contains two molecules of the protein L domain, related by a noncrystallographic 2-fold axis, as revealed by a self-rotation function calculated with native diffraction data. © 1995 Wiley-Liss, Inc.     

Temporal dynamics of estuarine phytoplankton: A case study of San Francisco Bay

Detailed surveys throughout San Francisco Bay over an annual cycle (1980) show that seasonal variations of phytoplankton biomass, community composition, and productivity can differ markedly among estuarine habitat types. For example, in the river-dominated northern reach (Suisun Bay) phytoplankton seasonality is characterized by a prolonged summer bloom of netplanktonic diatoms that results from the accumulation of suspended particulates at the convergence of nontidal currents (i.e. where residence time is long). Here turbidity is persistently high such that phytoplankton growth and productivity are severely limited by light availability, the phytoplankton population turns over slowly, and biological processes appear to be less important mechanisms of temporal change than physical processes associated with freshwater inflow and turbulent mixing. The South Bay, in contrast, is a lagoon-type estuary less directly coupled to the influence of river discharge. Residence time is long (months) in this estuary, turbidity is lower and estimated rates of population growth are high (up to 1–2 doublings d^–1), but the rapid production of phytoplankton biomass is presumably balanced by grazing losses to benthic herbivores. Exceptions occur for brief intervals (days to weeks) during spring when the water column stratifies so that algae retained in the surface layer are uncoupled from benthic grazing, and phytoplankton blooms develop. The degree of stratification varies over the neap-spring tidal cycle, so the South Bay represents an estuary where (1) biological processes (growth, grazing) and a physical process (vertical mixing) interact to cause temporal variability of phytoplankton biomass, and (2) temporal variability is highly dynamic because of the short-term variability of tides. Other mechanisms of temporal variability in estuarine phytoplankton include: zooplankton grazing, exchanges of microalgae between the sediment and water column, and horizontal dispersion which transports phytoplankton from regions of high productivity (shallows) to regions of low productivity (deep channels).Multi-year records of phytoplankton biomass show that large deviations from the typical annual cycles observed in 1980 can occur, and that interannual variability is driven by variability of annual precipitation and river discharge. Here, too, the nature of this variability differs among estuary types. Blooms occur only in the northern reach when river discharge falls within a narrow range, and the summer biomass increase was absent during years of extreme drought (1977) or years of exceptionally high discharge (1982). In South Bay, however, there is a direct relationship between phytoplankton biomass and river discharge. As discharge increases so does the buoyancy input required for density stratification, and wet years are characterized by persistent and intense spring blooms.     

The Genetics of Leaf Flecking in Maize and Its Relationship to Plant Defense and Disease Resistance

