野生与栽培黄花蒿净光合速率对光强和CO2浓度的响应

比较了相同种源的野生和栽培黄花蒿(Artemisia annua L.)净光合速率对光强和CO2浓度的响应特性。结果表明,野生和栽培黄花蒿的光饱和点(LSP)分别为1 183和1 564μmol m-2s-1,光补偿点(LCP)为17和18μmol m-2s-1,最大净光合速率(Pmax)为18.78和22.38μmol m-2s-1,表观量子效率(AQY)为0.08和0.075μmol m-2s-1,表明黄花蒿的光合能力强,能够利用很高的光强,且对弱光的适应性也较强。栽培黄花蒿的Pmax、LSP和最大羧化速率(Vcmax)显著高于野生黄花蒿,两者的LCP、不包括光下呼吸的CO2补偿点、AQY、光下呼吸速率和最大电子传递速率(Jmax)差异不显著。强光下栽培黄花蒿主要通过提高Vcmax和Jmax等来增强光合能力,强的光合能力有利于黄花蒿的生长,因此在人工栽培黄花蒿的过程中应选择阳光充足的开阔生境。     

ADP-ribosylation factor like 7 (ARL7) interacts with α-tubulin and modulates intracellular vesicular transport

ADP-ribosylation factor (ARF) like 7 (ARL7, also named ARL4C) is a member of ARL family and recent studies showed that it is involved in the AI-dependent cholesterol secretion process. Yet its biological function remains largely unknown. Using a MALDI-TOF/MS analysis, we identified α-tubulin interacted with ARL7. The interaction was confirmed by GST pull-down assay and co-immunoprecipitation in renal carcinoma cell 786-O in which we found the endogenous ARL7 is expressed. This is the second ARL member found interacting with tubulin after ARL8. In addition, ARL7Q72L, a GTP-binding form, promoted the transferrin transport from early endosome to recycling endosome significantly. The above data suggested that ARL7 might modulate the intracellular vesicular transport via interaction with microtubules.     

Elucidation of the effects of lipoperoxidation on the mitochondrial electron transport chain using yeast mitochondria with manipulated fatty acid content

Lipoperoxidative damage to the respiratory chain proteins may account for disruption in mitochondrial electron transport chain (ETC) function and could lead to an augment in the production of reactive oxygen species (ROS). To test this hypothesis, we investigated the effects of lipoperoxidation on ETC function and cytochromes spectra of Saccharomyces cerevisiae mitochondria. We compared the effects of Fe²⁺ treatment on mitochondria isolated from yeast with native (lipoperoxidation-resistant) and modified (lipoperoxidation-sensitive) fatty acid composition. Augmented sensitivity to oxidative stress was observed in the complex III-complex IV segment of the ETC. Lipoperoxidation did not alter the cytochromes content. Under lipoperoxidative conditions, cytochrome c reduction by succinate was almost totally eliminated by superoxide dismutase and stigmatellin. Our results suggest that lipoperoxidation impairs electron transfer mainly at cytochrome b in complex III, which leads to increased resistance to antimycin A and ROS generation due to an electron leak at the level of the Q_O site of complex III.     

The Persistent Question of Potassium Channel Permeation Mechanisms

Potassium channels play critical roles in many physiological processes, providing a selective permeation route for K⁺ ions in and out of a cell, by employing a carefully designed selectivity filter, evolutionarily conserved from viruses to mammals. The structure of the selectivity filter was determined at atomic resolution by x-ray crystallography, showing a tight coordination of desolvated K⁺ ions by the channel. However, the molecular mechanism of K⁺ ions permeation through potassium channels remains unclear, with structural, functional and computational studies often providing conflicting data and interpretations. In this review, we will present the proposed mechanisms, discuss their origins, and will critically assess them against all available data. General properties shared by all potassium channels are introduced first, followed by the introduction of two main mechanisms of ion permeation: soft and direct knock-on. Then, we will discuss critical computational and experimental studies that shaped the field. We will especially focus on molecular dynamics (MD) simulations, that provided mechanistic and energetic aspects of K⁺ permeation, but at the same time created long-standing controversies. Further challenges and possible solutions are presented as well.     

