热休克蛋白对电离辐射损伤的保护效应

近年来,热休克蛋白（HSPs）对电离辐射损伤的保护效应成为一个关注的热点。本文综述了热休克蛋白家族及其对电离辐射损伤的保护效应,包括HSPs对细胞凋亡的抑制作用和DNA损伤的保护作用两方面,对热休克蛋白与电离辐射损伤的关系进行了探讨。     

基于混沌映射和DNA编码的图像加密算法

为了有效改进图像的加密效果及安全性,在对已有的图像加密算法进行分析的基础上,提出基于混沌映射的位变换和DNA序列的图像加密算法。首先,采用混沌映射生成置乱序列对图像在位平面进行置乱,同时达到了图像置乱和扩散的双重加密效果。然后,利用DNA编码规则,对置乱后的图像编码,进行DNA运算,实现图像的扩散。实验结果表明,该算法密钥空间足够大,密钥敏感性较强,具有较好的安全性。     

DNA编码限制条件与编码策略

以评价DNA编码的基本限制条件之一——Hamming距离为出发点分析了DNA编码的三个参量：码字个数、码字长度与Watson-Crick Hamming距离,并得到它们之间的内在联系;讨论了Watson-Crick Hamming距离与DNA码字重量之间的关系;在此基础上得到了DNA编码的编码策略;提出了适合DNA编码的改进Watson-Crick Hamming距离及DNA编码模块化的定义,对DNA编码的优化做出了详细分析,为DNA计算的发展注入了活力。     

Oxidative Damage in Sporadic Colorectal Cancer: Molecular Mapping of Base Excision Repair Glycosylases MUTYH and hOGG1 in Colorectal Cancer Patients

Oxidative stress, oxidative DNA damage and resulting mutations play a role in colorectal carcinogenesis. Impaired equilibrium between DNA damage formation, antioxidant status, and DNA repair capacity is responsible for the accumulation of genetic mutations and genomic instability. The lesion-specific DNA glycosylases, e.g., hOGG1 and MUTYH, initiate the repair of oxidative DNA damage. Hereditary syndromes (MUTYH-associated polyposis, NTHL1-associated tumor syndrome) with germline mutations causing a loss-of-function in base excision repair glycosylases, serve as straight forward evidence on the role of oxidative DNA damage and its repair. Altered or inhibited function of above glycosylases result in an accumulation of oxidative DNA damage and contribute to the adenoma-adenocarcinoma transition. Oxidative DNA damage, unless repaired, often gives rise G:C > T:A mutations in tumor suppressor genes and proto-oncogenes with subsequent occurrence of chromosomal copy-neutral loss of heterozygosity. For instance, G>T transversions in position c.34 of a KRAS gene serves as a pre-screening tool for MUTYH-associated polyposis diagnosis. Since sporadic colorectal cancer represents more complex and heterogenous disease, the situation is more complicated. In the present study we focused on the roles of base excision repair glycosylases (hOGG1, MUTYH) in colorectal cancer patients by investigating tumor and adjacent mucosa tissues. Although we found downregulation of both glycosylases and significantly lower expression of hOGG1 in tumor tissues, accompanied with G>T mutations in KRAS gene, oxidative DNA damage and its repair cannot solely explain the onset of sporadic colorectal cancer. In this respect, other factors (especially microenvironment) per se or in combination with oxidative DNA damage warrant further attention. Base excision repair characteristics determined in colorectal cancer tissues and their association with disease prognosis have been discussed as well.     

Multiplexed-Based Assessment of DNA Damage Response to Chemotherapies Using Cell Imaging Cytometry

The current methods for measuring the DNA damage response (DDR) are relatively labor-intensive and usually based on Western blotting, flow cytometry, and/or confocal immunofluorescence analyses. They require many cells and are often limited to the assessment of a single or few proteins. Here, we used the Celigo^® image cytometer to evaluate the cell response to DNA-damaging agents based on a panel of biomarkers associated with the main DDR signaling pathways. We investigated the cytostatic or/and the cytotoxic effects of these drugs using simultaneous propidium iodide and calcein-AM staining. We also describe new dedicated multiplexed protocols to investigate the qualitative (phosphorylation) or the quantitative changes of eleven DDR markers (H2AX, DNA-PKcs, ATR, ATM, CHK1, CHK2, 53BP1, NBS1, RAD51, P53, P21). The results of our study clearly show the advantage of using this methodology because the multiplexed-based evaluation of these markers can be performed in a single experiment using the standard 384-well plate format. The analyses of multiple DDR markers together with the cell cycle status provide valuable insights into the mechanism of action of investigational drugs that induce DNA damage in a time- and cost-effective manner due to the low amounts of antibodies and reagents required.     

