Organism-sediment interactions govern post-hypoxia recovery of ecosystem functioning

Hypoxia represents one of the major causes of biodiversity and ecosystem functioning loss for coastal waters. Since eutrophication-induced hypoxic events are becoming increasingly frequent and intense, understanding the response of ecosystems to hypoxia is of primary importance to understand and predict the stability of ecosystem functioning. Such ecological stability may greatly depend on the recovery patterns of communities and the return time of the system properties associated to these patterns. Here, we have examined how the reassembly of a benthic community contributed to the recovery of ecosystem functioning following experimentally-induced hypoxia in a tidal flat. We demonstrate that organism-sediment interactions that depend on organism size and relate to mobility traits and sediment reworking capacities are generally more important than recovering species richness to set the return time of the measured sediment processes and properties. Specifically, increasing macrofauna bioturbation potential during community reassembly significantly contributed to the recovery of sediment processes and properties such as denitrification, bedload sediment transport, primary production and deep pore water ammonium concentration. Such bioturbation potential was due to the replacement of the small-sized organisms that recolonised at early stages by large-sized bioturbating organisms, which had a disproportionately stronger influence on sediment. This study suggests that the complete recovery of organism-sediment interactions is a necessary condition for ecosystem functioning recovery, and that such process requires long periods after disturbance due to the slow growth of juveniles into adult stages involved in these interactions. Consequently, repeated episodes of disturbance at intervals smaller than the time needed for the system to fully recover organism-sediment interactions may greatly impair the resilience of ecosystem functioning.

Accumulation of Biomass and Mineral Elements with Calendar Time by Corn: Application of the Expanded Growth Model

The expanded growth model is developed to describe accumulation of plant biomass (Mg ha−1) and mineral elements (kg ha−1) in with calendar time (wk). Accumulation of plant biomass with calendar time occurs as a result of photosynthesis for green land-based plants. A corresponding accumulation of mineral elements such as nitrogen, phosphorus, and potassium occurs from the soil through plant roots. In this analysis, the expanded growth model is tested against high quality, published data on corn (Zea mays L.) growth. Data from a field study in South Carolina was used to evaluate the application of the model, where the planting time of April 2 in the field study maximized the capture of solar energy for biomass production. The growth model predicts a simple linear relationship between biomass yield and the growth quantifier, which is confirmed with the data. The growth quantifier incorporates the unit processes of distribution of solar energy which drives biomass accumulation by photosynthesis, partitioning of biomass between light-gathering and structural components of the plants, and an aging function. A hyperbolic relationship between plant nutrient uptake and biomass yield is assumed, and is confirmed for the mineral elements nitrogen (N), phosphorus (P), and potassium (K). It is concluded that the rate limiting process in the system is biomass accumulation by photosynthesis and that nutrient accumulation occurs in virtual equilibrium with biomass accumulation

Model of Yield Response of Corn to Plant Population and Absorption of Solar Energy

Biomass yield of agronomic crops is influenced by a number of factors, including crop species, soil type, applied nutrients, water availability, and plant population. This article is focused on dependence of biomass yield (Mg ha−1 and g plant−1) on plant population (plants m−2). Analysis includes data from the literature for three independent studies with the warm-season annual corn (Zea mays L.) grown in the United States. Data are analyzed with a simple exponential mathematical model which contains two parameters, viz. Ym (Mg ha−1) for maximum yield at high plant population and c (m2 plant−1) for the population response coefficient. This analysis leads to a new parameter called characteristic plant population, xc = 1/c (plants m−2). The model is shown to describe the data rather well for the three field studies. In one study measurements were made of solar radiation at different positions in the plant canopy. The coefficient of absorption of solar energy was assumed to be the same as c and provided a physical basis for the exponential model. The three studies showed no definitive peak in yield with plant population, but generally exhibited asymptotic approach to maximum yield with increased plant population. Values of xc were very similar for the three field studies with the same crop species

1H, 13C and 15N resonance assignments of the Calmodulin-Munc13-1 peptide complex

Ca2+-Calmodulin binding to the variable N-terminal region of the diacylglycerol/phorbol ester-binding UNC13/Munc13 family of proteins modulates the short-term synaptic plasticity characteristics in neurons. Here, we report the sequential backbone and side chain resonance assignment of the Ca2+-Calmodulin/Munc13-1458–492 peptide complex at pH 6.8 and 35°C (BMRB No. 15470)

