植物系统获得的抗病性和信号传导

植物在长期的进化过程中,需要不断地抵抗病原微生物的侵害。在这种长期相互影响的共进化过程中,植物逐渐形成一系列复杂而行之有效的保护机制来抵御病原微生物的侵染。在植物抵御病原微生物侵染的过程中,宿主植物的抗病基因（R）产物与病原微生物无毒基因（Avr）产物的...     

Acquired Resistance Signal Transduction in Arabidopsis Is Ethylene Independent

To clarify the role of ethylene in systemic acquired resistance (SAR), we conducted experiments using Arabidopsis ethylene response mutants. Plants that are nonresponsive to ethylene (i.e., [theta]tr1 and [theta]in2) showed normal sensitivity to the SAR-inducing chemicals salicylic acid (SA) and 2,6-dichloroisonicotinic acid with respect to SAR gene induction and pathogen resistance. This indicated that chemically induced SAR is not an ethylene-dependent process in Arabidopsis. Ethephon, an ethylene-releasing chemical, induced SAR gene expression in both the wild type and ethylene mutants, whereas ethylene alone did not, suggesting that induction of these genes by ethephon is not due to the action of ethylene. Furthermore, transgenic plants expressing salicylate hydroxylase, a bacterial enzyme that degrades SA to catechol, did not accumulate SAR mRNAs in response to ethephon. Thus, SAR gene induction by ethephon appears to be mediated through SA. Other experiments suggested that ethylene may play a role in SAR by enhancing tissue sensitivity to the action of SA.     

Regulation of Salicylic Acid and N-Hydroxy-Pipecolic Acid in Systemic Acquired Resistance

In plants, salicylic acid (SA) is a central immune signal that is involved in both local and systemic acquired resistance (SAR). In addition to SA, several other chemical signals are also involved in SAR and these include N-hydroxy-pipecolic acid (NHP), a newly discovered plant metabolite that plays a crucial role in SAR. Recent discoveries have led to a better understanding of the biosynthesis of SA and NHP and their signaling during plant defense responses. Here, I review the recent progress in role of SA and NHP in SAR. In addition, I discuss how these signals cooperate with other SAR-inducing chemicals to regulate SAR.     

植物SAR和ISR中的乙烯信号转导网络

乙烯作为重要的信号分子在植物SAR和ISR中发挥重要作用。受病原物和其它激发子处理后,植物体内乙烯被合成,为内质网上一个His激酶类受体家族(Ⅰ型和Ⅱ型)所感知,在铜离子的转运活性下,乙烯与受体的结合使Raf-类Ser/Thr激酶CTR1失活。在CTR1的下游,EIN2、EIN3、EIN5/AIN1、EIN6、EIN7是乙烯反应的正调节子,负责乙烯信号的传导。EIN2编码功能未知的新的膜整合蛋白,而EIN5/AIN1、EIN6和EIN7尚未从分子水平上进行鉴定。定位在核内的DNA结合蛋白EIN3,直接作用于ERF1,调节乙烯反应基因的转录,激活植物防御素和病程相关蛋白基因的表达,使植物建立抗病性反应。     

Biochemical and Physiological Response to Salicylic Acid in Relation to the Systemic Acquired Resistance

In five genotypes of cowpea (Vigna unguiculata), the influence of salicylic acid (SA) on photosynthetic activity and biochemical constituents including peroxidase activity at the genotypic level was determined. After SA treatment the total free sugar content increased in IFC 8401 and IGFRI 450 genotypes, whereas the content of total leaf soluble proteins decreased significantly in IFC 902. The high chlorophyll (Chl) (a + b) content in IFC 902 showed a good correlation with the net photosynthetic rate (PN), as in this genotype a significant increase in PN was found after the SA treatment.     

转录因子WRKY和NPR1在系统获得抗性信号转导中的相互作用机制

WRKY和NPR1是系统获得抗性（SAR）信号转导途径中的2类重要转录因子。简要讨论了WRKY和NPR1在水杨酸（SA）诱导的SAR信号转导途径中的相互作用,以及进一步认识这种相互作用机制对提高植物自身抗性的广泛应用前景。     

Studies of Signal Transduction of Salicylic Acid in Cucumber Cells

For the first time, the signal transduction pathway of salicylic acid (SA) was investigated by using 3H-labelling, thin-layer chromatography and anion exchange column chromatography. It was found that SA stimulated the activity of membrane bound phospholipase C (PLC), accelerated the bm&down of phosphatidylinositol-4-monophosphate (PIP) and phosphatidylinositol-4,5-bisphos- phate (PIP2) and increased the levels of inositol-1,4-bisphosphate (IP2), inositol-1, 4,5-trisphos- phate (IP3) and diacylglycerol (DAG). These indicated that signal transduction of SA was probably accomplished through the mediation of phosphatidylinositide signal transduction system in cucumber ( Cucumis sativa L. ).     

