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Environmental stress and transposons in plants. 植物中的环境胁迫与转座子。
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-12-17 DOI: 10.1266/ggs.22-00045
Hidetaka Ito

Transposons were once thought to be junk repetitive DNA in the genome. However, their importance gradually became apparent as it became clear that they regulate gene expression, which is essential for organisms to survive, and that they are important factors in the driving force of evolution. Since there are multiple transposons in the genomes of all organisms, transposons have likely been activated and increased in copy number throughout their long history. This review focuses on environmental stress as a factor in transposon activation, paying particular attention to transposons in plants that are activated by environmental stresses. It is now known that plants respond to environmental stress in various ways, and correspondingly, many transposons respond to stress. The relationship between environmental stress and transposons is reviewed, including the mechanisms of their activation and the effects of transposon activation on host plants.

转座子曾被认为是基因组中的垃圾重复DNA。然而,它们的重要性逐渐变得明显,因为它们调节基因表达,这是生物体生存所必需的,它们是推动进化的重要因素。由于所有生物体的基因组中都存在多个转座子,因此转座子可能在其漫长的历史中被激活并增加拷贝数。本文综述了环境胁迫作为转座子激活的一个因素,特别关注植物中被环境胁迫激活的转座子。目前已知植物对环境胁迫有多种反应方式,相应的,许多转座子对胁迫也有反应。本文综述了环境胁迫与转座子的关系,包括转座子的激活机制以及转座子的激活对寄主植物的影响。
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引用次数: 5
Euchromatin factors HULC and Set1C affect heterochromatin organization and mating-type switching in fission yeast Schizosaccharomyces pombe. 常染色质因子HULC和Set1C影响裂糖酵母异染色质组织和交配型转换。
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-10-18 DOI: 10.1266/ggs.22-00012
Alfredo Esquivel-Chávez, Takahisa Maki, Hideo Tsubouchi, Testuya Handa, Hiroshi Kimura, James E Haber, Geneviève Thon, Hiroshi Iwasaki

Mating-type (P or M) of fission yeast Schizosaccharomyces pombe is determined by the transcriptionally active mat1 cassette and is switched by gene conversion using a donor, either mat2 or mat3, located in an adjacent heterochromatin region (mating-type switching; MTS). In the switching process, heterochromatic donors of genetic information are selected based on the P or M cell type and on the action of two recombination enhancers, SRE2 promoting the use of mat2-P and SRE3 promoting the use of mat3-M, leading to replacement of the content of the expressed mat1 cassette. Recently, we found that the histone H3K4 methyltransferase complex Set1C participates in donor selection, raising the question of how a complex best known for its effects in euchromatin controls recombination in heterochromatin. Here, we report that the histone H2BK119 ubiquitin ligase complex HULC functions with Set1C in MTS, as mutants in the shf1, brl1, brl2 and rad6 genes showed defects similar to Set1C mutants and belonged to the same epistasis group as set1Δ. Moreover, using H3K4R and H2BK119R histone mutants and a Set1-Y897A catalytic mutant, we found that ubiquitylation of histone H2BK119 by HULC and methylation of histone H3K4 by Set1C are functionally coupled in MTS. Cell-type biases in MTS in these mutants suggested that HULC and Set1C inhibit the use of the SRE3 recombination enhancer in M cells, thus favoring SRE2 and mat2-P. Consistent with this, imbalanced switching in the mutants was traced to compromised association of the directionality factor Swi6 with the recombination enhancers in M cells. Based on their known effects at other chromosomal locations, we speculate that HULC and Set1C control nucleosome mobility and strand invasion near the SRE elements. In addition, we uncovered distinct effects of HULC and Set1C on histone H3K9 methylation and gene silencing, consistent with additional functions in the heterochromatic domain.