Physiological leaf spotting, or flecking, is a mild-lesion phenotype observed on the leaves of several commonly used maize (Zea mays) inbred lines and has been anecdotally linked to enhanced broad-spectrum disease resistance. Flecking was assessed in the maize nested association mapping (NAM) population, comprising 4,998 recombinant inbred lines from 25 biparental families, and in an association population, comprising 279 diverse maize inbreds. Joint family linkage analysis was conducted with 7,386 markers in the NAM population. Genome-wide association tests were performed with 26.5 million single-nucleotide polymorphisms (SNPs) in the NAM population and with 246,497 SNPs in the association population, resulting in the identification of 18 and three loci associated with variation in flecking, respectively. Many of the candidate genes colocalizing with associated SNPs are similar to genes that function in plant defense response via cell wall modification, salicylic acid- and jasmonic acid-dependent pathways, redox homeostasis, stress response, and vesicle trafficking/remodeling. Significant positive correlations were found between increased flecking, stronger defense response, increased disease resistance, and increased pest resistance. A nonlinear relationship with total kernel weight also was observed whereby lines with relatively high levels of flecking had, on average, lower total kernel weight. We present evidence suggesting that mild flecking could be used as a selection criterion for breeding programs trying to incorporate broad-spectrum disease resistance.The plant hypersensitive response (HR) is a form of programmed cell death (PCD) characterized by rapid, localized cell death at the point of attempted pathogen penetration, usually resulting in disease resistance (Coll et al., 2011). It is often associated with other responses, including ion fluxes, an oxidative burst, lipid peroxidation, and cell wall fortification (Hammond-Kosack and Jones, 1996). van Doorn et al. (2011) suggested that HR is a type of PCD sharing features with, but distinct from, both vacuolar cell death and necrosis.HR has been associated with resistance to almost every class of pathogen and pest, including bacteria, viruses, fungi, nematodes, insects, and parasitic plants (Wu and Baldwin, 2010), and generally is most effective against biotrophic pathogens, since biotrophs require a long-term feeding relationship with living host cells. It is generally mediated by dominant resistance (R) genes whose activation is triggered by the direct or indirect detection of specific pathogen-derived effector proteins (Bent and Mackey, 2007). R proteins are maintained in their inactive state if their corresponding effector is not present. Mutants in which HR is constitutively active have been identified in many plant species, including maize/corn (Zea mays; Walbot et al., 1983; Johal, 2007), Arabidopsis (Arabidopsis thaliana; Lorrain et al., 2003), barley (Hordeum vulgare; Wolter et al., 1993), and rice (Oryza sativa; Yin et al., 2000).One well-known class of plant mutants spontaneously form lesions (patches of dead or chlorotic cells) in the absence of any obvious injury, stress, or infection to the plant. Since these lesions in some cases resemble HR, they have been termed disease-lesion mimics (Neuffer and Calvert, 1975). These mutants, which we will here collectively term Les mutants, have been studied extensively, especially in maize (Walbot et al., 1983; Johal et al., 1995; Johal, 2007) and Arabidopsis (Coll et al., 2011). While some of these lesion phenotypes are indeed caused by perturbations in the plant defense response (Hu et al., 1996; Rustérucci et al., 2001), some of the genes underlying this mutant class affect various other pathways that cause cell death if their function is perturbed (Johal, 2007). For instance, the Arabidopsis gene acd2 and the maize gene lls1 are defective in chlorophyll degradation (Gray et al., 1997; Mach et al., 2001).We have defined leaf flecking as the mild, genetically determined spotting observed on many maize inbred cultivars (Vontimitta et al., 2015; Fig. 1). The trait is qualitatively and visually similar to, but quantitatively less severe than, Les mutant phenotypes. The distinction between what constitutes a flecking versus a mild Les trait is necessarily somewhat arbitrary, but for our purposes, we have defined any nonproliferating and distinct leaf-spotting phenotype as flecking.Open in a separate windowFigure 1.A, Examples of variation in the flecking phenotype among inbred lines, with severity increasing from left to right (flecking scores in parentheses, from 0 to 4, scored on a scale of 1–10). B, Leaves of the lines nearly isogenic to inbred Mo20W, into which specific indicated dominant Les mutant genes have been introgressed (Rp1-D21 mutation in an H95 inbred background). Photographs were taken in Clayton, North Carolina, 12 weeks after planting. This figure is adapted from Figure 1 of Vontimitta et al. (2015).Leaf flecking is familiar to most corn breeders, appearing in such well-known and widely used lines such as Mo17 (Zehr et al., 1994) and in several other species such as barley (Makepeace et al., 2007), wheat (Triticum aestivum; Nair and Tomar, 2001), and oat (Avena sativa; Ferdinandsen and Winge, 1930). Flecking tends to be more noticeable in inbreds compared with their derived hybrids (M. Goodman and W. Dolezal, personal communication). Anecdotally, it is often thought to be indicative of a constitutive low-level defense response and as a marker for increased disease resistance.In previous work, we and others have defined the genetic architectures associated with resistance to several maize diseases, including southern leaf blight (SLB; causal agent, Cochliobolus heterostrophus), northern leaf blight (NLB; causal agent, Exserohilum turcicum), and gray leaf spot (GLS; causal agent, Cercospora zeae-maydis; Kump et al., 2011; Poland et al., 2011; Wisser et al., 2011; Benson et al., 2015), and with the control of the maize HR (Chintamanani et al., 2010; Chaikam et al., 2011; Olukolu et al., 2013). For much of this work, we used two powerful mapping populations: the maize association population (Flint-Garcia et al., 2005), a collection of 302 diverse inbred lines with low linkage disequilibrium, and the 5,000-line nested association mapping (NAM) population (McMullen et al., 2009), which is made up of 25 200-line recombinant inbred line (RIL) subpopulations derived from crosses between the common parent B73 and 25 diverse inbreds. Using these populations, it is possible to both sample a diverse array of germplasm and map quantitative trait loci (QTLs) precisely, in some cases to the gene level (Tian et al., 2011; Cook et al., 2012; Hung et al., 2012; Larsson et al., 2013; Olukolu et al., 2013; Wang and Balint-Kurti, 2016).A recent study using 300 lines from the maize intermated B73 × Mo17 population advanced intercross line mapping population identified low but moderately significant positive correlations between increased flecking and increased disease resistance and defense response (Vontimitta et al., 2015). Loci associated with variation in flecking were mapped, although these loci did not colocalize with QTLs identified previously for disease resistance and defense response traits (Balint-Kurti et al., 2007, 2008, 2010; Olukolu et al., 2013). In this study, we have extended this work to examine the genetic basis of leaf flecking over a much more diverse set of maize germplasm using a substantially larger population. We mapped loci associated with variation in leaf flecking and identified candidate genes and pathways that may be involved in this phenotype. Additionally, we have examined the correlations between leaf flecking and disease resistance, the hypersensitive defense response, and total kernel weight.     

