Salicylic acid-mediated innate immunity in Arabidopsis is regulated by SIZ1 SUMO E3 ligase

Reversible modifications of target proteins by small ubiquitin-like modifier (SUMO) proteins are involved in many cellular processes in yeast and animals. Yet little is known about the function of sumoylation in plants. Here, we show that the SIZ1 gene, which encodes an Arabidopsis SUMO E3 ligase, regulates innate immunity. Mutant siz1 plants exhibit constitutive systemic-acquired resistance (SAR) characterized by elevated accumulation of salicylic acid (SA), increased expression of pathogenesis-related (PR) genes, and increased resistance to the bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000. Transfer of the NahG gene to siz1 plants results in reversal of these phenotypes back to wild-type. Analyses of the double mutants, npr1 siz1, pad4 siz1 and ndr1 siz1 revealed that SIZ1 controls SA signalling. SIZ1 interacts epistatically with PAD4 to regulate PR expression and disease resistance. Consistent with these observations, siz1 plants exhibited enhanced resistance to Pst DC3000 expressing avrRps4, a bacterial avirulence determinant that responds to the EDS1/PAD4-dependent TIR-NBS-type R gene. In contrast, siz1 plants were not resistant to Pst DC3000 expressing avrRpm1, a bacterial avirulence determinant that responds to the NDR1-dependent CC-NBS-type R gene. Jasmonic acid (JA)-induced PDF1.2 expression and susceptibility to Botrytis cinerea were unaltered in siz1 plants. Taken together, these results demonstrate that SIZ1 is required for SA and PAD4-mediated R gene signalling, which in turn confers innate immunity in Arabidopsis.     

Spatial extinction or persistence: landscape‐temperature interactions perturb predator–prey dynamics

Recognising that species interact across a range of spatial scales, we explore how landscape structure interacts with temperature to influence persistence. Specifically, we recognise that few studies indicate thermal shifts as the proximal cause of species extinctions; rather, species interactions exacerbated by temperature result in extinctions. Using microcosm‐based experiments, as models of larger landscape processes, we test hypotheses that would be problematic to address through field work. A text‐book predator–prey system (the ciliates Didinium and Paramecium) was used to compare three landscapes: an unfragmented landscape subjected to uniform temperatures (10, 20, 30°C); a fragmented landscape (potentially hosting metapopulations) subjected to these three temperatures; and a fragmented landscape subjected to a spatial temperature gradient (～ 10 to 30°C) – despite the prevalence of natural temperature ecoclines this is the first time such an analysis has been conducted. Initial thermal response‐analysis (growth, mortality, and movement measured between 10 and 30°C) suggested that as temperature increased, the predator might drive the prey to extinction. Thermal preferences (measured at 5 temperatures between 10 and 30°C), indicated that both predator and prey preferred warmer temperatures, with the predator exhibiting the stronger preference, suggesting that cooler regions might act as a prey‐refuge. The landscape level observations, however, did not entirely support the predictions. First, in the unfragmented landscape, increased temperature led to extinctions, but at the highest temperature (where the predator growth can be reduced) the prey survived. Second, at high temperatures the fragmented landscape failed to host metapopulations that would allow predator–prey persistence. Third, the thermal ecocline did not provide heterogeneity that improved stability; rather it forced both species to occupy a smaller realized space, leading toward extinctions. These findings reveal that temperature‐impacted rates and temperature preferences combine to drive predator–prey dynamics and persistence across landscapes.     

受体酪氨酸激酶依赖的信号转导在突触可塑性中的研究

突触可塑性对于脑发育过程中的神经环路重构以及学习记忆等脑的高级功能是非常重要的。许多受体酪氨酸激酶家族成员,包括TrkB、ErbB和Eph在神经连接的建立和重构过程中起到核心作用。比如,突触后EphB依赖的信号会导致树突棘的产生和神经递质受体的聚集,而ephrinA引起的EphA4激活可以导致树突棘的回缩。但是,目前对EphA4依赖的树突棘重组和对神经递质受体的调节背后的机制还知之甚少。本文将集中探讨EphA4及其下游的信号通路在神经肌肉接头和中枢神经的突触中,对神经递质受体的调节功能。     

Mechanisms of Cadmium Mobility and Accumulation in Indian Mustard

Indian mustard (Brassica juncea L.), a high biomass crop plant, accumulated substantial amounts of cadmium, with bioaccumulation coefficients (concentration of Cd in dry plant tissue/concentration in solution) of up to 1100 in shoots and 6700 in roots at nonphytotoxic concentrations of Cd (0.1 [mu]g/mL) in solution. This was associated with a rapid accumulation of phytochelatins in the root, where the majority of the Cd was coordinated with sulfur ligands, probably as a Cd-S4 complex, as demonstrated by x-ray absorption spectroscopy. In contrast, Cd moving in the xylem sap was coordinated predominantly with oxygen or nitrogen ligands. Cd concentrations in the xylem sap and the rate of Cd accumulation in the leaves displayed similar saturation kinetics, suggesting that the process of Cd transport from solution through the root and into the xylem is mediated by a saturable transport system(s). However, Cd translocation to the shoot appeared to be driven by transpiration, since ABA dramatically reduced Cd accumulation in leaves. Within leaves, Cd was preferentially accumulated in trichomes on the leaf surface, and this may be a possible detoxification mechanism.     

