Tree identity and diversity directly affect soil moisture and temperature but not soil carbon ten years after planting

1. Soil C is the largest C pool in forest ecosystems that contributes to C sequestration and mitigates climate change. Tree diversity enhances forest productivity, so diversifying the tree species composition, notably in managed forests, could increase the quantity of organic matter being transferred to soils and alter other soil properties relevant to the C cycle.
2. A ten‐year‐old tree diversity experiment was used to study the effects of tree identity and diversity (functional and taxonomic) on soils. Surface (0–10 cm) mineral soil was repeatedly measured for soil C concentration, C:N ratio, pH, moisture, and temperature in twenty‐four tree species mixtures and twelve corresponding monocultures (replicated in four blocks).
3. Soil pH, moisture, and temperature responded to tree diversity and identity. Greater productivity in above‐ and below‐ground tree components did not increase soil C concentration. Soil pH increased and soil moisture decreased with functional diversity, more specifically, when species had different growth strategies and shade tolerances. Functional identity affected soil moisture and temperature, such that tree communities with more slow‐growing and shade‐tolerant species had greater soil moisture and temperature. Higher temperature was measured in communities with broadleaf‐deciduous species compared to communities with coniferous‐evergreen species.
4. We conclude that long‐term soil C cycling in forest plantations will likely respond to changes in soil pH, moisture, and temperature that is mediated by tree species composition, since tree species affect these soil properties through their litter quality, water uptake, and physical control of soil microclimates.

     

Stimulation of intestinal secretion of apolipoprotein AI by triiodothyronine

Rats were made hyperthyroid with triiodothyronine in an osmotic minipump implanted intraperitoneally for one week. Intestinal lymph was collected from euthyroid and hyperthyroid rats for 40-55 hours. The rate of apolipoprotein AI (apo AI) secreted into the lymph by hyperthyroid rats exceeded that of euthyroid rats (149 +/- 9 vs 95 +/- 2 micrograms/hr), and was not associated with a proportional increase in the output of triglyceride. The fall in plasma concentration of apoAI in the euthyroid (10 mg/dl) and hyperthyroid (23 mg/dl) could be accounted for by the loss due to diversion of lymph. It appears that the intestine may contribute significantly to the increased plasma levels of apoAI observed in the hyperthyroid rats.     

Replacement of the axial histidine ligand with imidazole in cytochrome c peroxidase. 1. Effects on structure

Replacement of the axial histidine ligand with exogenous imidazole has been accomplished in a number of heme protein mutants, where it often serves to complement the functional properties of the protein. In this paper, we describe the effects of pH and buffer ion on the crystal structure of the H175G mutant of cytochrome c peroxidase, in which the histidine tether between the heme and the protein backbone is replaced by bound imidazole. The structures show that imidazole can occupy the proximal H175G cavity under a number of experimental conditions, but that the details of the interaction with the protein and the coordination to the heme are markedly dependent on conditions. Replacement of the tethered histidine ligand with imidazole permits the heme to shift slightly in its pocket, allowing it to adopt either a planar or distally domed conformation. H175G crystallized from both high phosphate and imidazole concentrations exists as a novel, 5-coordinate phosphate bound state, in which the proximal imidazole is dissociated and the distal phosphate is coordinated to the iron. To accommodate this bound phosphate, the side chains of His-52 and Asn-82 alter their positions and a significant conformational change in the surrounding protein backbone occurs. In the absence of phosphate, imidazole binds to the proximal H175G cavity in a pH-dependent fashion. At pH 7, imidazole is directly coordinated to the heme (d(Fe--Im) = 2.0 A) with a nearby distal water (d(Fe--HOH) = 2.4 A). This is similar to the structure of WT CCP except that the iron lies closer in the heme plane, and the hydrogen bond between imidazole and Asp-235 (d(Im--Asp) = 3.1 A) is longer than for WT CCP (d(His--Asp) = 2.9 A). As the pH is dropped to 5, imidazole dissociates from the heme (d(Fe--Im) = 2.9 A), but remains in the proximal cavity where it is strongly hydrogen bonded to Asp-235 (d(Im--Asp) = 2.8 A). In addition, the heme is significantly domed toward the distal pocket where it may coordinate a water molecule. Finally, the structure of H175G/Im, pH 6, at low temperature (100 K) is very similar to that at room temperature, except that the water above the distal heme face is not present. This study concludes that steric restrictions imposed by the covalently tethered histidine restrain the heme and its ligand coordination from distortions that would arise in the absence of the restricted tether. Coupled with the functional and spectroscopic properties described in the following paper in this issue, these structures help to illustrate how the delicate and critical interactions between protein, ligand, and metal modulate the function of heme enzymes.     