Sterol Biosynthesis Is Required for Heat Resistance but Not Extracellular Survival in Leishmania

Sterol biosynthesis is a crucial pathway in eukaryotes leading to the production of cholesterol in animals and various C24-alkyl sterols (ergostane-based sterols) in fungi, plants, and trypanosomatid protozoa. Sterols are important membrane components and precursors for the synthesis of powerful bioactive molecules, including steroid hormones in mammals. Their functions in pathogenic protozoa are not well characterized, which limits the development of sterol synthesis inhibitors as drugs. Here we investigated the role of sterol C14α-demethylase (C14DM) in Leishmania parasites. C14DM is a cytochrome P450 enzyme and the primary target of azole drugs. In Leishmania, genetic or chemical inactivation of C14DM led to a complete loss of ergostane-based sterols and accumulation of 14-methylated sterols. Despite the drastic change in lipid composition, C14DM-null mutants (c14dm ⁻) were surprisingly viable and replicative in culture. They did exhibit remarkable defects including increased membrane fluidity, failure to maintain detergent resistant membrane fraction, and hypersensitivity to heat stress. These c14dm ⁻ mutants showed severely reduced virulence in mice but were highly resistant to itraconazole and amphotericin B, two drugs targeting sterol synthesis. Our findings suggest that the accumulation of toxic sterol intermediates in c14dm ⁻ causes strong membrane perturbation and significant vulnerability to stress. The new knowledge may help improve the efficacy of current drugs against pathogenic protozoa by exploiting the fitness loss associated with drug resistance.     

在伤信号传导中茉莉酸与水杨酸的关系

近年来,发现茉莉酸和水杨酸都是植物体对外界伤害作出反应,表达抗性基因的信号分子。水杨酸可抑制茉莉酸类的合成及其所诱导的蛋白基因的表达;茉莉酸能阻止病原侵染后所产生的水杨酸的增加。茉莉酸信号转导途径和水杨酸信号转导途径存在着交叉,小GTP结合蛋白和细胞分裂素可能起着信号开关的作用。     

在伤信号传导中茉莉酸与水杨酸的关系

近年来,发现茉莉酸和水杨酸都是植物体对外界伤害作出反应,表达抗性基因的信号分子。水杨酸可抑制茉莉酸类的合成及其所诱导的蛋白基因的表达;茉莉酸能阻止病原侵染后所产缮乃钏岬脑黾印＼岳蛩嵝藕抛纪揪逗退钏嵝藕抛纪揪洞嬖谧沤徊妫。牵裕薪岷蛋白和细胞分裂素可能起着信号开关的作用。     

A Fatty Acid Messenger Is Responsible for Inducing Dispersion in Microbial Biofilms

