线粒体稳定高钙信号诱发超氧炫

线粒体对于细胞钙信号和活性氧信号转导有重要的调控作用．超氧炫是新近发现的单个线粒体超氧阴离子短时程爆发现象,反映了活性氧生成动力学的一种新形式．线粒体钙信号作为重要的细胞功能调控信号,能否及如何调控超氧炫尚待深入研究．本研究对HeLa细胞进行高胞外钙和离子霉素刺激,或用皂苷穿孔细胞质膜后置于高钙细胞内液中,两种方法均显著增加了超氧炫发生的频率．其中,穿孔细胞胞浆高钙诱导的超氧炫依赖于线粒体钙单向转运体,表明超氧炫由线粒体基质内高钙信号所诱发．重要的是,离子霉素诱导的超氧炫发生频率与线粒体稳态钙水平线性相关,而与瞬态线粒体钙无相关性,提示钙离子对超氧炫的调控是一个多步骤、相对缓慢的过程．综上,线粒体基质的稳态高钙是超氧炫的重要调控因子．     

植物叶绿体发育及调控研究进展

植物的光合作用几乎是所有生物生存和发展的物质基础。叶绿体是绿色植物进行光合作用的重要细胞器。尽管叶绿体发育及调控一直受到人们的关注,但其装备及调控的分子机制尚不完全清楚。该文对叶绿体装备过程、叶绿体发育调控及质体-细胞核反向信号的研究进展进行概述,以使人们从整体上认识叶绿体发育及调控机制。     

Mitogen-Activated Protein Kinase 4 Is a Salicylic Acid-Independent Regulator of Growth But Not of Photosynthesis in Arabidopsis

Mitogen-activated protein kinase （MAPK） pathways regulate signal transduction from different cellular com- partments and from the extracellular environment to the nucleus in all eukaryotes. One of the best-characterized MAPKs in Arabidopsis thaliana is MPK4, which was shown to be a negative regulator of systemic-acquired resistance. The mpk4 mutant accumulates salicylic acid （SA）, possesses constitutive expression of pathogenesis-related （PR） genes, and has an extremely dwarf phenotype. We show that suppression of SA and phylloquinone synthesis in chloroplasts by knocking down the IC51 gene （by crossing it with the icsl mutant） in the mpk4 mutant background did not revert mpk4-impaired growth. However, it did cause changes in the photosynthetic apparatus and severely impaired the quantum yield of pho- tosystem Ih Transmission microscopy analysis revealed that the chloroplasts＇ structure was strongly altered in the mpk4 and mpk4/icsl double mutant. Analysis of reactive oxygen species （ROS）-scavenging enzymes expression showed that suppression of SA and phylloquinone synthesis in the chloroplasts of the mpk4 mutant caused imbalances in ROS homeo- stasis which were more pronounced in mpk4/icsl than in mpk4. Taken together, the presented results strongly suggest that MPK4 is an ROS/hormonal rheostat hub that negatively, in an SA-dependent manner, regulates immune defenses, but at the same time positively regulates photosynthesis, ROS metabolism, and growth. Therefore, we concluded that MPK4 is a complex regulator of chloroplastic retrograde signaling for photosynthesis, growth, and immune defenses in Arabidopsis.     

调控肿瘤上皮–间质转化及肿瘤干细胞样特性的信号通路串话

上皮–间质转化（epithelial-mesenchymal transition,EMT）是上皮来源肿瘤细胞获得侵袭和转移能力的重要生物学过程。肿瘤干细胞样细胞（cancer stem-like cells,CSLCs）在肿瘤发生、侵袭、转移和复发中亦起着关键作用。近年发现,EMT与肿瘤干细胞样特性获得存在密切关联,二者通过TGF-β、Wnt/β-catenin、Notch、Hedgehog、FGF、PI3k/Akt等多种信号通路及通路间的信号串话而交互作用,共同影响着肿瘤发生、侵袭及转移,了解调控EMT/CSLCs关键信号分子的功能及相互作用对于肿瘤靶向治疗具有重要意义。     

Mitochondrial protein import in plants – Signals,Sorting, Targeting,Processing and Regulation

Plant Molecular Biology - Mitochondrial biogenesis requires a coordinated expression of both the nuclear and the organellar genomes and specific intracellular protein trafficking, processing and...     

Distinct Functions of Nuclear Distribution Proteins LIS1, Ndel1 and NudCL in Regulating Axonal Mitochondrial Transport

Neurons critically depend on the long‐distance transport of mitochondria. Motor proteins kinesin and dynein control anterograde and retrograde mitochondrial transport, respectively in axons. The regulatory molecules that link them to mitochondria need to be better characterized. Nuclear distribution (Nud) family proteins LIS1, Ndel1 and NudCL are critical components of cytoplasmic dynein complex. Roles of these Nud proteins in neuronal mitochondrial transport are unknown. Here we report distinct functions of LIS1, Ndel1 and NudCL on axonal mitochondrial transport in cultured hippocampal neurons. We found that LIS1 interacted with kinsein family protein KIF5b. Depletion of LIS1 enormously suppressed mitochondrial motility in both anterograde and retrograde directions. Inhibition of either Ndel1 or NudCL only partially reduced retrograde mitochondrial motility. However, knocking down both Ndel1 and NudCL almost blocked retrograde mitochondrial transport, suggesting these proteins may work together to regulate retrograde mitochondrial transport through linking dynein‐LIS1 complex. Taken together, our results uncover novel roles of LIS1, Ndel1 and NudCL in the transport of mitochondria in axons.      

