温度胁迫对植物花粉发育的影响

温度是影响开花植物有性繁殖的重要环境因子之一,在雌雄配子的发育过程中,温度胁迫常导致花粉败育。该文总结了目前研究已知的温度胁迫对植物花粉发育的影响,包括花粉发育对温度胁迫的最敏感时期、温度胁迫引起的花药绒毡层、糖代谢、激素水平的变化,并对低温与高温胁迫对花粉发育的影响进行了比较讨论。文章同时还概述了花粉响应温度胁迫的分子机理研究进展,重点介绍了目前已知的6个参与花粉响应低温胁迫的基因的功能,并总结了此研究领域中存在的不足及展望了今后研究重点,以期为进一步解析花粉响应温度胁迫的机制提供参考。     

高温影响番茄小孢子发育的细胞学研究

以番茄‘Micro-Tom’为材料,利用形态观察、DAPI染色、石蜡切片等方法对正常情况下番茄小孢子发生过程进行时期划分.通过连续7d的高温胁迫((35±1)℃/(30±1)℃)处理试验,结合细胞学观察,研究高温对番茄花粉小孢子发育的影响.研究表明,高温胁迫不仅导致花粉畸形或败育、花粉数量减少、活力低萌发力差,而且还导致花药绒毡层、药隔组织、药室内壁、花药表皮、环状细胞簇等花药细胞结构的发育异常.结果有助于阐明热胁迫对番茄小孢子发育的影响,并为培育耐高温农作物新品种提供思路.     

植物感知和传递低温信号的分子机制

低温胁迫是影响植物生长、发育及作物产量的重要环境胁迫之一。植物通过感知低温信号并快速启动低温应答，以降低低温胁迫对其损伤。近年来，低温潜在感受器和低温调控网络逐渐被解析。植物可以在多个层面感知低温信号，但具体机制依然不清楚。当植物感知低温信号后，一些低温诱导的次级信号分子（如钙离子和活性氧）被植物解码并传递，以激活下游低温应答基因表达。同时，蛋白翻译后修饰可调控蛋白活性和稳定性，在植物早期低温信号传递中起关键作用。本文重点阐述植物感知和传递低温早期信号的分子机制，并讨论和展望低温胁迫领域面临的挑战及研究方向。     

农作物花粉高温胁迫研究进展

高温现已成为农作物生产不可忽视的环境因素,而花粉是农作物对高温最敏感的器官.本文从细胞学、生理学和分子生物学等方面对近年来国内外有关农作物花粉高温胁迫的研究进行了综述,以期为保持农作物在高温胁迫下的高生产力提供思路.高温对农作物花粉的细胞学影响表现在绒毡层粗糙型内质网排列方式改变、药隔维管束鞘细胞形状异常、花粉管高尔基体小泡产生减少等方面;生理学影响表现在Ca²⁺动态平衡无法及时恢复、生长调节物质含量改变以及糖代谢减慢等方面;分子生物学影响表现在热激蛋白诱导表达不足和其他花粉功能基因表达被抑制等方面.     

植物响应镉胁迫的生理生化机制研究进展

镉(Cd)是一种分布广泛且污染严重的重金属;其毒性大,不仅影响植物的生长发育,而且危害人类健康。该文对植物Cd胁迫的生理生化响应方面的最新研究进展进行了总结概括。从植物光合系统、活性氧、活性氮、抗氧化防御系统、激素、钙信号、蛋白和基因等方面,概述了植物对Cd胁迫的响应及应答机制,探讨了植物对Cd胁迫响应机制的研究方向,...     