It is well established that in nature, bacteria are found primarily as residents of surface-associated communities called biofilms. These structures form in a sequential process initiated by attachment of cells to a surface, followed by the formation of matrix-enmeshed microcolonies, and culminating in dispersion of the bacteria from the mature biofilm. In the present study, we have demonstrated that, during growth, Pseudomonas aeruginosa produces an organic compound we have identified as cis-2-decenoic acid, which is capable of inducing the dispersion of established biofilms and of inhibiting biofilm development. When added exogenously to P. aeruginosa PAO1 biofilms at a native concentration of 2.5 nM, cis-2-decenoic acid was shown to induce the dispersion of biofilm microcolonies. This molecule was also shown to induce dispersion of biofilms, formed by Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Streptococcus pyogenes, Bacillus subtilis, Staphylococcus aureus, and the yeast Candida albicans. Active at nanomolar concentrations, cis-2-decenoic acid appears to be functionally and structurally related to the class of short-chain fatty acid signaling molecules such as diffusible signal factor, which act as cell-to-cell communication molecules in bacteria and fungi.Biofilms are comprised of microorganisms enmeshed in a hydrated polymer matrix attached to a solid surface. Biofilm growth is a leading cause of materials damage, product quality degradation, and risk to public health. Bacterial biofilms are an important cause of chronic inflammatory and infectious diseases in plants and animals. In humans, biofilms have been implicated in chronic otitis media, native valve endocarditis, gastrointestinal ulcers, urinary tract and middle ear infections, and chronic lung infections in patients with cystic fibrosis (8, 11, 13, 15, 16, 29). Unfortunately, the control of biofilm growth and persistence has been problematic due to the enhanced resistance of biofilms to treatment with microbicides and antibiotics when compared to planktonic cells (30).Biofilm formation has been most intensively studied in the bacterium Pseudomonas aeruginosa, which has been shown to progress through multiple developmental stages, beginning with reversible attachment to a surface, followed by irreversible attachment and the development of microcolonies, which continue to grow to the final stage of development when dispersion occurs, releasing cells into the bulk liquid (27, 32). Bacteria have been shown to display unique phenotypes at each stage of biofilm development and possess properties that are markedly different from planktonic cells of the same species (27, 28, 32, 33, 36, 38). As a behavioral characteristic of bacteria, biofilm dispersion is of major significance because of its promise to provide a mechanism for the control of the growth and persistence of biofilms, particularly in household, medical, and industrial settings.The search for an extracellular signal responsible for biofilm dispersion has uncovered a range of factors that have been shown to stimulate biofilm disruption. In 2000, Chen and Stewart (6) reported that reactive chemicals (e.g., NaCl, CaCl₂, hypochlorite, monochloramine, and concentrated urea), chelating agents, surfactants (e.g., sodium dodecyl sulfate, Tween 20, and Triton X-100), and lysozyme, as well as a number of antimicrobial agents, when added to mixed biofilms of P. aeruginosa and Klebsiella pneumoniae, resulted in the removal of more than 25% of protein from the surface, indicating cell release from the biofilms. Sauer et al. (27) have shown that a sudden increase in the concentration of organic carbon causes bacteria to disaggregate from a biofilm. Thormann et al. (33) reported that a rapid reduction in oxygen could induce biofilm dispersion after cessation of flow in an oxygen-limited growth medium. Other studies have shown that starvation may be a trigger for dispersion (14), that a prophage in P. aeruginosa may mediate cell death and provide a vehicle for cell cluster disaggregation (37), and that nitric oxide may play a role in the biofilm dispersion process (3). Finally, the chelator EDTA has been shown to induce killing and dispersion in P. aeruginosa biofilms (1). Although the mechanism of dispersion induction is unknown in these cases, a common thread throughout these studies is that they induce major perturbations of cellular metabolism and likely also activate stress regulons, which may be involved in biofilm dispersion.The identification of a cell-to-cell communication molecule responsible for biofilm dispersion has been the focus of a number of researchers over the past decade. Recently, indole has been shown to act as an intercellular messenger, inhibiting biofilm formation in Escherichia coli but enhancing biofilm formation in P. aeruginosa (19, 20). To date, however, indole has not been shown to activate a dispersion response in existing biofilms. Rice et al. (23) described a limited role for N-butanoyl-l-homoserine lactone in modulating detachment, or sloughing, of Serratia marcescens; however, the role of quorum-sensing molecules in biofilm dispersion remains controversial. Dow et al. (10) have characterized a substituted fatty acid messenger, cis-11-methyl-2-dodecenoic acid, called diffusible signal factor (DSF), recovered from Xanthomonas campestris and shown it to be responsible for virulence, as well as induction of the release of endo-β-1,4-mannanase. Intriguingly, DSF was shown to be able to disaggregate cell flocs formed in broth culture by X. campestris, although no activity against extracellular xanthan was detected (10).In the present study we demonstrate that an unsaturated fatty acid, cis-2-decenoic acid, produced by P. aeruginosa both in batch and biofilm cultures is responsible for inducing a dispersion response in biofilms formed by a range of gram-negative bacteria, including P. aeruginosa, and by gram-positive bacteria. Furthermore, cis-2-decenoic acid was also capable of inducing dispersion in biofilms of Candida albicans, indicating that this molecule has cross-kingdom functional activity.     