10个线粒体基因在甘蓝型油菜NCa不育系统不同组织中的转录调控及其与育性的关系

用10个线粒体基因为探针,对NCα不育系、保持系和可育F1的苗期叶片、幼蕾及未成熟种子的线粒体RNA进行了Northern分析。结果表明,这10个线粒体基因除atp6外,其余9个基因在同一材料的不同组织中没有表达差异,都属于组成型表达的线粒体基因。其中,off139、orf222、atp1、cox1、cox2、cob、rm5S、rm26S等8个线粒体基因在不育系、保持系和可育F1的苗期叶片、幼蕾及未成熟种子中有着相同的表达,属于表达不受核基因型影响,没有组织特异性的类型：atp9基因分别在同一材料的不同组织中的转录也基本没有变化,但是在3个不同的材料间具有表达差异：可能属于表达受核基因型影响、没有组织特异性的线粒体基因。atp6基因也在3个材料的叶、蕾和种子中都产生相同大小的转录本,但是在各个材料的不同组织中存在着信号强度的差异,可能是属于表达既受核基因型影响、又有组织特异性的线粒体基因。Orf222和off139分别在不育系和可育F1幼蕾中产生相同大小和丰度的转录本,但是在保持系幼蕾中没有检测到转录本;orf222检测到的3条转录本分别为1．1kb、0．9kb、0．6kb,而off139检测到0．8kb和0．6kb两条带。atp9探针在不育系和保持系幼蕾中都检测到1条0．6kb的转录本,而在可育F1幼蕾中检测到0．6kb和1．2kb的转录本。讨论了orf222、off139、atp9基因的表达与NCα细胞质雄性不育的可能关系。     

miR172-AP2模块调控植物生长发育及逆境响应的研究进展

MicroRNA (miRNA)是一类具有调控能力的非编码小分子RNA, 通过与靶基因mRNA特异或非特异性结合, 诱导靶基因mRNA降解或抑制其翻译, 从而调控植物的生长发育。其中, miR172的靶基因AP2所编码的转录因子为植物所特有, miR172在转录后或翻译水平对AP2进行表达调控, 进而调控植物的花发育、时序转换、小穗形态、块茎和果实发育、结瘤(豆科)以及逆境响应等过程。该文综述了近年来miR172-AP2模块在植物生长发育调控方面的最新研究进展。     

水稻病程相关PR1家族蛋白质在叶片生长及与白叶枯病菌互作反应中的表达

病程相关(PR)蛋白质经常被用作抗病反应的分子标记。利用免疫印迹(WB)技术检测了7个PR1家族蛋白质在水稻(Oryza sativa)叶片生长及与白叶枯病菌互作反应过程中的表达,发现6个PR1家族蛋白质在叶片生长中有表达。检测PR1蛋白质在Xa21介导的抗白叶枯病过程中的表达,结果显示PR1#052、PR1#072、PR1#073和PR1#121四个蛋白质在抗病反应后期呈上调或诱导表达,PR1#071则表达下调。进一步比较它们在抗病、感病和对照(Mock)反应中的表达丰度,发现在抗病和感病反应中的变化幅度均明显大于对照反应,推测这些PR蛋白质在水稻-白叶枯病菌互作反应中发挥作用。另外,对PR1基因上游启动子区的cis元件进行了分析。该研究初步揭示了水稻PR1家族蛋白质的表达谱,为进一步了解PR1蛋白质的功能提供了线索。     

miRNA调控药用植物生长发育和次生代谢

microRNA(miRNA)作为一类内源性的短链非编码RNA,广泛存在于真核细胞中,主要通过对转录本剪切和抑制翻译等方式,参与转录后基因的表达调控。近年来研究表明,多种药用植物中鉴定出大量的miRNA。这些miRNA对药用植物的生长发育和次生代谢产物合成具有调控功能。次生代谢产物是药用植物的主要有效成分,研究miRNA对药用植物次生代谢过程的调控作用具有十分重要的意义。本文综述了miRNA在植物中的产生途径、作用方式和体内功能,在此基础上重点介绍了miRNA对药用植物生长发育和次生代谢产物生物合成的调控作用,并对药用植物miRNA的研究进行了展望,以期为提高药用植物产量,高效获得药用植物有效成分以及临床应用开拓新的思路。     

Mitochondrial unfolded protein response gene Clpp is required to maintain ovarian follicular reserve during aging,for oocyte competence,and development of pre‐implantation embryos

Caseinolytic peptidase P mediates degradation of unfolded mitochondrial proteins and activates mitochondrial unfolded protein response (mtUPR) to maintain protein homeostasis. Clpp^?/? female mice generate a lower number of mature oocytes and two‐cell embryos, and no blastocysts. Clpp^?/? oocytes have smaller mitochondria, with lower aspect ratio (length/width), and decreased expression of genes that promote fusion. A 4‐fold increase in atretic follicles at 3 months, and reduced number of primordial follicles at 6–12 months are observed in Clpp^?/? ovaries. This is associated with upregulation of p‐S6, p‐S6K, p‐4EBP1 and p‐AKT473, p‐mTOR2481 consistent with mTORC1 and mTORC2 activation, respectively, and Clpp^?/? oocyte competence is partially rescued by mTOR inhibitor rapamycin. Our findings demonstrate that CLPP is required for oocyte and embryo development and oocyte mitochondrial function and dynamics. Absence of CLPP results in mTOR pathway activation, and accelerated depletion of ovarian follicular reserve.