酿酒酵母氧化胁迫应答反应机制

氧化胁迫是生物体面对逆境时的重要反应。在与逆境和活性氧做斗争的过程中,细胞进化出一套完整的应答调控机制,通过调节体内活性氧的代谢平衡,来保护DNA、脂质和蛋白质等免受氧化攻击。本文以酿酒酵母为例,根据近年来国内外研究的进展,围绕其在氧化胁迫应答过程中的三道保护屏障,即抗氧化物质和防御酶系统、转录调节和氧化物降解以及细胞器自噬,综述了其抗氧化代谢机理,为深入认识细胞的抗氧化应答机制奠定基础。     

高温逆境下植物叶片衰老机理研究进展

叶片衰老是植物叶片发育的最后阶段,其作为一个主动的生理过程,对植物体内的营养循环再利用以及种子形成具有重要的生理意义。在植物的生长过程中,多种环境因素会影响叶片衰老进程。高温是影响叶片衰老最重要的环境因素之一。随着温室效应的加剧,研究高温胁迫下叶片衰老的调节机制对于通过调控叶片衰老进程,从而增加植物产量具有重要意义。本文对高温胁迫下叶绿体及类囊体膜的损伤、光合电子传递活力的改变、活性氧累积、光合作用相关蛋白质降解及细胞自噬方面的研究进展进行了综述。     

植物有性生殖对温度胁迫反应的研究进展

开花植物的有性生殖阶段对温度胁迫高度敏感,高温热害和低温冷害都会对这一过程造成严重影响。本文全面总结了温度胁迫对作物有性生殖的影响,明确花粉发育过程是有性生殖过程中对温度胁迫最敏感的时期;转录组和蛋白质组的研究结果表明,蛋白激酶、热激转录因子、热休克蛋白等可能参与花粉发育期对热胁迫的信号转导。理解植物在有性生殖发育阶段如何适应温度胁迫的机理,为遗传育种实践中筛选对温度耐受的作物品种提供指导,也为基因工程选育对温度耐受的品种提供可能。     

非生物胁迫影响水稻颖花育性机理的研究进展

本文从颖花发育的形态学和生理学角度,综述了水稻穗分化期至抽穗开花期非生物胁迫导致颖花不育的机理,旨在揭示非生物胁迫导致水稻颖花败育的关键过程及其内在联系.颖花是否可育主要与绒毡层细胞行为、花药开裂与散粉、花粉萌发、受精4个关键过程有关,胁迫通过影响这些关键过程,导致颖花不育.花药发育早期异常变化影响生殖细胞发育与授粉作用.可以通过喷施外源物质或增施硅肥等方法减缓非生物胁迫对颖花育性的伤害.今后需要加强交叉胁迫对颖花育性的影响、不同胁迫对花器官形态结构和生理特性的影响、不同水稻品种对胁迫的响应差异,以及胁迫影响花器官发育的分子生物学机制等方面的研究.     

高等植物小孢子胚发生的启动

高等植物小孢子在受到胁迫时能改变正常的花粉发育途径而启动胚发生途径.小孢子胚发生的启动主要包括胚发生的诱导、对胁迫的细胞应答和抑制花粉发育程序.目前,国内外对于小孢子胚发生研究大多限于形态学观察,对小孢子由正常花粉发育途径转向胚发生途径过程中所涉及的相关分子机制缺乏系统报道,而上述研究是精确、高效诱导小孢子胚发生的关键.结合目前最新研究,对小孢子胚发生的早期事件,尤其是小孢子启动胚发生的生理生化和分子机制作一简要论述.以期为相关研究提供参考.     

Protective mechanisms of heat tolerance in crop plants

High temperature (HT) has become a global concern because it severely affects the growth and production of crops. Heat stress causes an abrupt increase in the expression of stress-associated proteins which provide tolerance by stimulating the defense response in plants. Heat-shock proteins (Hsps) and antioxidant enzymes are important in encountering heat stress in plants. The heat-shock response is characterized by repression of normal cellular protein synthesis and induction of Hsp synthesis. Under HT stress, upregulation of various enzymatic and nonenzymatic antioxidants, maintenance of cell membrane stability, production of various compatible solutes and hormonal changes occurs. Reactive oxygen species involving several pathways such as water–water cycle, Halliwell–Asada, glutathione peroxidase, Haber–Weiss and Fenton reactions helps in protecting plants against toxic radicals which otherwise could cause damage to lipophilic protein. Genetic approaches to elucidate and map genes or quantitative trait loci conferring thermotolerance will facilitate marker-assisted breeding for heat tolerance and also pave the way for characterizing genetic factors which could be useful for engineering plants with improved heat tolerance. This review discusses the protective mechanism of heat stress responses encompassing different pathways that provide tolerance during HT stress.     