Calmodulin Interaction with hEAG1 Visualized by FRET Microscopy

BACKGROUND: Ca(2+)-mediated regulation of ion channels provides a link between intracellular signaling pathways and membrane electrical activity. Intracellular Ca(2+) inhibits the voltage-gated potassium channel EAG1 through the direct binding of calmodulin (CaM). Three CaM binding sites (BD-C1: 674-683, BD-C2: 711-721, BD-N: 151-165) have been identified in a peptide screen and were proposed to mediate binding. The participation of the three sites in CaM binding to the native channel, however, remains unclear. METHODOLOGY/PRINCIPAL FINDINGS: Here we studied the binding of Ca(2+)/CaM to the EAG channel by visualizing the interaction between YFP-labeled CaM and Cerulean-labeled hEAG1 in mammalian cells by FRET. The results of our cellular approach substantiate that two CaM binding sites are predominantly involved; the high-affinity 1-8-14 based CaM binding domain in the N-terminus and the second C-terminal binding domain BD-C2. Mutations at these sites completely abolished CaM binding to hEAG1. CONCLUSIONS/SIGNIFICANCE: We demonstrated that the BD-N and BD-C2 binding domains are sufficient for CaM binding to the native channel, and, therefore, that BD-C1 is unable to bind CaM independently

Smoking status and common carotid artery intima-medial thickness among middle-aged men and women based on ultrasound measurement: a cohort study

BACKGROUND: Cigarette smoking is an established causal factor for atherosclerosis. However, the smoking effect on different echogenic components of carotid arterial wall measured by ultrasound is not well elucidated. METHODS: Middle-aged men and women who had IMT measurement ≥ 0.7 mm at baseline and follow-up were included (N = 413, age 40–60 years at baseline in 1995). Intima-media thickness of common carotid artery (CCA-IMT) and its components (echogenic and echolucent layers) were measured at baseline and in the follow-up examination 3 years later. IMT and its components were compared across current, former and never smokers. Individual growth models were used to examine how smoking status was related to the baseline and progression of overall IMT and IMT components. RESULTS: For both men and women, current smoking was associated with thicker echogenic layer than never smokers; former smokers exhibited thinner echogenic layer than current smokers after adjustment for cigarette pack-years. Among women, current smoking was also associated with a thinned echolucent layer that resulted in a non-significant overall association of current smoking with IMT for women. CONCLUSION: Cigarette smoking is associated with carotid artery morphological changes and the association is sex-dependent. The atherogenic effect of smoking appears to be partly reversible among former smokers. IMT measurement alone may not be adequate to detect carotid atherosclerosis associated with cigarette smoking among middle-age women

Identification of Genes that Elicit Disuse Muscle Atrophy via the Transcription Factors p50 and Bcl-3

Skeletal muscle atrophy is a debilitating condition associated with weakness, fatigue, and reduced functional capacity. Nuclear factor-kappaB (NF-κB) transcription factors play a critical role in atrophy. Knockout of genes encoding p50 or the NF-κB co-transactivator, Bcl-3, abolish disuse atrophy and thus they are NF-κB factors required for disuse atrophy. We do not know however, the genes targeted by NF-κB that produce the atrophied phenotype. Here we identify the genes required to produce disuse atrophy using gene expression profiling in wild type compared to Nfkb1 (gene encodes p50) and Bcl-3 deficient mice. There were 185 and 240 genes upregulated in wild type mice due to unloading, that were not upregulated in Nfkb1−/− and Bcl-3−/− mice, respectively, and so these genes were considered direct or indirect targets of p50 and Bcl-3. All of the p50 gene targets were contained in the Bcl-3 gene target list. Most genes were involved with protein degradation, signaling, translation, transcription, and transport. To identify direct targets of p50 and Bcl-3 we performed chromatin immunoprecipitation of selected genes previously shown to have roles in atrophy. Trim63 (MuRF1), Fbxo32 (MAFbx), Ubc, Ctsl, Runx1, Tnfrsf12a (Tweak receptor), and Cxcl10 (IP-10) showed increased Bcl-3 binding to κB sites in unloaded muscle and thus were direct targets of Bcl-3. p50 binding to the same sites on these genes either did not change or increased, supporting the idea of p50:Bcl-3 binding complexes. p65 binding to κB sites showed decreased or no binding to these genes with unloading. Fbxo9, Psma6, Psmc4, Psmg4, Foxo3, Ankrd1 (CARP), and Eif4ebp1 did not show changes in p65, p50, or Bcl-3 binding to κB sites, and so were considered indirect targets of p50 and Bcl-3. This work represents the first study to use a global approach to identify genes required to produce the atrophied phenotype with disuse

