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131.
洞庭湖湿地土壤环境及其对退田还湖方式的响应 总被引:1,自引:0,他引:1
土壤物理、化学和生物学特性是构成土壤环境的主要组分,综合影响湿地生态系统的调蓄功能和演替恢复。本文以农田(水田和旱地)和自然湿地系统(苔草地和芦苇地)为对照,以3种退田还湖生态系统(种植杨树、芦苇和自然恢复)为研究对象,采用主成分和聚类分析,探索湿地土壤总体环境与生态系统演替过程的相关性。研究结果表明,土壤总体环境与生态系统恢复有很好的一致性。退田还湖为自然水域后,土壤环境的恢复接近于自然湿地系统,在3种退田还湖方式中恢复最好;杨树林地对土壤环境的恢复效果优于人工芦苇地,在一定程度上对湿地土壤环境有所改善,特别是对土壤有机质积累、土壤粘粒形成等过程的改善,但是其土壤环境与苔草等自然湿地发育的土壤仍然有较大差异;因子重要性分析表明水文情势是控制湿地土壤环境恢复的决定性因素,其次是人类干扰强度和方式。 相似文献
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ChunMei Yin JunJiao Li Dan Wang DanDan Zhang Jian Song ZhiQiang Kong BaoLi Wang XiaoPing Hu Steven J. Klosterman Krishna V. Subbarao JieYin Chen XiaoFeng Dai 《Molecular Plant Pathology》2022,23(8):1122
The arms race between fungal pathogens and plant hosts involves recognition of fungal effectors to induce host immunity. Although various fungal effectors have been identified, the effector functions of ribonucleases are largely unknown. Herein, we identified a ribonuclease secreted by Verticillium dahliae (VdRTX1) that translocates into the plant nucleus to modulate immunity. The activity of VdRTX1 causes hypersensitive response (HR)‐related cell death in Nicotiana benthamiana and cotton. VdRTX1 possesses a signal peptide but is unlikely to be an apoplastic effector because its nuclear localization in the plant is necessary for cell death induction. Knockout of VdRTX1 significantly enhanced V. dahliae virulence on tobacco while V. dahliae employs the known suppressor VdCBM1 to escape the immunity induced by VdRTX1. VdRTX1 homologs are widely distributed in fungi but transient expression of 24 homologs from other fungi did not yield cell death induction, suggesting that this function is specific to the VdRTX1 in V. dahliae. Expression of site‐directed mutants of VdRTX1 in N. benthamiana leaves revealed conserved ligand‐binding sites that are important for VdRTX1 function in inducing cell death. Thus, VdRTX1 functions as a unique HR‐inducing effector in V. dahliae that contributes to the activation of plant immunity. 相似文献
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Zhengquan Yang Chengliang Zhang Guojun Lian Shijie Dong Menghui Song Hengrong Shao Jingmei Wang Tao Zhong Zhenni Luo Shengnan Jin Chunming Ding 《Nucleic acids research》2022,50(13):7560
5′-Adenylated oligonucleotides (AppOligos) are widely used for single-stranded DNA/RNA ligation in next-generation sequencing (NGS) applications such as microRNA (miRNA) profiling. The ligation between an AppOligo adapter and target molecules (such as miRNA) no longer requires ATP, thereby minimizing potential self-ligations and simplifying library preparation procedures. AppOligos can be produced by chemical synthesis or enzymatic modification. However, adenylation via chemical synthesis is inefficient and expensive, while enzymatic modification requires pre-phosphorylated substrate and additional purification. Here we cloned and characterized the Pfu RNA ligase encoded by the PF0353 gene in the hyperthermophilic archaea Pyrococcus furiosus. We further engineered fusion enzymes containing both Pfu RNA ligase and T4 polynucleotide kinase. One fusion enzyme, 8H-AP, was thermostable and can directly catalyze 5′-OH-terminated DNA substrates to adenylated products. The newly discovered Pfu RNA ligase and the engineered fusion enzyme may be useful tools for applications using AppOligos. 相似文献
137.
Aldo Spanjaard Ronak Shah Daniël de
Groot Olimpia Alessandra Buoninfante Ben Morris Cor Lieftink Colin Pritchard Lisa
M Zürcher Shirley Ormel Joyce J I Catsman Renske de
Korte-Grimmerink Bjrn Siteur Natalie Proost Terry Boadum Marieke van
de
Ven Ji-Ying Song Maaike Kreft Paul C M van
den
Berk Roderick
L Beijersbergen Heinz Jacobs 《Nucleic acids research》2022,50(13):7420
Crosslink repair depends on the Fanconi anemia pathway and translesion synthesis polymerases that replicate over unhooked crosslinks. Translesion synthesis is regulated via ubiquitination of PCNA, and independently via translesion synthesis polymerase REV1. The division of labor between PCNA-ubiquitination and REV1 in interstrand crosslink repair is unclear. Inhibition of either of these pathways has been proposed as a strategy to increase cytotoxicity of platinating agents in cancer treatment. Here, we defined the importance of PCNA-ubiquitination and REV1 for DNA in mammalian ICL repair. In mice, loss of PCNA-ubiquitination, but not REV1, resulted in germ cell defects and hypersensitivity to cisplatin. Loss of PCNA-ubiquitination, but not REV1 sensitized mammalian cancer cell lines to cisplatin. We identify polymerase Kappa as essential in tolerating DNA damage-induced lesions, in particular cisplatin lesions. Polk-deficient tumors were controlled by cisplatin treatment and it significantly delayed tumor outgrowth and increased overall survival of tumor bearing mice. Our results indicate that PCNA-ubiquitination and REV1 play distinct roles in DNA damage tolerance. Moreover, our results highlight POLK as a critical TLS polymerase in tolerating multiple genotoxic lesions, including cisplatin lesions. The relative frequent loss of Polk in cancers indicates an exploitable vulnerability for precision cancer medicine. 相似文献
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