Enhancement of Reproductive Heat Tolerance in Plants

Comparison of average crop yields with reported record yields has shown that major crops exhibit annual average yields three- to seven-fold lower than record yields because of unfavorable environments. The current study investigated the enhancement of pollen heat tolerance through expressing an Arabidopsis thaliana heat shock protein 101 (AtHSP101) that is not normally expressed in pollen but reported to play a crucial role in vegetative thermotolerance. The AtHSP101 construct under the control of the constitutive ocs/mas ‘superpromoter’ was transformed into cotton Coker 312 and tobacco SRI lines via Agrobacterium mediated transformation. Thermotolerance of pollen was evaluated by in vitro pollen germination studies. Comparing with those of wild type and transgenic null lines, pollen from AtHSP101 transgenic tobacco and cotton lines exhibited significantly higher germination rate and much greater pollen tube elongation under elevated temperatures or after a heat exposure. In addition, significant increases in boll set and seed numbers were also observed in transgenic cotton lines exposed to elevated day and night temperatures in both greenhouse and field studies. The results of this study suggest that enhancing heat tolerance of reproductive tissues in plant holds promise in the development of crops with improved yield production and yield sustainability in unfavorable environments.     

Heat stress phenotypes of Arabidopsis mutants implicate multiple signaling pathways in the acquisition of thermotolerance

To investigate the importance of different processes to heat stress tolerance, 45 Arabidopsis (Arabidopsis thaliana) mutants and one transgenic line were tested for basal and acquired thermotolerance at different stages of growth. Plants tested were defective in signaling pathways (abscisic acid, salicylic acid, ethylene, and oxidative burst signaling) and in reactive oxygen metabolism (ascorbic acid or glutathione production, catalase) or had previously been found to have temperature-related phenotypes (e.g. fatty acid desaturase mutants, uvh6). Mutants were assessed for thermotolerance defects in seed germination, hypocotyl elongation, root growth, and seedling survival. To assess oxidative damage and alterations in the heat shock response, thiobarbituric acid reactive substances, heat shock protein 101, and small heat shock protein levels were determined. Fifteen mutants showed significant phenotypes. Abscisic acid (ABA) signaling mutants (abi1 and abi2) and the UV-sensitive mutant, uvh6, showed the strongest defects in acquired thermotolerance of root growth and seedling survival. Mutations in nicotinamide adenine dinucleotide phosphate oxidase homolog genes (atrbohB and D), ABA biosynthesis mutants (aba1, aba2, and aba3), and NahG transgenic lines (salicylic acid deficient) showed weaker defects. Ethylene signaling mutants (ein2 and etr1) and reactive oxygen metabolism mutants (vtc1, vtc2, npq1, and cad2) were more defective in basal than acquired thermotolerance, especially under high light. All mutants accumulated wild-type levels of heat shock protein 101 and small heat shock proteins. These data indicate that, separate from heat shock protein induction, ABA, active oxygen species, and salicylic acid pathways are involved in acquired thermotolerance and that UVH6 plays a significant role in temperature responses in addition to its role in UV stress.     

The protein kinase CPK28 phosphorylates ascorbate peroxidase and enhances thermotolerance in tomato

