植物类病变坏死突变体及其基因的研究进展

在植物中类病变坏死突变现象广泛存在,突变体植株在无病害侵染也未受逆境或损伤的条件下自发形成与病原物侵染后坏死类似的症状,它们与植物抗病及细胞程序化死亡相关,并可能增强系统抗病性。综述了几种植物的典型类病变坏死突变体及其基因的研究情况,探讨了其发生的机制并对今后的应用前景进行了展望。     

植物细胞程序性死亡研究进展

植物细胞死亡分为坏死和程序性死亡。细胞程序性死亡是具有信号或一系列分子参与,并且由细胞内在的死亡程序介导的有序过程。它在植物生长发育和抵御外界胁迫中具有重要作用。简要介绍了植物PCD的特征,对植物PCD中的信号分子和类caspase的作用等进行了综述,并对植物PCD存在的问题进行分析和展望,为深入研究植物PCD提供参考。     

水稻类病斑突变体研究进展

植物类病变突变体是一类在没有病原物侵染情况下就能自发产生坏死斑的突变体。这类突变往往导致植株的抗病增强和防御相关基因的组成性表达。水稻中已报道了将近200个来源不同的类病变突变体,截至2014年12月73个水稻类病变突变体已被鉴定和命名,其中11个控制类病变性状的基因被克隆,它们分别编码不同的蛋白,包括热激蛋白转录因子、E3泛素连接酶、质膜蛋白激酶、锌指蛋白、酰基转移酶。尽管这些蛋白不是直接与植物抗病途径相关,但是在已鉴定的水稻类病变突变体中,绝大多数提高了对白叶枯病或稻瘟病的抗性,表明这些类病变基因的突变激活了植株的防御系统,并且不同的类病变基因可能参与了不同的抗病信号传导途径。深入研究水稻类病变突变体对作物抗病的分子机理研究和栽培品种的遗传改良都具有重要的意义。     

植物细胞程序性死亡分子机制和信号转导

细胞程序化死亡(PCD)在植物的发育、抗病及植物与环境互作等过程中发挥着极其重要的作用.总结了植物细胞凋亡发生的特征及其检测技术,概括了植细胞凋亡的分子机制,综述了植物细胞凋亡相关激素种类及其信号转导机制,并对植物细胞凋亡存在的问题进行分析和展望.     

拟南芥MMD1基因编码一个花药减数分裂所需的PHD指纹蛋白

虽然在植物中已鉴定了一些影响减数分裂的突变体 ,但分子水平上的调节机理还知之甚少 ,而且也尚未鉴定出减数分裂特异的转录调节子。马红实验室在此文中报告 ,从拟南芥中分离和鉴定了一种新的雄性不育突变体 ,它不能完成减数分裂 ;其小孢子母细胞在终变期之前还是正常的 ,但从终变期开始就表现出程序性死亡的特征———染色体行为异常、细胞质收缩、染色质片段化 ,在胞质分裂之前细胞即已死亡。因此 ,该突变体被命名为mmd1 (malemeiocytedeath 1 )。遗传和DNA凝胶印迹分析指出mmd1突变体有 1个Ds插入子 ,且与败育表型连锁。利用离散 (diss…     

神经细胞死亡的细胞和分子机制（续）

神经细胞死亡的细胞和分子机制（续）朱国璋，张永莲，龚岳亭（中国科学院上海生物化学研究所，上海２０００３１）３．神经细胞死亡和细胞增殖、细胞周期的关系处于死亡的神经元表现着一系列事件的定向顺序性。在死亡的较后阶段，死亡细胞常出现同增殖细胞相似的形态，特...     

植物细胞程序化死亡研究进展

细胞程序化死亡（PCD）是一种由基因控制的、主动的细胞死亡过程,它在植物正常生长发育过程中起着重要作用。本文就植物PCD的近期研究进展和其分子信号调控机制作一综合阐述。     

植物在逆境胁迫中的细胞程序性死亡

细胞程序性死亡(programmed cell death,PCD)是一种由基因控制的、主动的细胞死亡过程,它对植物正常生长发育起重要作用.在逆境胁迫因子如病原体、高盐、低氧、低温、热激和金属离子等作用下,植物为了抵御不良环境的侵害,以活性氧、Ca2+、乙烯和NO等为信号因子,诱导植物体的特定部位发生PCD,形成细胞主动死亡,从而避免逆境对其他组织进一步伤害,并使植物获得对不良环境的适应性.对植物PCD的一般特征、环境胁迫因子及诱导PCD信号分子等进行了综述,为在逆境条件下深入研究植物细胞程序性死亡提供参考.     

