Herbivory limits the yellow water lily in an overgrown lake and in flowing water

Aquatic macrophytes with floating leaves are often key ecological species that affect entire aquatic ecosystems. Here we describe an investigation of the importance of insect herbivory for population growth and leaf senescence in the yellow water lily (Nuphar lutea). In order to gain a general picture of the importance of herbivory under different conditions, we experimentally manipulated herbivory in a large lily population in natural still water and observed the natural development of 32 smaller populations in flowing water. Herbivory drastically increased leaf senescence, reducing leaf density. In the still water, over one summer, leaf density increased by a factor of 1.23 in the presence of water lily leaf beetles and 1.61 when herbivory was eliminated. In flowing water, population growth was restricted mainly by leaf crowdedness, which limited large dense populations. Herbivory by water lily leaf beetles also had a limiting effect on yellow water lily, again mainly in large dense populations. Small populations supported a lower density of beetles. Previous studies have not addressed population-level responses of vascular plants with floating leaves. Our results suggest that herbivory can result in greater light penetration into the water and reduce “enemy-free space” for aquatic species that find such space in water lily stands. We suggest that the water lily leaf beetle should be considered an “ecological engineer.”     

Active site of epoxide hydrolases revisited: a noncanonical residue in potato StEH1 promotes both formation and breakdown of the alkylenzyme intermediate

The carboxylate of Glu35 in the active site of potato epoxide hydrolase StEH1 interacts with the catalytic water molecule and is the first link in a chain of hydrogen bonds connecting the active site with bulk solvent. To probe its importance to catalysis, the carboxylate was replaced with an amide through an E35Q mutation. Comparing enzyme activities using the two trans-stilbene oxide (TSO) enantiomers as substrates revealed the reaction with R,R-TSO to be the one more severely affected by the E35Q mutation, as judged by determined kinetic parameters describing the pre-steady states or the steady states of the catalyzed reactions. The hydrolysis of S,S-TSO afforded by the E35Q mutant was comparable with that of the wild-type enzyme, with only a minor decrease in activity, or a change in pH dependencies of kcat, and the rate of alkylenzyme hydrolysis, k3. The pH dependence of E35Q-catalyzed hydrolysis of R,R-TSO, however, exhibited an inverted titration curve as compared to that of the wild-type enzyme, with a minimal catalytic rate at pH values where the wild-type enzyme exhibited maximum rates. To simulate the pH dependence of the E35Q mutant, a shift in the acidity of the alkylenzyme had to be invoked. The proposed decrease in the pKa of His300 in the E35Q mutant was supported by computer simulations of the active site electrostatics. Hence, Glu35 participates in activation of the Asp nucleophile, presumably by facilitating channeling of protons out of the active site, and during the hydrolysis half-reaction by orienting the catalytic water for optimal hydrogen bonding, to fine-tune the acid-base characteristics of the general base His300.     

Caprolactam,a light-promoted growth inhibitor in sunflower seedlings

A neutral growth inhibitor, isolated from methanolic extracts of sunflower seedlings, was characterized by spectral data as caprolactam. Light-grown se     

What life cycle graphs can tell about the evolution of life histories

We analyze long-term evolutionary dynamics in a large class of life history models. The model family is characterized by discrete-time population dynamics and a finite number of individual states such that the life cycle can be described in terms of a population projection matrix. We allow an arbitrary number of demographic parameters to be subject to density-dependent population regulation and two or more demographic parameters to be subject to evolutionary change. Our aim is to identify structural features of life cycles and modes of population regulation that correspond to specific evolutionary dynamics. Our derivations are based on a fitness proxy that is an algebraically simple function of loops within the life cycle. This allows us to phrase the results in terms of properties of such loops which are readily interpreted biologically. The following results could be obtained. First, we give sufficient conditions for the existence of optimisation principles in models with an arbitrary number of evolving traits. These models are then classified with respect to their appropriate optimisation principle. Second, under the assumption of just two evolving traits we identify structural features of the life cycle that determine whether equilibria of the monomorphic adaptive dynamics (evolutionarily singular points) correspond to fitness minima or maxima. Third, for one class of frequency-dependent models, where optimisation is not possible, we present sufficient conditions that allow classifying singular points in terms of the curvature of the trade-off curve. Throughout the article we illustrate the utility of our framework with a variety of examples.     

Zn2+ binding to human calbindin D(28k) and the role of histidine residues

We have studied the binding of Zn2+ to the hexa EF-hand protein, calbindin D(28k)-a strong Ca2+-binder involved in apoptosis regulation-which is highly expressed in brain tissue. By use of radioblots, isothermal titration calorimetry, and competition with a fluorescent Zn2+ chelator, we find that calbindin D(28k) binds Zn2+ to three rather strong sites with dissociation constants in the low micromolar range. Furthermore, we conclude based on spectroscopic investigations that the Zn2+-bound state is structurally distinct from the Ca2+-bound state and that the two forms are incompatible, yielding negative allosteric interaction between the zinc- and calcium-binding events. ANS titrations reveal a change in hydrophobicity upon binding Zn2+. The binding of Zn2+ is compatible with the ability of calbindin to activate myo-inositol monophosphatase, one of the known targets of calbindin. Through site-directed mutagenesis, we address the role of cysteine and histidine residues in the binding of Zn2+. Mutation of all five cysteines into serines has no effect on Zn2+-binding affinity or stoichiometry. However, mutating histidine 80 into a glutamine reduces the binding affinity of the strongest Zn2+ site, indicating that this residue is involved in coordinating the Zn2+ ion in this site. Mutating histidines 5, 22, or 114 has significantly smaller effects on Zn2+-binding affinity.     