Plant KT/KUP/HAK potassium transporters: single family - multiple functions

BACKGROUND AND AIMS: Potassium transporters belonging to the KT/KUP/HAK family are important for various aspects of plant life including mineral nutrition and the regulation of development. Genes encoding these transporters are present in the genomes of all plants, but have not been found in the genomes of Protista or Animalia. The aim of this Botanical Briefing is to analyse the function of KT/KUP/HAK transporters from evolutionary, molecular and physiological perspectives. SCOPE: This Briefing covers the phylogeny and evolution of KT/KUP/HAK transporters, the role of transporters in plant mineral nutrition and potassium homeostasis, and the role of KT/KUP/HAK transporters in plant development.     

Motor impairment in Alzheimer's disease and transgenic Alzheimer's disease mouse models

In this commentary, we accent the accumulating evidence for motor impairment as a common feature of early Alzheimer's disease (AD) pathology. In addition, we summarize the state of knowledge on this phenotype in experimental mouse models, expressing AD-associated genes like tau or amyloid precursor protein.     

Distinct isocomplexes of the TRAPP trafficking factor coexist inside human cells

The transport protein particle (TRAPP) complex is required for proper vesicular transport from the ER to the Golgi. The composition of yeast TRAPP is well characterized, but the organization of mammalian TRAPP complex remains elusive. Using a tandem affinity purification (TAP) approach, we provide first experimental proof for the association of NIBP (NIK/IKKβ binding protein) with Bet3 and find two human paralogs of Trs33 (A and B) associated with Bet3. Interaction studies and gel filtration analysis reveal that both proteins are part of human TRAPP and might mark two distinct isocomplexes that exert different functions in the regulation of ER-to-Golgi traffic.

Structured summary

MINT-6784845:

Bet3 (uniprotkb:O43617) physically interacts (MI:0218) with Trs33B (uniprotkb:Q86SZ2) by anti bait coimmunoprecipitation (MI:0006)

MINT-6785053:

Trs33B (uniprotkb:Q86SZ2) physically interacts (MI:0218) with Bet3 (uniprotkb:O43617) and Sedl (uniprotkb:O14582) by anti bait coimmunoprecipitation (MI:0006)

MINT-6784856:

Bet3 (uniprotkb:O43617) physically interacts (MI:0218) with Trs33A2 (uniprotkb:O75865-2) by anti bait coimmunoprecipitation (MI:0006)

MINT-6785038:

Trs33A1 (uniprotkb:O75865-2) physically interacts (MI:0218) with Sedl (uniprotkb:O14582) and Bet3 (uniprotkb:O43617) by anti bait coimmunoprecipitation (MI:0006)

MINT-6784879:

Bet3 (uniprotkb:O43617) physically interacts (MI:0218) with NIBP (uniprotkb:Q96Q05) by tandem affinity purification (MI:0676)

MINT-6785068:

Trs33B (uniprotkb:Q86SZ2), Trs33A2 (uniprotkb:O75865-2) and Bet3 (uniprotkb:O43617) colocalize (MI:0403) by molecular sieving (MI:0071)

MINT-6785415:

Bet3 (uniprotkb:O43617) physically interacts (MI:0218) with Trs33A1 (uniprotkb:O75865) by anti bait coimmunoprecipitation (MI:0006)

     

Monitoring the fluvial palynomorph load in a lowland temperate catchment and its relationship to suspended sediment and discharge

Despite it being a component of the seston we know very little about fluvial (waterborne) pollen and spore (palynomorph) transport. This paper presents the results of a monitoring programme conducted over two years and at a catchment scale in South West England. A hierarchical monitoring network was established with flood peak samples taken at 9 sub-catchments, intra-hydrograph samples taken in two sub-catchments and time-integrated sampling undertaken at one location. In addition sampling was undertaken of probable palynomorph sources such as channel bed and bank sediments, and the airborne pollen flux was monitored using modified Tauber traps. The results support previous research in illustrating how the vast majority of fluvial pollen and spores are transported during floods (91%) and that the main control on waterborne palynomorph assemblages is the catchment vegetation and its spatial distribution but with a long-distance (extra-catchment) component. However, strong seasonal effects are also shown, and the importance of distinctive sources such as the riparian input, bed re-suspension and overland flow into drains and tributaries is revealed. Fine sediment in river pools appears to act as a selective store of damaged cereal type pollen grains derived from arable fields. Although pollen does form part of composite particles the data presented here suggest that the majority of the pollen is transported as single grains. Fluvial palynomorph loading is strongly dependant upon discharge and so concentrations in laminated or varved sediments could be regarded as a proxy for flood magnitude. Handling editor: J. Saros     