环境因子诱导的植物细胞程序性死亡

细胞发生程序性死亡（Programmed cell death,PCD）是多细胞生物用以消除多余的或有害的细胞的一种重要方式。对于植物个体来说,细胞发生程序性死亡（PCD）是抵抗逆境的一种十分有效的途径。因此,揭示环境因子诱导的植物PCD现象的分子本质就具有十分重要的现实意义。近十年来,有关环境因子诱导的植物PCD研究报道逐年增加。本文重点综述了环境因子与植物PCD相关的研究进展,并对植物PCD的主要生物学意义和研究展望进行了讨论。     

miRNA在心肌梗死中的作用及其机制研究进展

急性心肌梗死（AMI）是最常见的心血管事件,具有高发病率和高死亡率,严重威胁人类生命健康。微小RNA（miRNA）通过调节心肌细胞炎症、纤维化、细胞自噬及新生血管形成的表型机制发挥功能。本综述探讨了心肌梗死后miRNA上调及下调的分子机制,以及miRNA对心肌梗死早期诊断中的价值。     

Characterizing rice lesion mimic mutants and identifying a mutant with broad-spectrum resistance to rice blast and bacterial blight

Many plant mutants develop spontaneous lesions that resemble disease symptoms in the absence of pathogen attack. In several pathosystems, lesion mimic mutations have been shown to be involved in programmed cell death, which in some instances leads to enhanced disease resistance to multiple pathogens. We investigated the relationship between spontaneous cell death and disease resistance in rice with nine mutants with a range of lesion mimic phenotypes. All nine mutations are controlled by recessive genes and some of these mutants have stunted growth and other abnormal characteristics. The lesion mimics that appeared on the leaves of these mutants were caused by cell death as measured by trypan blue staining. Activation of six defense-related genes was observed in most of the mutants when the mimic lesions developed. Four mutants exhibited significant enhanced resistance to rice blast. One of the mutants, spl11, confers non-race-specific resistance not only to blast but also to bacterial blight. The level of resistance in the spl11 mutant to the two pathogens correlates with the defense-related gene expression and lesion development on the leaves. The results suggest that some lesion mimic mutations in rice may be involved in disease resistance, and cloning of these genes may provide a clue to developing broad-spectrum resistance to diverse pathogens.     

SDR7-6, a short-chain alcohol dehydrogenase/reductase family protein,regulates light-dependent cell death and defence responses in rice

Lesion mimic mutants resembling the hypersensitive response without pathogen attack are an ideal material to understand programmed cell death, the defence response, and the cross-talk between defence response and development in plants. In this study, mic, a lesion mimic mutant from cultivar Yunyin treated with ethyl methanesulphonate (EMS), was screened. By map-based cloning, a short-chain alcohol dehydrogenase/reductase with an atypical active site HxxxK was isolated and designated as SDR7-6. It functions as a homomultimer in rice and is localized at the endoplasmic reticulum. The lesion mimic phenotype of the mutant is light-dependent. The mutant displayed an increased resistance response to bacterial blight, but reduced resistance to rice blast disease. The mutant and knockout lines showed increased reactive oxygen species, jasmonic acid content, antioxidant enzyme activity, and expression of pathogenicity-related genes, while chlorophyll content was significantly reduced. The knockout lines showed significant reduction in grain size, seed setting rate, 1000-grain weight, grain weight per plant, panicle length, and plant height. SDR7-6 is a new lesion mimic gene that encodes a short-chain alcohol dehydrogenase with atypical catalytic site. Disruption of SDR7-6 led to cell death and had adverse effects on multiple agricultural characters. SDR7-6 may act at the interface of the two defence pathways of bacterial blight and rice blast disease in rice.     

Regulators of cell death in disease resistance

Cell death and disease resistance are intimately connected in plants. Plant disease resistance genes (R genes) are key components in pathogen perception and have a potential to activate cell death pathways. Analysis of R proteins suggests common molecular mechanisms for pathogen recognition and signal emission whereas the subsequent signalling unexpectedly involves a network of pathways of parallel, branching and converging action. Disease resistance signalling mutants have revealed novel types of regulatory proteins whose biochemical functions are still unknown. Accumulation of small molecules such as salicylic acid, reactive oxygen intermediates, and nitric oxide amplifies resistance responses and directs cells to initiate cell death programs. Genetic analyses of lesion mimic mutants provide a glimpse of how cell death thresholds are set via an interplay of positive and negative regulatory components.     

Vascular associated death1, a novel GRAM domain-containing protein, is a regulator of cell death and defense responses in vascular tissues

The hypersensitive response (HR) is a programmed cell death that is commonly associated with plant disease resistance. A novel lesion mimic mutant, vad1 (for vascular associated death1), that exhibits light conditional appearance of propagative HR-like lesions along the vascular system was identified. Lesion formation is associated with expression of defense genes, production of high levels of salicylic acid (SA), and increased resistance to virulent and avirulent strains of Pseudomonas syringae pv tomato. Analyses of the progeny from crosses between vad1 plants and either nahG transgenic plants, sid1, nonexpressor of PR1 (npr1), enhanced disease susceptibility1 (eds1), or non-race specific disease resistance1 (ndr1) mutants, revealed the vad1 cell death phenotype to be dependent on SA biosynthesis but NPR1 independent; in addition, both EDS1 and NDR1 are necessary for the proper timing and amplification of cell death as well as for increased resistance to Pseudomonas strains. VAD1 encodes a novel putative membrane-associated protein containing a GRAM domain, a lipid or protein binding signaling domain, and is expressed in response to pathogen infection at the vicinity of the hypersensitive lesions. VAD1 might thus represent a new potential function in cell death control associated with cells in the vicinity of vascular bundles.     