Arabidopsis pdr2 reveals a phosphate-sensitive checkpoint in root development

Plants have evolved complex strategies to maintain phosphate (Pi) homeostasis and to maximize Pi acquisition when the macronutrient is limiting. Adjustment of root system architecture via changes in meristem initiation and activity is integral to the acclimation process. However, the mechanisms that monitor external Pi status and interpret the nutritional signal remain to be elucidated. Here, we present evidence that the Pi deficiency response, pdr2, mutation disrupts local Pi sensing. The sensitivity and amplitude of metabolic Pi-starvation responses, such as Pi-responsive gene expression or accumulation of anthocyanins and starch, are enhanced in pdr2 seedlings. However, the most conspicuous alteration of pdr2 is a conditional short-root phenotype that is specific for Pi deficiency and caused by selective inhibition of root cell division followed by cell death below a threshold concentration of about 0.1 mm external Pi. Measurements of general Pi uptake and of total phosphorus (P) in root tips exclude a defect in high-affinity Pi acquisition. Rescue of root meristem activity in Pi-starved pdr2 by phosphite (Phi), a non-metabolizable Pi analog, and divided-root experiments suggest that pdr2 disrupts sensing of low external Pi availability. Thus, PDR2 is proposed to function at a Pi-sensitive checkpoint in root development, which monitors environmental Pi status, maintains and fine-tunes meristematic activity, and finally adjusts root system architecture to maximize Pi acquisition.     

Redundant roles of four ZIP family members in zinc homeostasis and seed development in Arabidopsis thaliana

Zinc (Zn) is essential for normal plant growth and development. The Zn-regulated transporter, iron-regulated transporter (IRT)-like protein (ZIP) family members are involved in Zn transport and cellular Zn homeostasis throughout the domains of life. In this study, we have characterized four ZIP transporters from Arabidopsis thaliana (IRT3, ZIP4, ZIP6, and ZIP9) to better understand their functional roles. The four ZIP proteins can restore the growth defect of a yeast Zn uptake mutant and are upregulated under Zn deficiency. Single and double mutants show no phenotypes under Zn-sufficient or Zn-limited growth conditions. In contrast, triple and quadruple mutants show impaired growth irrespective of external Zn supply due to reduced Zn translocation from root to shoot. All four ZIP genes are highly expressed during seed development, and siliques from all single and higher-order mutants exhibited an increased number of abnormal seeds and decreased Zn levels in mature seeds relative to wild type. The seed phenotypes could be reversed by supplementing the soil with Zn. Our data demonstrate that IRT3, ZIP4, ZIP6, and ZIP9 function redundantly in maintaining Zn homeostasis and seed development in A. thaliana.     

The preparation and use of media based on a simple fish waste extract

An aqueous extract of trypsin-degraded fish waste is a good substitute for beef extract in culture media. With beef extract and proteose peptone, it promoted luxuriant growth and staphylococcal toxin production. Though growth occurred in dilute solutions of the extract alone, alpha-toxin production was suppressed. It was synergistic with proteose peptone in the production of alpha-toxin. Separated fish lipids may be used to demonstrate lipase activity.     

Imaging multiple phases of neurodegeneration: a novel approach to assessing cell death in vivo

Nerve cell death is the key event in all neurodegenerative disorders, with apoptosis and necrosis being central to both acute and chronic degenerative processes. However, until now, it has not been possible to study these dynamically and in real time. In this study, we use spectrally distinct, well-recognised fluorescent cell death markers to enable the temporal resolution and quantification of the early and late phases of apoptosis and necrosis of single nerve cells in different disease models. The tracking of single-cell death profiles in the same living eye over hours, days, weeks and months is a significant advancement on currently available techniques. We identified a numerical preponderance of late-phase versus early-phase apoptotic cells in chronic models, reinforcing the commonalities between cellular mechanisms in different disease models. We showed that MK801 effectively inhibited both apoptosis and necrosis, but our findings support the use of our technique to investigate more specific anti-apoptotic and anti-necrotic strategies with well-defined targets, with potentially greater clinical application. The optical properties of the eye provide compelling opportunities for the quantitative monitoring of disease mechanisms and dynamics in experimental neurodegeneration. Our findings also help to directly observe retinal nerve cell death in patients as an adjunct to refining diagnosis, tracking disease status and assessing therapeutic intervention.