Inhibition of hepatoma cell growth in vitro by arylating and non-arylating K vitamin analogs. Significance of protein tyrosine phosphatase inhibition

We recently found that a thioether analog of K vitamin (Cpd 5) inhibited the activity of protein-tyrosine phosphatases (PTPases) and induced protein-tyrosine phosphorylation in a human hepatoma cell line (Hep3B). We have now examined the structural requirements for induction of protein-tyrosine phosphorylation and PTPase inhibition by several K vitamin analogs. Thioether analogs with sulfhydryl arylation capacity, especially those with a hydroxy (Cpd 5) or a methoxy group at the end of the side chain, induced protein-tyrosine phosphorylation, but non-arylating analogs, such as those with an all-carbon or O-ether side chain, did not. Among the receptor-tyrosine kinases, epidermal growth factor receptors were tyrosine-phosphorylated by treatment with thioether analogs, whereas insulin and hepatocyte growth factor receptors were not. An increase in tyrosine-phosphorylated ERK2 mitogen-activated protein kinase was also observed. The activity of purified T cell PTPase was inhibited only by the thioether analogs, but not by non-arylating analogs. Furthermore, the epidermal growth factor receptor dephosphorylation activity of Hep3B cell lysates was inhibited by Cpd 5 treatment. A similar induction of protein-tyrosine phosphorylation by Cpd 5 was seen in other human hepatoma cell lines together with growth inhibition. However, one cell line (HepG2), which was relatively resistant to growth inhibition by Cpd 5, did not increase its phosphorylation levels upon Cpd 5 treatment. These results suggest that cell growth inhibition by thioether analogs is closely associated with inhibition of PTPases by sulfhydryl arylation and with tyrosine phosphorylation of selected proteins.     

Maitotoxin and P2Z/P2X7 purinergic receptor stimulation activate a common cytolytic pore

The effects ofmaitotoxin (MTX) on plasmalemma permeability are similar to thosecaused by stimulation of P2Z/P2X₇ionotropic receptors, suggesting that1) MTX directly activatesP2Z/P2X₇ receptors or2) MTX andP2Z/P2X₇ receptor stimulationactivate a common cytolytic pore. To distinguish between these twopossibilities, the effect of MTX was examined in1) THP-1 monocytic cells before andafter treatment with lipopolysaccharide and interferon-, a maneuverknown to upregulate P2Z/P2X₇receptor, 2) wild-type HEK cells andHEK cells stably expressing theP2Z/P2X₇ receptor, and3) BW5147.3 lymphoma cells, a cellline that expresses functional P2Z/P2X₇ channels that are poorlylinked to pore formation. In control THP-1 monocytes, addition of MTXproduced a biphasic increase in the cytosolic freeCa²⁺ concentration([Ca²⁺]_i);the initial increase reflects MTX-inducedCa²⁺ influx, whereas the secondphase correlates in time with the appearance of large pores and theuptake of ethidium. MTX produced comparable increases in[Ca²⁺]_iand ethidium uptake in THP-1 monocytes overexpressing theP2Z/P2X₇ receptor. In bothwild-type HEK and HEK cells stably expressing theP2Z/P2X₇ receptor, MTX-inducedincreases in[Ca²⁺]_iand ethidium uptake were virtually identical. The response of BW5147.3cells to concentrations of MTX that produced large increases in[Ca²⁺]_ihad no effect on ethidium uptake. In both THP-1 and HEK cells, MTX- andBz-ATP-induced pores activate with similar kinetics and exhibit similarsize exclusion. Last, MTX-induced pore formation, but not channelactivation, is greatly attenuated by reducing the temperature to22°C, a characteristic shared by theP2Z/P2X₇-induced pore. Together,the results demonstrate that, although MTX activates channels that aredistinct from those activated byP2Z/P2X₇ receptor stimulation, thecytolytic/oncotic pores activated by MTX- and Bz-ATP are indistinguishable.

     

Local polynomial regression modeling of human plasma melatonin levels

Accurate characterization of features of the melatonin production curve is important for research in chronobiology. Local polynomial regression is used to model the plasma melatonin concentration curve and obtain consistent and asymptotically normally distributed estimates of synthesis onset and offset times, duration, peak concentration, and area under the curve. A simple production-clearance model for melatonin kinetics provides the connection between plasma concentrations and the melatonin production curve. This model identifies onset and offset times with critical points of derivatives of the concentration curve. The method proposed has the advantage of flexibility and ease of implementation. Local polynomial regression can be shown to produce consistent estimates of the regression curve and parameters of interest. Furthermore, the method can be implemented in any software package with weighted least squares routines.     

The evolution of cooperation

Darwin recognized that natural selection could not favor a trait in one species solely for the benefit of another species. The modern, selfish-gene view of the world suggests that cooperation between individuals, whether of the same species or different species, should be especially vulnerable to the evolution of noncooperators. Yet, cooperation is prevalent in nature both within and between species. What special circumstances or mechanisms thus favor cooperation? Currently, evolutionary biology offers a set of disparate explanations, and a general framework for this breadth of models has not emerged. Here, we offer a tripartite structure that links previously disconnected views of cooperation. We distinguish three general models by which cooperation can evolve and be maintained: (i) directed reciprocation--cooperation with individuals who give in return; (ii) shared genes--cooperation with relatives (e.g., kin selection); and (iii) byproduct benefits--cooperation as an incidental consequence of selfish action. Each general model is further subdivided. Several renowned examples of cooperation that have lacked explanation until recently--plant-rhizobium symbioses and bacteria-squid light organs--fit squarely within this framework. Natural systems of cooperation often involve more than one model, and a fruitful direction for future research is to understand how these models interact to maintain cooperation in the long term.