Selective loss of innate CD4(+) V alpha 24 natural killer T cells in human immunodeficiency virus infection

V alpha 24 natural killer T (NKT) cells are innate immune cells involved in regulation of immune tolerance, autoimmunity, and tumor immunity. However, the effect of human immunodeficiency virus type 1 (HIV-1) infection on these cells is unknown. Here, we report that the V alpha 24 NKT cells can be subdivided into CD4(+) or CD4(-) subsets that differ in their expression of the homing receptors CD62L and CD11a. Furthermore, both CD4(+) and CD4(-) NKT cells frequently express both CXCR4 and CCR5 HIV coreceptors. We find that the numbers of NKT cells are reduced in HIV-infected subjects with uncontrolled viremia and marked CD4(+) T-cell depletion. The number of CD4(+) NKT cells is inversely correlated with HIV load, indicating depletion of this subset. In contrast, CD4(-) NKT-cell numbers are unaffected in subjects with high viral loads. HIV infection experiments in vitro show preferential depletion of CD4(+) NKT cells relative to regular CD4(+) T cells, in particular with virus that uses the CCR5 coreceptor. Thus, HIV infection causes a selective loss of CD4(+) lymph node homing (CD62L(+)) NKT cells, with consequent skewing of the NKT-cell compartment to a predominantly CD4(-) CD62L(-) phenotype. These data indicate that the key immunoregulatory NKT-cell compartment is compromised in HIV-1-infected patients.     

The impact of Helicobacter pylori on atopic disorders in childhood

Background: The prevalence of Helicobacter pylori in Western populations has steadily decreased. This has been suggested as one of the factors involved in the recent increase of asthma and allergy. Some studies have reported a negative association between H. pylori and asthma and allergy, but data are inconsistent and there are a few studies in children. Aim: We investigated whether the prevalence of H. pylori was associated with asthma symptoms, allergic rhinitis, and atopic dermatitis in childhood. Methods: We determined IgG anti‐H. pylori and CagA antibodies in serum of Dutch children, who took part in the PIAMA birth cohort study. Serum was collected from 545 children, aged 7–9 years (Dutch ethnicity 91.5%). Symptoms of asthma and atopy were assessed by yearly questionnaires. Chi‐square tests and logistic regression were used. Results: We found 9%H. pylori and 0.9% CagA seropositivity. Twelve (5.9%) children with reported wheezing ever were H. pylori positive, compared to 37 (10.9%) of the non‐wheezers (p = .05). No significant differences in H. pylori prevalence were found between children with or without allergic rhinitis (8.5% vs 9.5%), atopic dermatitis (8.7% vs 9.2%), and physician‐diagnosed asthma (7.1% vs 9.4%). Multivariate analysis showed no significant associations between H. pylori seropositivity and wheezing (OR 0.52; 95% CI 0.25–1.06), allergic rhinitis (OR 0.96; 95% CI 0.51–1.81), atopic dermatitis (OR 1.05; 95% CI 0.56–1.98) or physician‐diagnosed asthma (OR 0.87; 95% CI 0.37–2.08). Conclusion: We found a borderline significantly lower H. pylori seropositivity in children with wheezing compared to non‐wheezers, but no association between H. pylori serum‐antibody status and allergic rhinitis, atopic dermatitis, or asthma.     

Quantitative assessment of methyl‐esterification and other side reactions in a standard propionylation protocol for detection of histone modifications

Histone modifications play an important role in regulating chromatin stability and gene expression, but to date, investigating them remains challenging. In order to obtain peptides suitable for MS‐based analysis, chemical derivatization of N‐terminus and lysine residues by propionic anhydride is commonly performed. Several side reactions (methyl‐esterification, amidation, solvolysis, overpropionylation, and missed propionylation) during propionylation protocols have been described, yet their relative abundances remain vague. Because methyl‐esterification could interfere with correct interpretation of the modification pattern, it is essential to take measures to avoid it. Here we present in‐depth quantitative analyses of methyl‐esterification and the other side reactions in a standard propionylation protocol containing methanol, and when replacing methanol with isopropanol or acetonitrile. We show that the use of alternative solvents can eliminate methyl‐esterification and that even though other side reactions are not prevented, their contribution can be kept relatively small. We also show that replacing methanol can be of importance also in other proteomics methods, such as mixed cation exchange, using methanol under acidic conditions.