水稻基因组MSAP指纹图谱构建及DNA甲基化修饰位点分离与鉴定

采用EcoR I和Hpa II/Msp I双酶切建立了适合于水稻基因组的甲基化敏感扩增多态性(MSAP)分析体系,在全基因组水平检测了水稻DNA甲基化修饰位点.以12对MSAP引物进行选择性扩增,共检测到甲基化修饰位点120个,"CCGG/GGCC"位点甲基化修饰比例为20.17%.对部分水稻基因组甲基化修饰位点进行回收,最终分离了55条存在甲基化位点变异的DNA序列,通过BLAST比对分析将其联配到水稻基因组序列上.分析表明,这些甲基化修饰位点主要集中于基因启动子区(47%)和第一外显子区(22%),在其侧翼序列中存在类似"CpG island" 典型序列特征的"CpG"二核苷酸成簇富集区.在此基础上,对应用MSAP技术分离水稻基因组DNA甲基化修饰位点的有效性以及水稻基因组序列中"CpG island"类似序列分布特征和生物意义进行了讨论.     

An Adaptive Role for DNA Double-Strand Breaks in Hippocampus-Dependent Learning and Memory

DNA double-strand breaks (DSBs), classified as the most harmful type of DNA damage based on the complexity of repair, lead to apoptosis or tumorigenesis. In aging, DNA damage increases and DNA repair decreases. This is exacerbated in disease, as post-mortem tissue from patients diagnosed with mild cognitive impairment (MCI) or Alzheimer’s disease (AD) show increased DSBs. A novel role for DSBs in immediate early gene (IEG) expression, learning, and memory has been suggested. Inducing neuronal activity leads to increases in DSBs and upregulation of IEGs, while increasing DSBs and inhibiting DSB repair impairs long-term memory and alters IEG expression. Consistent with this pattern, mice carrying dominant AD mutations have increased baseline DSBs, and impaired DSB repair is observed. These data suggest an adaptive role for DSBs in the central nervous system and dysregulation of DSBs and/or repair might drive age-related cognitive decline (ACD), MCI, and AD. In this review, we discuss the adaptive role of DSBs in hippocampus-dependent learning, memory, and IEG expression. We summarize IEGs, the history of DSBs, and DSBs in synaptic plasticity, aging, and AD. DSBs likely have adaptive functions in the brain, and even subtle alterations in their formation and repair could alter IEGs, learning, and memory.     

Plant DNA Methylation: An Epigenetic Mark in Development,Environmental Interactions,and Evolution

DNA methylation is an epigenetic modification of the genome involved in the regulation of gene expression and modulation of chromatin structure. Plant genomes are widely methylated, and the methylation generally occurs on the cytosine bases through the activity of specific enzymes called DNA methyltransferases. On the other hand, methylated DNA can also undergo demethylation through the action of demethylases. The methylation landscape is finely tuned and assumes a pivotal role in plant development and evolution. This review illustrates different molecular aspects of DNA methylation and some plant physiological processes influenced by this epigenetic modification in model species, crops, and ornamental plants such as orchids. In addition, this review aims to describe the relationship between the changes in plant DNA methylation levels and the response to biotic and abiotic stress. Finally, we discuss the possible evolutionary implications and biotechnological applications of DNA methylation.     

ENet-6mA: Identification of 6mA Modification Sites in Plant Genomes Using ElasticNet and Neural Networks

N6-methyladenine (6mA) has been recognized as a key epigenetic alteration that affects a variety of biological activities. Precise prediction of 6mA modification sites is essential for understanding the logical consistency of biological activity. There are various experimental methods for identifying 6mA modification sites, but in silico prediction has emerged as a potential option due to the very high cost and labor-intensive nature of experimental procedures. Taking this into consideration, developing an efficient and accurate model for identifying N6-methyladenine is one of the top objectives in the field of bioinformatics. Therefore, we have created an in silico model for the classification of 6mA modifications in plant genomes. ENet-6mA uses three encoding methods, including one-hot, nucleotide chemical properties (NCP), and electron–ion interaction potential (EIIP), which are concatenated and fed as input to ElasticNet for feature reduction, and then the optimized features are given directly to the neural network to get classified. We used a benchmark dataset of rice for five-fold cross-validation testing and three other datasets from plant genomes for cross-species testing purposes. The results show that the model can predict the N6-methyladenine sites very well, even cross-species. Additionally, we separated the datasets into different ratios and calculated the performance using the area under the precision–recall curve (AUPRC), achieving 0.81, 0.79, and 0.50 with 1:10 (positive:negative) samples for F. vesca, R. chinensis, and A. thaliana, respectively.