Direct binding and activation of protein kinase C isoforms by steroid hormones

The non-genomic action of steroid hormones regulates a wide variety of cellular responses including regulation of ion transport, cell proliferation, migration, death and differentiation. In order to achieve such plethora of effects steroid hormones utilize nearly all known signal transduction pathways. One of the key signalling molecules regulating the non-genomic action of steroid hormones is protein kinase C (PKC). It is thought that rapid action of steroids hormones results from the activation of plasma membrane receptors; however, their molecular identity remains elusive. In recent years, an increasing number of studies have pointed at the selective binding and activation of specific PKC isoforms by steroid hormones. This has led to the hypothesis that PKC could act as a receptor as well as a transducer of the non-genomic effects of these hormones. In this review we summarize the current knowledge of the direct binding and activation of PKC by steroid hormones.     

A high-density admixture scan in 1,670 African Americans with hypertension

Hypertension (HTN) is a devastating disease with a higher incidence in African Americans than European Americans, inspiring searches for genetic variants that contribute to this difference. We report the results of a large-scale admixture scan for genes contributing HTN risk, in which we screened 1,670 African Americans with HTN and 387 control individuals for regions of the genome with elevated proportion of African or European ancestry. No loci were identified that were significantly associated with HTN. We also searched for evidence of an admixture signal at 40 candidate genes and eight previously reported linkage peaks, but none appears to contribute substantially to the differential HTN risk between African and European Americans. Finally, we observed nominal association at one of the loci detected in the admixture scan of Zhu et al. 2005 (p = 0.016 at 6q24.3 correcting for four hypotheses tested), although we caution that the significance is marginal and the estimated odds ratio of 1.19 per African allele is less than what would be expected from the original report; thus, further work is needed to follow up this locus.     

Peroxynitrite inhibits myofibrillar protein function in an in vitro assay of motility

We determined the effects of peroxynitrite (ONOO-) on cardiac myosin, actin, and thin filaments in order to more clearly understand the impact of this reactive compound in ischemia/reperfusion injury and heart failure. Actin filaments, native thin filaments, and alpha-cardiac myosin from rat hearts were exposed to ONOO- in the presence of 2 mM bicarbonate. Filament velocities over myosin, calcium sensitivity, and relative force generated by myosin were assessed in an in vitro motility assay in the absence of reducing agents. ONOO- concentrations > or =10 microM significantly reduced the velocities of thin filaments or bare actin filaments over alpha-cardiac myosin when any of these proteins were exposed individually. These functional deficits were linearly related to the degree of tyrosine nitration, with myosin being the most sensitive. However, at 10 microM ONOO- the calcium sensitivity of thin filaments remained unchanged. Cotreatment of myosin and thin filaments, analogous to the in vivo situation, resulted in a significantly greater functional deficit. The load supported by myosin after ONOO- exposure was estimated using mixtures experiments to be increased threefold. These data suggest that nitration of myofibrillar proteins can contribute to cardiac contractile dysfunction in pathologic states in which ONOO- is liberated.     

Cardiac-restricted overexpression of extracellular matrix metalloproteinase inducer causes myocardial remodeling and dysfunction in aging mice

The matrix metalloproteinases (MMPs) play a pivotal role in adverse left ventricular (LV) myocardial remodeling. The transmembrane protein extracellular MMP inducer (EMMPRIN) causes increased MMP expression in vitro, and elevated levels occur in patients with LV failure. However, the direct consequences of a prolonged increase in the myocardial expression of EMMPRIN in vivo remained unexplored. Cardiac-restricted EMMPRIN expression (EMMPRINexp) was constructed in mice using the full-length human EMMPRIN gene ligated to the myosin heavy chain promoter, which yielded approximately a twofold increase in EMMPRIN compared with that of the age/strain-matched wild-type (WT) mice; EMMPRINexp (n=27) and WT (n=33) mice were examined at 3.2+/-0.1 or at 13.3+/-0.5 mo of age (n=43 and 26, respectively). LV end-diastolic volume (EDV) was similar in young EMMPRINexp and WT mice (54+/-2 vs. 57+/-3 microl), but LV ejection fraction (EF) was reduced (51+/-1 vs. 57+/-1%; P<0.05). In old EMMPRINexp mice, LV EDV was increased compared with WT mice values (76+/-3 vs. 58+/-3 microl; P<0.05) and LV EF was significantly reduced (45+/-1 vs. 57+/-2%; P<0.05). In EMMPRINexp old mice, myocardial MMP-2 and membrane type-1 MMP levels were increased by >50% from WT values (P<0.05) and were accompanied by a twofold higher collagen content (P<0.05). Persistent myocardial EMMPRINexp in aging mice caused increased levels of both soluble and membrane type MMPs, fibrosis, and was associated with adverse LV remodeling. These findings suggest that EMMPRIN is an upstream signaling pathway that can play a mechanistic role in adverse remodeling within the myocardium.