Metabolic Adaptation in Transplastomic Plants Massively Accumulating Recombinant Proteins

BACKGROUND: Recombinant chloroplasts are endowed with an astonishing capacity to accumulate foreign proteins. However, knowledge about the impact on resident proteins of such high levels of recombinant protein accumulation is lacking. METHODOLOGY/PRINCIPAL FINDINGS: Here we used proteomics to characterize tobacco (Nicotiana tabacum) plastid transformants massively accumulating a p-hydroxyphenyl pyruvate dioxygenase (HPPD) or a green fluorescent protein (GFP). While under the conditions used no obvious modifications in plant phenotype could be observed, these proteins accumulated to even higher levels than ribulose 1,5-bisphosphate carboxylase/oxygenase (Rubisco), the most abundant protein on the planet. This accumulation occurred at the expense of a limited number of leaf proteins including Rubisco. In particular, enzymes involved in CO(2) metabolism such as nuclear-encoded plastidial Calvin cycle enzymes and mitochondrial glycine decarboxylase were found to adjust their accumulation level to these novel physiological conditions. CONCLUSIONS/SIGNIFICANCE: The results document how protein synthetic capacity is limited in plant cells. They may provide new avenues to evaluate possible bottlenecks in recombinant protein technology and to maintain plant fitness in future studies aiming at producing recombinant proteins of interest through chloroplast transformation

Transcriptome Analysis of Epithelial and Stromal Contributions to Mammogenesis in Three Week Prepartum Cows

Transcriptome analysis of bovine mammary development has provided insight into regulation of mammogenesis. However, previous studies primarily examined expression of epithelial and stromal tissues combined, and consequently did not account for tissue specific contribution to mammary development. Our objective was to identify differences in gene expression in epithelial and intralobular stromal compartments. Tissue was biopsied from non-lactating dairy cows 3 weeks prepartum, cut into explants and incubated for 2 hr with insulin and hydrocortisone. Epithelial and intralobular stromal tissues were isolated with laser capture microdissection. Global gene expression was measured with Bovine Affymetrix GeneChips, and data were preprocessed using RMA method. Moderated t-tests from gene-specific linear model analysis with cell type as a fixed effect showed more than 3,000 genes were differentially expressed between tissues (P<0.05; FDR<0.17). Analysis of epithelial and stromal transcriptomes using Database for Annotation, Visualization and Integrated Discovery (DAVID) and Ingenuity Pathways Analysis (IPA) showed that epithelial and stromal cells contributed distinct molecular signatures. Epithelial signatures were enriched with gene sets for protein synthesis, metabolism and secretion. Stromal signatures were enriched with genes that encoded molecules important to signaling, extracellular matrix composition and remodeling. Transcriptome differences also showed evidence for paracrine interactions between tissues in stimulation of IGF1 signaling pathway, stromal reaction, angiogenesis, neurogenesis, and immune response. Molecular signatures point to the dynamic role the stroma plays in prepartum mammogenesis and highlight the importance of examining the roles of cell types within the mammary gland when targeting therapies and studying mechanisms that affect milk production

Interplay between phosphorylation and palmitoylation mediates plasma membrane targeting and sorting of GAP43.

Phosphorylation and lipidation provide posttranslational mechanisms that contribute to the distribution of cytosolic proteins in growing nerve cells. The growth-associated protein GAP43 is susceptible to both phosphorylation and S-palmitoylation and is enriched in the tips of extending neurites. However, how phosphorylation and lipidation interplay to mediate sorting of GAP43 is unclear. Using a combination of biochemical, genetic, and imaging approaches, we show that palmitoylation is required for membrane association and that phosphorylation at Ser-41 directs palmitoylated GAP43 to the plasma membrane. Plasma membrane association decreased the diffusion constant fourfold in neuritic shafts. Sorting to the neuritic tip required palmitoylation and active transport and was increased by phosphorylation-mediated plasma membrane interaction. Vesicle tracking revealed transient association of a fraction of GAP43 with exocytic vesicles and motion at a fast axonal transport rate. Simulations confirmed that a combination of diffusion, dynamic plasma membrane interaction and active transport of a small fraction of GAP43 suffices for efficient sorting to growth cones. Our data demonstrate a complex interplay between phosphorylation and lipidation in mediating the localization of GAP43 in neuronal cells. Palmitoylation tags GAP43 for global sorting by piggybacking on exocytic vesicles, whereas phosphorylation locally regulates protein mobility and plasma membrane targeting of palmitoylated GAP43