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1.
Zenghui Hu Yingbai Shen Fanyi Shen Youqing Luo Xiaohua Su 《Trees - Structure and Function》2009,23(5):1003-1011
Interplant communication has been widely demonstrated in plants, especially in herbaceous plants. In this study, mechanical
damage was shown to affect the levels of pyrochatechol, chlorogenic acid, gallic acid and p-hydroxyl benzoic acid in poplar (Populus simonii × P. pyramidalis ‘Opera 8277’) cuttings, indicating the activation of defense response. In neighboring intact cuttings, the levels of those
phenolics also varied when compared to the control, suggesting the interplant communication between poplar cuttings. Three
volatiles, methyl jasmonate, methyl salicylate and benzothiazole, were detected in volatiles emitted from mechanically damaged
poplar cuttings. All of them can induce changes in the levels of four phenolics. Therefore, they could act as airborne signals
between P. simonii × P. pyramidalis ‘Opera 8277’ cuttings. The different change patterns of phenolic contents induced by different volatiles imply that the defense
response activated in neighboring plants may be regulated by multiple signaling pathways. The results also suggest that the
entire defense response of plants involves a variety of airborne signals in wound-induced volatiles. 相似文献
2.
不同年龄大鼠主动脉壁凝集素组织化学的图像分析研究 总被引:1,自引:0,他引:1
本文利用凝集素组织化学的方法,结合应用IBAS图像分析系统对不同年龄(10天,6个月及2年)大鼠主动脉壁的凝集素受体进行研究。在所采用的六种生物素化凝集素中(ConA、RCAI、UEA-I、PNA、SBA及WGA),ConA、RCA-I及WGA在大鼠主动脉壁呈阳性反应,它们在各年龄组大鼠主动脉壁内膜及外膜均表现出强阳性反应,而在中膜反应较弱。UEA-I、PNA和SBA表现出无明显反应。此外,三种阳性反应凝集素在主动脉壁的反应产物随增龄而减少,图像分析结果显示其灰度值随增龄的变化趋势是逐渐增加。上述结果提示,大鼠主动脉壁含α-D-Mannose、β-DGalactose、sialicacid或N-acetyl-D-Glucosamine残基的糖复合物含量随增龄而减少,可能使LDL易于通透而致脂质在动脉壁沉积,加速脂纹病变的形成,从而易于导致动脉粥样硬化。 相似文献
3.
4.
Xiaohua Li Susanne M. Mumby Angela Greenwood Richard S. Jope 《Journal of neurochemistry》1995,64(3):1107-1117
Abstract: Monoclonal antibodies were produced that are specific for the three major pertussis toxin-sensitive G protein α-subunits present in mammalian brain—αo, αi1, and αi2—using purified bovine brain G proteins, purified rat brain G proteins, and purified recombinant αi2, respectively. These monoclonal antibodies were used to monitor changes in the concentrations of the three G protein α-subunits during differentiation of PC12 cells and human neuroblastoma LA-N-5 cells. In PC12 cells, levels of αi1 but not αi2 increased during nerve growth factor-induced differentiation. In contrast, αi2 but not αi1 increased when LA-N-5 cells were differentiated with retinoic acid. The concentration of αo increased in both cell lines during differentiation. Electrophoretic resolution of αo subtypes revealed that although αo2 was the major subtype in undifferentiated cells, only the concentration of αo1 increased during differentiation of both PC12 and LA-N-5 cells. The level of 43-kDa growth-associated protein, a protein known to associate with αo, increased similarly to that of αo1. ADP-ribosylation of αo, αi1, and αi2 with pertussis toxin did not alter the reactivities of the monoclonal antibodies, but toxin treatment of cells reduced the concentrations of each protein after 24 h. There was no change in the concentration of αq, which is not ADP-ribosylated by pertussis toxin. Thus, these new monoclonal antibodies enabled the detection of differential increases in subtypes of αi and αo associated with neuronal differentiation. 相似文献
5.
罗汉果双受精过程的细胞学观察 总被引:3,自引:1,他引:2
罗汉果(Siraitiagrosvenori(Swingle)C.Jemey)双受精过程属有丝分裂前配子融合类型,授粉后24~48h,花粉管进入胚囊,穿过一个助细胞,放出两个精子。雌雄核融合和雄核与次生核融合同时发生在授粉后62~72,雄核与次生核融合速度快于配子融合,72h后即可见到初生胚乳核分裂。合子中的雌雄核仁在授粉后第5~6d融合,授粉后8~9d合成分裂形成二细胞胚。在双受精过程中,多次观察到有多条花粉管进入胚囊和多精入极核现象。原胚期有附加花粉管从珠孔进入。 相似文献
6.
A subsystem impactor test for pedestrian lower limb injury evaluation has been brought in China New Car Assessment Protocol(CNCAP).Concerning large anthropometr... 相似文献
7.
8.