A unifying conceptual model for the environmental responses of isoprene emissions from plants

Background and Aims

Isoprene is the most important volatile organic compound emitted by land plants in terms of abundance and environmental effects. Controls on isoprene emission rates include light, temperature, water supply and CO₂ concentration. A need to quantify these controls has long been recognized. There are already models that give realistic results, but they are complex, highly empirical and require separate responses to different drivers. This study sets out to find a simpler, unifying principle.

Methods

A simple model is presented based on the idea of balancing demands for reducing power (derived from photosynthetic electron transport) in primary metabolism versus the secondary pathway that leads to the synthesis of isoprene. This model''s ability to account for key features in a variety of experimental data sets is assessed.

Key results

The model simultaneously predicts the fundamental responses observed in short-term experiments, namely: (1) the decoupling between carbon assimilation and isoprene emission; (2) a continued increase in isoprene emission with photosynthetically active radiation (PAR) at high PAR, after carbon assimilation has saturated; (3) a maximum of isoprene emission at low internal CO₂ concentration (c_i) and an asymptotic decline thereafter with increasing c_i; (4) maintenance of high isoprene emissions when carbon assimilation is restricted by drought; and (5) a temperature optimum higher than that of photosynthesis, but lower than that of isoprene synthase activity.

Conclusions

A simple model was used to test the hypothesis that reducing power available to the synthesis pathway for isoprene varies according to the extent to which the needs of carbon assimilation are satisfied. Despite its simplicity the model explains much in terms of the observed response of isoprene to external drivers as well as the observed decoupling between carbon assimilation and isoprene emission. The concept has the potential to improve global-scale modelling of vegetation isoprene emission.     

Effects of Barbiturates on Facilitative Glucose Transporters are Pharmacologically Specific and Isoform Selective

Barbiturates inhibit GLUT-1-mediated glucose transport across the blood-brain barrier, in cultured mammalian cells, and in human erythrocytes. Barbiturates also interact directly with GLUT-1. The hypotheses that this inhibition of glucose transport is (i) selective, preferring barbiturates over halogenated hydrocarbon inhalation anesthetics, and (ii) specific, favoring some GLUT-# isoforms over others were tested. Several oxy- and thio-barbiturates inhibited [³H]-2-deoxyglucose uptake by GLUT-1 expressing murine fibroblasts with IC₅₀s of 0.2–2.9 mm. Inhibition of GLUT-1 by barbiturates correlates with their overall lipid solubility and pharmacology, and requires hydrophobic side chains on the core barbiturate structure. In contrast, several halogenated hydrocarbons and ethanol (all ≤10 mm) do not significantly inhibit glucose transport. The interaction of these three classes of anesthetics with purified GLUT-1 was evaluated by quenching of intrinsic protein fluorescence and displayed similar specificities and characteristics. The ability of barbiturates to inhibit other facilitative glucose transporters was determined in cell types expressing predominantly one isoform. Pentobarbital inhibits [³H]-2-deoxyglucose and [¹⁴C]-3-O-methyl-glucose uptake in cells expressing GLUT-1, GLUT-2, and GLUT-3 with IC₅₀s of ∼1 mm. In contrast, GLUT-4 expressed in insulin-stimulated rat adipocytes was much less sensitive than the other isoforms to inhibition by pentobarbital (IC₅₀ of >10 mm). Thus, barbiturates selectively inhibit glucose transport by some, but not all, facilitative glucose transporter isoforms. Received: 10 November 1998/Revised: 3 February 1999