Signal Molecules Inducing Systemic Resistance and Susceptibility in Barley Seedlings

Exudate collected from the cut end of barley seedlings exhibited both activities that induced systemic resistance and susceptibility against Erysiphe graminis f. sp. hordei race Hh4 depending on the time after pruning. Exudates collected between 3–6 h after pruning showed maximum activity that induced systemic resistance, whereas those during 9–12 h conversely induced susceptibility in barley seedlings. The accumulation of antifungal substances in barley leaves correlates to the timing, of induced resistance. The antifuntingal substances were watersoluble and severely affected the infection of E. graminis f. sp. hordei.     

STAT3 but Not STAT1 Is Required for Astrocyte Differentiation

The JAK-STAT signaling pathway has been implicated in astrocyte differentiation. Both STAT1 and STAT3 are expressed in the central nervous system and are thought to be important for glial differentiation, as mainly demonstrated in vitro; however direct in vivo evidence is missing. We investigated whether STAT1 and STAT3 are essential for astrocyte development by testing the STAT responsiveness of astrocyte progenitors. STAT3 was absent in the ventricular zone where glial progenitors are born but begins to appear at the marginal zone at E16.5. At E18.5, both phospho-STAT1 and phospho-STAT3 were present in glial fibrillary acidic protein (GFAP)-expressing white matter astrocytes. Overexpression of STAT3 by electroporation of chicks in ovo induced increased numbers of astrocyte progenitors in the spinal cord. Likewise, elimination of STAT3 in Stat3 conditional knockout (cKO) mice resulted in depletion of white matter astrocytes. Interestingly, elimination of STAT1 in Stat1 null mice did not inhibit astrocyte differentiation and deletion of Stat1 failed to aggravate the glial defects in Stat3 cKO mice. Measuring the activity of STAT binding elements and the gfap promoter in the presence of various STAT mutants revealed that transactivation depended on the activity of STAT3 not STAT1. No synergistic interaction between STAT1 and STAT3 was observed. Cortical progenitors of Stat1 null; Stat3 cKO mice generated astrocytes when STAT3 or the splice variant Stat3β was supplied, but not when STAT1 was introduced. Together, our results suggest that STAT3 is necessary and sufficient for astrocyte differentiation whereas STAT1 is dispensable.     

Actin Polymerization Is Required for Negative Feedback Regulation of Epidermal Growth Factor-Induced Signal Transduction

Epidermal growth factor (EGF) induces rapid actin filament assembly in the membrane skeleton of a variety of cells. To investigate the significance of this process for signal transduction, actin polymerization is inhibited by dihydrocytochalasin B (CB). CB almost completely abolishes EGF-induced actin polymerization, as assessed by quantitative confocal laser scanning microscopy. Under these conditions, EGF induces enhanced EGF receptor (EGFR) tyrosine kinase activity, as well as superinduction of the c-fosproto-oncogene. These data suggest that EGF-induced actin polymerization may be important for negative feedback regulation of signal transduction by the EGFR. The phosphorylation of Thr⁶⁵⁴by protein kinase C (PKC) is a well-characterized negative feedback control mechanism for signal transduction by the EGFR tyrosine kinase. A synthetic peptide, corresponding to the regions flanking Thr⁶⁵⁴of the EGFR, is used to analyze EGF stimulated PKC activity by incorporation of³²P into the peptide. Cotreatment of cells with CB and EGF results in a complete loss of EGF-induced phosphorylation of the peptide. These data suggest that actin polymerization is obligatory for negative feedback regulation of the EGFR tyrosine kinase through the C-kinase pathway.     

MicroRNA-223 Regulates Granulopoiesis but Is Not Required for HSC Maintenance in Mice

MIR233 is genetically or epigenetically silenced in a subset of acute myeloid leukemia (AML). MIR223 is normally expressed throughout myeloid differentiation and highly expressed in hematopoietic stem cells (HSCs). However, the contribution of MIR223 loss to leukemic transformation and HSC function is largely unknown. Herein, we characterize HSC function and myeloid differentiation in Mir223 deficient mice. We show that Mir223 loss results in a modest expansion of myeloid progenitors, but is not sufficient to induce a myeloproliferative disorder. Loss of Mir223 had no discernible effect on HSC quiescence, long-term repopulating activity, or self-renewal capacity. These results suggest that MIR223 loss is likely not an initiating event in AML but may cooperate with other AML associated oncogenes to induce leukemogenesis.