Qiang Lv Shuang Han Lei Wang Jinchan Xia Peng Li Ruoyang Hu Jinzheng Wang Lei Gao Yuli Chen Yu Wang Jing Du Fang Bao Yong Hu Xingzhi Xu Wei Xiao Yikun He 《Nucleic acids research》2022,50(12):6820
Nitric oxide (NO) is a key player in numerous physiological processes. Excessive NO induces DNA damage, but how plants respond to this damage remains unclear. We screened and identified an Arabidopsis NO hypersensitive mutant and found it to be allelic to TEBICHI/POLQ, encoding DNA polymerase θ. The teb mutant plants were preferentially sensitive to NO- and its derivative peroxynitrite-induced DNA damage and subsequent double-strand breaks (DSBs). Inactivation of TEB caused the accumulation of spontaneous DSBs largely attributed to endogenous NO and was synergistic to DSB repair pathway mutations with respect to growth. These effects were manifested in the presence of NO-inducing agents and relieved by NO scavengers. NO induced G2/M cell cycle arrest in the teb mutant, indicative of stalled replication forks. Genetic analyses indicate that Polθ is required for translesion DNA synthesis across NO-induced lesions, but not oxidation-induced lesions. Whole-genome sequencing revealed that Polθ bypasses NO-induced base adducts in an error-free manner and generates mutations characteristic of Polθ-mediated end joining. Our experimental data collectively suggests that Polθ plays dual roles in protecting plants from NO-induced DNA damage. Since Polθ is conserved in higher eukaryotes, mammalian Polθ may also be required for balancing NO physiological signaling and genotoxicity. 相似文献
9.
Aaron Mendez-Bermudez Liudmyla Lototska Melanie Pousse Florent Tessier Oliver Croce Chrysa
M Latrick Veronica Cherdyntseva Joe Nassour Jiang Xiaohua Yiming Lu Corinne Abbadie Sarantis Gagos Jing Ye Eric Gilson 《Nucleic acids research》2022,50(13):7493
Cellular senescence triggers various types of heterochromatin remodeling that contribute to aging. However, the age-related mechanisms that lead to these epigenetic alterations remain elusive. Here, we asked how two key aging hallmarks, telomere shortening and constitutive heterochromatin loss, are mechanistically connected during senescence. We show that, at the onset of senescence, pericentromeric heterochromatin is specifically dismantled consisting of chromatin decondensation, accumulation of DNA breakages, illegitimate recombination and loss of DNA. This process is caused by telomere shortening or genotoxic stress by a sequence of events starting from TP53-dependent downregulation of the telomere protective protein TRF2. The resulting loss of TRF2 at pericentromeres triggers DNA breaks activating ATM, which in turn leads to heterochromatin decondensation by releasing KAP1 and Lamin B1, recombination and satellite DNA excision found in the cytosol associated with cGAS. This TP53–TRF2 axis activates the interferon response and the formation of chromosome rearrangements when the cells escape the senescent growth arrest. Overall, these results reveal the role of TP53 as pericentromeric disassembler and define the basic principles of how a TP53-dependent senescence inducer hierarchically leads to selective pericentromeric dismantling through the downregulation of TRF2. 相似文献
10.
Lihua Qu Yi Li Chao Chen Tong Yin Qian Fang Yijin Zhao Wenting Lv Ziqi Liu Yangye Chen Li Shen 《Cell death & disease》2022,13(8)
Acute lung injury (ALI) is a potentially life-threatening, devastating disease with an extremely high rate of mortality. The underlying mechanism of ALI is currently unclear. In this study, we aimed to confirm the hub genes associated with ALI and explore their functions and molecular mechanisms using bioinformatics methods. Five microarray datasets available in GEO were used to perform Robust Rank Aggregation (RRA) to identify differentially expressed genes (DEGs) and the key genes were identified via the protein-protein interaction (PPI) network. Lipopolysaccharide intraperitoneal injection was administered to establish an ALI model. Overall, 40 robust DEGs, which are mainly involved in the inflammatory response, protein catabolic process, and NF-κB signaling pathway were identified. Among these DEGs, we identified two genes associated with ALI, of which the CAV-1/NF-κB axis was significantly upregulated in ALI, and was identified as one of the most effective targets for ALI prevention. Subsequently, the expression of CAV-1 was knocked down using AAV-shCAV-1 or CAV-1-siRNA to study its effect on the pathogenesis of ALI in vivo and in vitro. The results of this study indicated that CAV-1/NF-κB axis levels were elevated in vivo and in vitro, accompanied by an increase in lung inflammation and autophagy. The knockdown of CAV-1 may improve ALI. Mechanistically, inflammation was reduced mainly by decreasing the expression levels of CD3 and F4/80, and activating autophagy by inhibiting AKT/mTOR and promoting the AMPK signaling pathway. Taken together, this study provides crucial evidence that CAV-1 knockdown inhibits the occurrence of ALI, suggesting that the CAV-1/NF-κB axis may be a promising therapeutic target for ALI treatment.Subject terms: Cell signalling, Respiratory tract diseases 相似文献