A method for reconstructing temporal changes in vegetation functional trait composition using Holocene pollen assemblages.

Methods of reconstructing changes in plant traits over long time scales are needed to understand the impact of changing environmental conditions on ecosystem processes and services. Although Holocene pollen have been extensively used to provide records of vegetation history, few studies have adopted a functional trait approach that is pertinent to changes in ecosystem processes. Here, for woody and herbaceous fen peatland communities, we use modern pollen and vegetation data combined with pollen records from Holocene deposits to reconstruct vegetation functional dynamics. The six traits chosen (measures of leaf area-to-mass ratio and leaf nutrient content) are known to modulate species' fitness and to vary with changes in ecosystem processes. We fitted linear mixed effects models between community weighted mean (CWM) trait values of the modern pollen and vegetation to determine whether traits assigned to pollen types could be used to reconstruct traits found in the vegetation from pollen assemblages. We used relative pollen productivity (RPP) correction factors in an attempt to improve this relationship. For traits showing the best fit between modern pollen and vegetation, we applied the model to dated Holocene pollen sequences from Fenland and Romney Marsh in eastern and southern England and reconstructed temporal changes in trait composition. RPP adjustment did not improve the linear relationship between modern pollen and vegetation. Leaf nutrient traits (leaf C and N) were generally more predictable from pollen data than mass-area traits. We show that inferences about biomass accumulation and decomposition rates can be made using Holocene trait reconstructions. While it is possible to reconstruct community-level trends for some leaf traits from pollen assemblages preserved in sedimentary archives in wetlands, we show the importance of testing methods in modern systems first and encourage further development of this approach to address issues concerning the pollen-plant abundance relationship and pollen source area.

Relation between modern pollen rain, vegetation and climate in northern China: Implications for quantitative vegetation reconstruction in a steppe environment.

Vegetation reconstructions from palaeoecological records depend on adequate understanding of relationships between modern pollen, vegetation and climate. A key parameter for quantitative vegetation reconstructions is the Relative Pollen Productivity (RPP). Differences in both environmental and methodological factors are known to alter the RPP estimated significantly, making it difficult to determine whether the underlying pollen productivity does actually vary, and if so, why. In this paper, we present the results of a replication study for the Bashang steppe region, a typical steppe area in northern China, carried out in 2013 and 2014. In each year, 30 surface samples were collected for pollen analysis, with accompanying vegetation survey using the "Crackles Bequest Project" methodology. Sampling designs differed slightly between the two years: in 2013, sites were located completely randomly, whilst in 2014 sampling locations were constrained to be within a few km of roads. There is a strong inter-annual variability in both the pollen and the vegetation spectra therefore in RPPs, and annual precipitation may be a key influence on these variations. The pollen assemblages in both years are dominated by herbaceous taxa such as Artemisia, Amaranthaceae, Poaceae, Asteraceae, Cyperaceae, Fabaceae and Allium. Artemisia and Amaranthaceae pollen are significantly over-represented for their vegetation abundance. Poaceae, Cyperaceae and Fabaceae seem to have under-represented pollen for vegetation with correspondingly lower RPPs. Asteraceae seems to be well-represented, with moderate RPPs and less annual variation. Estimated Relevant Source Area of Pollen (RSAP) ranges from 2000 to 3000m. Different sampling designs have an effect both on RSAP and RPPs and random sample selection may be the best strategy for obtaining robust estimates. Our results have implications for further pollen-vegetation relationship and quantitative vegetation reconstruction research in typical steppe areas and in other open habitats with strong inter-annual variation.

A mouse model of familial porphyria cutanea tarda.

Approximately one-third of patients with porphyria cutanea tarda (PCT), the most common porphyria in humans, inherit a single mutant allele of the uroporphyrinogen decarboxylase (URO-D) gene. PCT associated with URO-D mutations is designated familial PCT. The phenotype is characterized by a photosensitive dermatosis with hepatic accumulation and urinary excretion of uroporphyrin and hepta-carboxylic porphyrins. Most heterozygotes for URO-D mutations do not express a porphyric phenotype unless hepatic siderosis is present. Hemochromatosis gene (HFE) mutations are frequently found when the phenotype is expressed. We used homologous recombination to disrupt one allele of murine URO-D. URO-D(+/-) mice had half-wild type (wt) URO-D protein and enzymatic activity in all tissues but did not accumulate hepatic porphyrins, indicating that half-normal URO-D activity is not rate limiting. When URO-D(+/-) mice were injected with iron-dextran and given drinking water containing delta-aminolevulinic acid for 21 days, hepatic porphyrins accumulated, and hepatic URO-D activity was reduced to 20% of wt. We bred mice homozygous for an HFE gene disruption (HFE(-/-)) to URO-D(+/-) mice, generating mice with the URO-D(+/-)/HFE(-/-) genotype. These animals developed a porphyric phenotype by 14 weeks of age without ALA supplementation, and URO-D activity was reduced to 14% of wt. These data indicate that iron overload alone is sufficient to reduce URO-D activity to rate-limiting levels in URO-D(+/-) mice. The URO-D(+/-) mouse serves as an excellent model of familial PCT and affords the opportunity to define the mechanism by which iron influences URO-D activity.