裂糖酵母(Schizosaccharomyces pombe)的交配型(P或M)由转录活性的mat1盒决定,并通过位于相邻异染色质区域的供体mat2或mat3的基因转换来切换(交配型切换;MTS)。在转换过程中,根据P或M细胞类型以及两种重组增强子(SRE2促进mat2-P的使用,SRE3促进mat3-M的使用)的作用选择遗传信息的异色供体,导致表达的mat1盒的内容被替换。最近,我们发现组蛋白H3K4甲基转移酶复合物Set1C参与供体选择,提出了一个以其在常染色质中的作用而闻名的复合物如何控制异染色质中的重组的问题。在这里,我们报道了组蛋白H2BK119泛素连接酶复合体HULC在MTS中与Set1C一起起作用,因为shf1、brl1、brl2和rad6基因的突变体表现出与Set1C突变体相似的缺陷,并且与set1Δ属于同一组。此外,利用H3K4R和H2BK119R组蛋白突变体以及Set1-Y897A催化突变体,我们发现在MTS中,HULC对组蛋白H2BK119的泛素化和Set1C对组蛋白H3K4的甲基化在功能上偶联,这些突变体在MTS中的细胞类型偏倚表明,HULC和Set1C抑制了M细胞中SRE3重组增强子的使用,从而有利于SRE2和mat2-P。与此一致,突变体中的不平衡开关可追溯到M细胞中方向性因子Swi6与重组增强子的关联受损。基于它们在其他染色体位置的已知作用,我们推测HULC和Set1C控制核小体的流动性和SRE元件附近的链入侵。此外,我们发现了HULC和Set1C对组蛋白H3K9甲基化和基因沉默的明显影响,这与异色结构域的其他功能一致。
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引用次数: 0
Role of Error Catastrophe in Transmission Ability of Virus 错误突变在病毒传播能力中的作用
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-07-04 DOI: 10.1101/2022.06.28.22276997
N. Takahata, Hirotaka Sugawara
The role played by "error catastrophe" is explicitly taken into account in the mathematical formulation to analyze the COVID-19 data. The idea is to combine the mathematical genetics formalism of the error catastrophe of mutations in the virus gene loci with the standard model of epidemics which lacks the explicit incorporation of the mutation effect on the spreading of the viruses. We apply the formalism to the case of SARS-CoV-2 virus. We assume the "universality" of the error catastrophe in the process of analyzing the data. This means that some basic parameter to describe the error catastrophe is independent of which group (country or city) we deal with. Concretely, we analyze the omicron data of South Africa and then analyze the cases of Japan using the same value of the basic parameter derived in the South Africa analysis. The result shows the validity of our universality assumption.
在分析新冠肺炎数据的数学公式中,明确考虑了“错误灾难”所扮演的角色。其想法是将病毒基因座突变的错误突变的数学遗传学形式与流行病的标准模型相结合,后者缺乏对病毒传播的突变效应的明确结合。我们将形式主义应用于严重急性呼吸系统综合征冠状病毒2型的病例。在分析数据的过程中,我们假设了误差突变的“普遍性”。这意味着,描述误差突变的一些基本参数与我们处理的群体(国家或城市)无关。具体来说,我们分析了南非的奥密克戎数据,然后使用南非分析中得出的基本参数的相同值分析了日本的病例。结果表明了我们的普遍性假设的有效性。
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引用次数: 0
S100A9 and SOCS3 as diagnostic biomarkers of acute myocardial infarction and their association with immune infiltration. S100A9和SOCS3作为急性心肌梗死的诊断性生物标志物及其与免疫浸润的关系
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-06-09 DOI: 10.1266/ggs.21-00073
Ze-Liang Lin, Yan-Cun Liu, Yu-lei Gao, Xinsen Chen, Chao Wang, Song-Tao Shou, Y. Chai
Acute myocardial infarction (AMI) is one of the leading causes of death globally, with a mortality rate of over 20%. However, the diagnostic biomarkers frequently used in current clinical practice have limitations in both sensitivity and specificity, likely resulting in delayed diagnosis. This study aimed to identify potential diagnostic biomarkers for AMI and explored the possible mechanisms involved. Datasets were retrieved from the Gene Expression Omnibus. First, we identified differentially expressed genes (DEGs) and preserved modules, from which we identified candidate genes by LASSO (least absolute shrinkage and selection operator) regression and the SVM-RFE (support vector machine-recursive feature elimination) algorithm. Subsequently, we used ROC (receiver operating characteristic) analysis to evaluate the diagnostic accuracy of the candidate genes. Thereafter, functional enrichment analysis and an analysis of immune infiltration were implemented. Finally, we assessed the association between biomarkers and biological processes, infiltrated cells, clinical traits, tissues and time points. We identified nine preserved modules containing 1,016 DEGs and managed to construct a diagnostic model with high accuracy (GSE48060: AUC = 0.923; GSE66360: AUC = 0.973) incorporating two genes named S100A9 and SOCS3. Functional analysis revealed the pivotal role of inflammation; immune infiltration analysis indicated that eight cell types (monocytes, epithelial cells, neutrophils, CD8+ T cells, Th2 cells, NK cells, NKT cells and platelets) were likely involved in AMI. Furthermore, we observed that S100A9 and SOCS3 were correlated with inflammation, variably infiltrated cells, clinical traits of patients, sampling tissues and sampling time points. In conclusion, we suggested S100A9 and SOCS3 as diagnostic biomarkers of AMI and discovered their association with inflammation, infiltrated immune cells and other factors.