High temperatures are a major threat to plant growth and development, leading to yield losses in crops. Calcium-dependent protein kinases (CPKs) act as critical components of Ca²⁺ sensing in plants that transduce rapid stress-induced responses to multiple environmental stimuli. However, the role of CPKs in plant thermotolerance and their mechanisms of action remain poorly understood. To address this issue, tomato (Solanum lycopersicum) cpk28 mutants were generated using a CRISPR-Cas9 gene-editing approach. The responses of mutant and wild-type plants to normal (25°C) and high temperatures (45°C) were documented. Thermotolerance was significantly decreased in the cpk28 mutants, which showed increased heat stress-induced accumulation of reactive oxygen species (ROS) and levels of protein oxidation, together with decreased activities of ascorbate peroxidase (APX) and other antioxidant enzymes. The redox status of ascorbate and glutathione were also modified. Using a yeast two-hybrid library screen and protein interaction assays, we provide evidence that CPK28 directly interacts with cytosolic APX2. Mutations in APX2 rendered plants more sensitive to high temperatures, whereas the addition of exogenous reduced ascorbate (AsA) rescued the thermotolerance phenotype of the cpk28 mutants. Moreover, protein phosphorylation analysis demonstrated that CPK28 phosphorylates the APX2 protein at Thr-59 and Thr-164. This process is suggested to be responsive to Ca²⁺ stimuli and may be required for CPK28-mediated thermotolerance. Taken together, these results demonstrate that CPK28 targets APX2, thus improving thermotolerance. This study suggests that CPK28 is an attractive target for the development of improved crop cultivars that are better adapted to heat stress in a changing climate.

The protein kinase CPK28 regulates thermotolerance in plants by targeting APX2, thus regulating cellular redox homeostasis.     

The calcium‐dependent protein kinase ZmCDPK7 functions in heat‐stress tolerance in maize

Global warming poses a serious threat to crops. Calcium‐dependent protein kinases (CDPKs)/CPKs play vital roles in plant stress responses, but their exact roles in plant thermotolerance remains elusive. Here, we explored the roles of heat‐induced ZmCDPK7 in thermotolerance in maize. ZmCDPK7‐overexpressing maize plants displayed higher thermotolerance, photosynthetic rates, and antioxidant enzyme activity but lower H₂O₂ and malondialdehyde (MDA) contents than wild‐type plants under heat stress. ZmCDPK7‐knockdown plants displayed the opposite patterns. ZmCDPK7 is attached to the plasma membrane but can translocate to the cytosol under heat stress. ZmCDPK7 interacts with the small heat shock protein sHSP17.4, phosphorylates sHSP17.4 at Ser‐44 and the respiratory burst oxidase homolog RBOHB at Ser‐99, and upregulates their expression. Site‐directed mutagenesis of sHSP17.4 to generate a Ser‐44‐Ala substitution reduced ZmCDPK7's enhancement of catalase activity but enhanced ZmCDPK7's suppression of MDA accumulation in heat‐stressed maize protoplasts. sHSP17.4, ZmCDPK7, and RBOHB were less strongly upregulated in response to heat stress in the abscisic acid‐deficient mutant vp5 versus the wild type. Pretreatment with an RBOH inhibitor suppressed sHSP17.4 and ZmCDPK7 expression. Therefore, abscisic acid‐induced ZmCDPK7 functions both upstream and downstream of RBOH and participates in thermotolerance in maize by mediating the phosphorylation of sHSP17.4, which might be essential for its chaperone function.     

A mutation in Thermosensitive Male Sterile 1, encoding a heat shock protein with DnaJ and PDI domains, leads to thermosensitive gametophytic male sterility in Arabidopsis

In most flowering plant species, pollination and fertilization occur during the hot summer, so plants must have evolved a mechanism that ensures normal growth of their pollen tubes at high temperatures. Despite its importance to plant reproduction, little is known about the molecular basis of thermotolerance in pollen tubes. Here we report the identification and characterization of a novel Arabidopsis gene, THERMOSENSITIVE MALE STERILE 1 ( TMS1 ), which plays an important role in thermotolerance of pollen tubes. TMS1 encodes a Hsp40-homologous protein with a DnaJ domain and an a_ERdj5_C domain found in protein disulfide isomerases (PDI). Purified TMS1 expressed in Escherichia coli (BL21 DE3) had the reductive activity of PDI. TMS1 was expressed in pollen grains, pollen tubes and other vegetative tissues, including leaves, stems and roots. Heat shock treatment at 37°C increased its expression levels in growing pollen tubes as well as in vegetative tissues. A knockout mutation in TMS1 grown at 30°C had greatly retarded pollen tube growth in the transmitting tract, resulting in a significant reduction in male fertility. Our study suggests that TMS1 is required for thermotolerance of pollen tubes in Arabidopsis, possibly by functioning as a co-molecular chaperone.