Lesion mimic mutants: keys for deciphering cell death and defense pathways in plants?

The identification of several lesion mimic mutants (LMM) that misregulate cell death constitutes a powerful tool to unravel programmed cell death (PCD) pathways in plants, particularly the hypersensitive response (HR), a form of PCD associated with resistance to pathogens. Recently, the characterization of novel LMM has enabled genes that might regulate cell death programmes to be identified as well as the dissection of defense signaling pathways and of crosstalk between multiple pathways in ways that might not be possible by studying the responses of wild-type plants to pathogens.     

Rice lesion mimic mutants with enhanced resistance to diseases

Lesion mimic mutants are characterized by the formation of necrotic lesions in the absence of pathogens. Such genetic defects often result in enhanced resistance to pathogen infection and constitutive expression of defense response genes. To understand the genetic mechanisms leading to these mutations, we characterized 21 lesion mimic mutants isolated from IR64 rice mutant populations produced by mutagenesis with diepoxybutane (D), gamma rays (G), and fast neutrons (F). Four mutations are controlled by single dominant genes, one of which is inherited maternally. Five lesion mimics are allelic to known spotted leaf (spl) mutants spl1, spl2, spl3, or spl6. In total, 11 new lesion mimic mutations, named spl16, spl17, and spl19 through Spl27, were established based on allelism tests. Two lesion mimics, spl17 and Spl26 showed enhanced resistance to multiple strains of Magnaporthe oryzae, the rice blast pathogen, and Xanthomonas oryzae pv. oryzae, the bacterial blight (BB) pathogen. Co-segregation analyses of blast and BB resistance and lesion mimic phenotypes in segregating populations of spl17 and Spl26 indicate that enhanced resistance to the two diseases is conferred by mutations in the lesion mimic genes. A double mutant produced from two independent lesion mimics showed more severe lesions and higher level of resistance to X. o. pv. oryzae than their single mutant parents indicating a synergistic effect of the two mutations. In mutants that exhibit enhanced disease resistance to both pathogens, increases in expression of defense response genes PR-10a, POX22.3, and PO-C1 were correlated with lesion mimic development and enhancement of resistance. These lesion mimic mutants may provide essential materials for a comprehensive dissection of the disease resistance pathways in rice.     

Defence signalling pathways in cereals.

The combination of mutational and molecular studies has shed light on the role of reactive oxygen intermediates and programmed cell death in cereal disease resistance mechanisms. Rice Rac1 and barley Rar1 represent conserved disease resistance signalling genes, which may have related functions in animals. The analysis of non-pathogenic Magnaporthe grisea mutants may provide novel tools to study host defence pathways.     

Disease lesion mimics of maize: A model for cell death in plants

A class of maize mutants, collectively known as disease lesion mimics, display discrete disease-like symptoms in the absence of pathogens. It is intriguing that a majority of these lesion mimics behave as dominant gain-of-function mutations. The production of lesions is strongly influenced by light, temperature, developmental state and genetic background. Presently, the biological significance of this lesion mimicry is not clear, although suggestions have been made that they may represent defects in the plants' recognition of, or response to, pathogens. One feature that is common to all lesion mimics is their association with cell death. In plants, as in animals, a number of developmental and pathological processes exist where controlled cell death, whether programmed or triggered in response to physiological or environmental stimuli, constitutes the normal aspect of life. Might disease lesion mimic mutations represent variants where regulation of desirable cell death has gone awry? In this paper we argue that this might be the case, and further conjecture that these mutants offer a unique opportunity for studying the genetic and cellular mechanisms of cell death in plants.     

Autophagy and plant innate immunity

Plant innate immunity is often associated with specialized programmed cell death at or near the site of pathogen infection. Despite the isolation of several lesion mimic mutants, the molecular mechanisms that regulate cell death during an immune response remain obscure. Recently, autophagy, an evolutionarily conserved process of bulk protein and organelle turnover, was shown to play an important role in limiting cell death initiated during plant innate immune responses. Consistent with its role in plants, several studies in animals also demonstrate that the autophagic machinery is involved in innate as well as adaptive immunities. Here, we review the role of autophagy in plant innate immunity. Because autophagy is observed in healthy and dying plant cells, we will also examine whether autophagy plays a protective or a destructive role during an immune response.