急性心肌梗死(AMI)是全球死亡的主要原因之一,死亡率超过20%。然而,当前临床实践中经常使用的诊断生物标志物在敏感性和特异性方面都有局限性,可能导致诊断延迟。本研究旨在确定AMI的潜在诊断生物标志物,并探讨其可能的机制。从基因表达综合数据库中检索数据集。首先,我们鉴定了差异表达基因(DEG)和保留的模块,并通过LASSO(最小绝对收缩和选择算子)回归和SVM-RFE(支持向量机递归特征消除)算法从中鉴定了候选基因。随后,我们使用ROC(受体操作特征)分析来评估候选基因的诊断准确性。此后,进行功能富集分析和免疫浸润分析。最后,我们评估了生物标志物与生物学过程、浸润细胞、临床特征、组织和时间点之间的关系。我们鉴定了9个含有1016个DEG的保存模块,并成功构建了一个高准确度的诊断模型(GSE48060:AUC=0.923;GSE66360:AUC=0.0973),该模型包含两个名为S100A9和SOCS3的基因。功能分析揭示了炎症的关键作用;免疫浸润分析表明,8种细胞类型(单核细胞、上皮细胞、中性粒细胞、CD8+T细胞、Th2细胞、NK细胞、NKT细胞和血小板)可能参与AMI。此外,我们观察到S100A9和SOCS3与炎症、可变浸润细胞、患者的临床特征、采样组织和采样时间点相关。总之,我们建议S100A9和SOCS3作为AMI的诊断生物标志物,并发现它们与炎症、浸润的免疫细胞和其他因素有关。
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引用次数: 1
BpEIL1 negatively regulates resistance to Rhizoctonia solani and Alternaria alternata in birch. BpEIL1负调控白桦对茄枯丝核菌和互花病菌的抗性。
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-06-09 DOI: 10.1266/ggs.21-00098
Ranhong Li, Jingjing Sun, Xiaomeng Ning, Dan Liu, Xin Chen
Pathogen attacks affect tree health, causing considerable economic losses as well as serious damage to the surrounding environment. Understanding the disease resistance mechanisms of trees is important for tree breeding. In previous studies on birch (Betula platyphylla × B. pendula), we identified a lesion mimic mutant called lmd. We found that reduced expression of BpEIL1 was responsible for the phenotype in lmd. Following cloning, we acquired several BpEIL1 overexpression and suppression lines in birch. In this study, we cloned the BpEIL1 promoter and found that BpEIL1 was primarily expressed in leaves, particularly in veins. We further studied the traits of transgenic lines and the function of BpEIL1 in disease resistance in birch using the BpEIL1 overexpression line OE9, the suppression line SE13 and the non-transgenic line NT. We found that hydrogen peroxide accumulated in SE13 leaves. Ascorbate peroxidase and catalase activity significantly increased in SE13. SE13 was more resistant to the fungal pathogens Alternaria alternata and Rhizoctonia solani than were the OE9 and NT lines. RNA-seq indicated that pathways related to signal transduction, disease resistance and plant immunity were enriched in SE13. BpEIL1 is thus a negative regulatory transcription factor for disease resistance in birch. This study provides a reference for disease resistance of birch and other trees.