Molecular cloning of a novel human diacylglycerol kinase highly selective for arachidonate-containing substrates.

Diacylglycerol (DAG) is a second messenger that activates protein kinase C and also occupies a central role in phospholipid biosynthesis. Conversion of DAG to phosphatidic acid by DAG kinase regulates the amount of DAG and the route it takes. We used degenerate primers to amplify polymerase chain reaction products from cDNA derived from human endothelial cells. A product with a novel sequence was identified and used to clone a 2.6-kilobase cDNA from an endothelial cell library. When transfected with a truncated version of this cDNA, COS-7 cells had a marked increase in DAG kinase activity, which demonstrated clear selectivity for arachidonoyl-containing species of diacylglycerol. The open reading frame of this clone has 567 residues with a predicted protein of 64 kDa. This enzyme, which we designated DGK epsilon, has two distinctive zinc finger-like structures in its N-terminal region, but does not contain the E-F hand motifs found in several other mammalian DGKs. The catalytic domain of DGK epsilon, which is related to other DGKs, contains two ATP-binding motifs. Northern blotting demonstrated that DGK epsilon is expressed predominantly in testis. This unique diacylglycerol kinase may terminate signals transmitted through arachidonoyl-DAG or may contribute to the synthesis of phospholipids with defined fatty acid composition.

Lack of a centrally-mediated antihypertensive effect following acute or chronic central treatment with AT1-receptor antagonists in spontaneously hypertensive rats.

1. The role of the central renin-angiotensin system in the pathogenesis of hypertension in spontaneously hypertensive rats (SHR) was examined following acute and chronic intracerebroventricular (i.c.v.) infusions of angiotensin1 (AT1) receptor antagonists. 2. Groups of SHR were chronically instrumented for acute i.c.v. administration of the AT1 receptor antagonists, losartan and CV-11974, on mean arterial blood pressure (MAP) and heart rate (HR). Other groups of SHR also had mini-osmotic pumps implanted for chronic i.c.v. infusion of CV-11974. 3. Initially both young (15-18 weeks, n = 8) and old (25-29 weeks, n = 9) SHR received acute i.c.v. injections of losartan (10 micrograms) while a third group of young SHR received CV-11974 (1 microgram, n = 6). In all three groups of SHR, MAP and HR did not change up to 24 h after antagonist injection. However, changes in MAP and HR in response to i.c.v. angiotensin II (AII, 100 ng) were abolished 15 min after administration of the AT1 receptor antagonists. These responses had returned to control levels after 3 h in both groups given losartan but were still significantly depressed at 24 h in the CV-11974-treated group. By contrast, responses to i.v. AII (25 ng) before and 1 h after administration of AT1 receptor antagonists were not significantly different. 4. For chronic studies, four groups of SHR received chronic i.c.v. infusion of either vehicle (n = 9) or CV-11974 (1, 5 and 100 micrograms kg-1 day-1) (n = 4, 7 and 8 respectively) for 4 days. Baseline cardiovascular parameters were monitored daily together with changes in MAP and HR in response to both i.c.v. and i.v. AII (100 ng and 50 ng respectively) and i.v. phenylephrine (3 micrograms). Responses to i.c.v. carbachol (5 micrograms) were also recorded on day 4 while baroreflex function was assessed between days 1-3. In SHR treated chronically with i.c.v. vehicle or CV-11974, at 1 or 5 micrograms kg-1 day-1, resting MAP and HR did not vary over the four day infusion period. However, SHR treated with 100 micrograms kg-1 day-1 CV-11974 had significantly lower MAP compared to vehicle-treated SHR. While there was some variation in resting HR, there were no differences between the drug-treated and vehicle-treated groups. Pressor responses following i.c.v. AII administration were slightly, but significantly, inhibited on days 3 and 4 in the low dose CV-11974-treated (1 microgram kg-1 day-1) SHR. However, these responses were abolished on all 4 days in the 5 and 100 micrograms kg-1 day-1 CV-11974-treated groups. By contrast, changes in MAP and HR following i.v. AII injection did not vary over the 4 day infusion between SHR treated with the 2 lowest doses of CV-11974 and the vehicle-treated group. However, in the high dose CV-11974-treated SHR (100 micrograms kg-1 day-1), the cardiovascular effects of AII were abolished. In addition, phenylephrine (i.v.) and carbachol (i.c.v.) induced changes in MAP and HR were not significantly different in all four treatment groups. Similarly, baroreflex function was unaffected by i.c.v. infusion of 100 micrograms kg-1 day-1 CV-11974, except for a significant fall in BP50 which paralleled the fall in resting MAP. 5. Collectively, these results indicate that acute and chronic central AT1 receptor antagonism does not lower MAP in conscious SHR in doses which only block central AII-induced pressor activity. Chronic central infusion of CV-11974 at sufficiently high doses will lower MAP, as has been reported by others, but not without the abolition of the peripheral effects of AII. Therefore it is most likely that peripheral AT1 receptor blockade contributes to the hypotensive action of CV-11974 under these conditions.