病原体攻击影响树木健康,造成相当大的经济损失,并对周围环境造成严重破坏。了解树木的抗病机制对树木育种很重要。在之前对桦树(Betula platyphylla×B.pendula)的研究中,我们鉴定了一种称为lmd的病变模拟突变体。我们发现BpEIL1的表达减少是lmd表型的原因。克隆后,我们在桦树中获得了几个BpEIL1过表达和抑制系。在这项研究中,我们克隆了BpEIL1启动子,发现BpEIL 1主要在叶片中表达,尤其是在叶脉中。利用BpEIL1过表达株系OE9、抑制株系SE13和非转基因株系NT,进一步研究了转基因株系的特性和BpEIL 1在桦树抗病性中的作用。在SE13中抗坏血酸过氧化物酶和过氧化氢酶活性显著增加。SE13对真菌病原Alternaria alternata和Rhizoctonia solani的抗性高于OE9和NT系。RNA-seq表明,SE13中富集了与信号转导、抗病性和植物免疫相关的途径。因此BpEIL1是桦树抗病性的负调控转录因子。本研究为桦树及其他树木的抗病性提供了参考。
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引用次数: 0
Regulation of spermatogenic stem cell homeostasis by mitogen competition in an open niche microenvironment. 开放生态位微环境中丝裂原竞争对生精干细胞稳态的调节。
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-06-04 Epub Date: 2022-02-06 DOI: 10.1266/ggs.21-00062
Yu Kitadate, Shosei Yoshida

Continuity of spermatogenesis in mammals is underpinned by spermatogenic (also called spermatogonial) stem cells (SSCs) that self-renew and differentiate into sperm that pass on genetic information to the next generation. Despite the fundamental role of SSCs, the mechanisms underlying SSC homeostasis are only partly understood. During homeostasis, the stem cell pool remains constant while differentiating cells are continually produced to replenish the lost differentiated cells. One of the outstanding questions here is how self-renewal and differentiation of SSCs are balanced to achieve a constant self-renewing pool. In this review, we shed light on the regulatory mechanism of SSC homeostasis, with focus on the recently proposed mitogen competition model in a facultative (or open) niche microenvironment.

哺乳动物精子发生的连续性是由生精(也称为生精)干细胞(SSCs)支撑的,这些干细胞自我更新并分化成将遗传信息传递给下一代的精子。尽管SSC的基本作用,但SSC稳态的机制只被部分理解。在稳态过程中,干细胞库保持恒定,分化细胞不断产生,以补充失去的分化细胞。这里的一个突出问题是如何平衡ssc的自我更新和分化,以实现一个持续的自我更新池。在这篇综述中,我们阐明了SSC稳态的调控机制,重点介绍了最近提出的兼性(或开放)微环境中有丝分裂原竞争模型。
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引用次数: 1
MEIOSIN directs initiation of meiosis and subsequent meiotic prophase program during spermatogenesis. 减数分裂蛋白在精子发生过程中指导减数分裂的开始和随后的减数分裂前期程序。
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-06-04 Epub Date: 2021-12-25 DOI: 10.1266/ggs.21-00054
Kei-Ichiro Ishiguro, Ryuki Shimada

Meiosis is a crucial process for spermatogenesis and oogenesis. Initiation of meiosis coincides with spermatocyte differentiation and is followed by meiotic prophase, a prolonged G2 phase that ensures the completion of numerous meiosis-specific chromosome events. During meiotic prophase, chromosomes are organized into axis-loop structures, which underlie meiosis-specific events such as meiotic recombination and homolog synapsis. In spermatocytes, meiotic prophase is accompanied by robust alterations of gene expression programs and chromatin status for subsequent sperm production. The mechanisms regulating meiotic initiation and subsequent meiotic prophase programs are enigmatic. Recently, we discovered MEIOSIN (Meiosis initiator), a DNA-binding protein that directs the switch from mitosis to meiosis. This review mainly focuses on how MEIOSIN is involved in meiotic initiation and the meiotic prophase program during spermatogenesis. Further, we discuss the downstream genes activated by MEIOSIN, which are crucial for meiotic prophase-specific events, from the viewpoint of chromosome dynamics and the gene expression program.

减数分裂是精子发生和卵子发生的重要过程。减数分裂的开始与精母细胞分化一致,随后是减数分裂前期,这是一个延长的G2期,确保完成许多减数分裂特异性染色体事件。在减数分裂前期,染色体被组织成轴环结构,这是减数分裂特异性事件的基础,如减数分裂重组和同源突触。在精母细胞中,减数分裂前期伴随着基因表达程序和染色质状态的强烈改变,从而导致随后的精子产生。调控减数分裂起始和随后的减数分裂前期程序的机制是谜。最近,我们发现了MEIOSIN(减数分裂启动器),这是一种dna结合蛋白,指导从有丝分裂到减数分裂的转换。本文主要综述了减数分裂蛋白在精子发生过程中如何参与减数分裂起始和减数分裂前期程序。进一步,我们从染色体动力学和基因表达程序的角度讨论了减数分裂前期特异性事件中至关重要的下游基因被MEIOSIN激活。
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引用次数: 1
DNA methylation plays an important role in iron-overloaded Tibetans. DNA甲基化在铁超载的藏族人中起着重要作用。
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-05-28 DOI: 10.1266/ggs.21-00006
Qin Zhao, Zhijing Ge, Suhong Fu, Shan Wan, Jing Shi, Yunhong Wu, Yongqun Zhang
The prevalence of iron overload in Tibetans in Tibet is higher than that in Han. DNA methylation (DNAm) is closely related to iron metabolism and iron level. Nevertheless, the epigenetic status of Tibetans with iron overload is unknown, and we therefore aimed to explore whether the phenomenon observed in the Tibetan population is regulated by epigenetics. The results showed that 2.26% of cytosine was methylated in the whole genome, and that the rate of CG cytosine methylation was higher in individuals in the iron overload (TH) group than in those in the iron normal (TL) group. We analyzed differentially methylated genes (DMGs) in whole-genome bisulfite sequencing data from the TH and TL groups of high-altitude Tibetans. Protein-protein interaction and pathway analyses of candidate DMGs related to iron uptake and transport showed that epigenetic changes in 10 candidate genes (ACO1, CYBRD1, FLVCR1, HFE, HMOX2, IREB2, NEDD8, SLC11A2, SLC40A1 and TFRC) are likely to relate to iron overload. This work reveals, for the first time, changes of DNAm in Tibetan people with iron overload, which suggest that DNAm is a mechanism underlying differences in iron content between individuals in the high-altitude Tibetan population. Our findings should contribute to the study of iron metabolism and the overall health status of Tibetans.
藏族铁超载患病率高于汉族。DNA甲基化(DNAm)与铁代谢和铁水平密切相关。然而,铁过载藏人的表观遗传学状况尚不清楚,因此我们旨在探索在藏人群体中观察到的现象是否受表观遗传学的调节。结果显示,全基因组中2.26%的胞嘧啶被甲基化,并且铁过载(TH)组的CG胞嘧啶甲基化率高于铁正常(TL)组。我们分析了高海拔藏族TH和TL群体亚硫酸氢盐全基因组测序数据中的差异甲基化基因(DMG)。与铁摄取和转运相关的候选DMG的蛋白质-蛋白质相互作用和通路分析表明,10个候选基因(ACO1、CYBRD1、FLVCR1、HFE、HMOX2、IREB2、NEDD8、SLC11A2、SLC40A1和TFRC)的表观遗传学变化可能与铁过载有关。这项工作首次揭示了铁过载藏族人群DNAm的变化,这表明DNAm是高海拔藏族人群个体间铁含量差异的潜在机制。我们的发现应该有助于研究铁代谢和藏人的整体健康状况。
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引用次数: 3
Genetic purity of a rear-edge population of Carex podogyna Franch. et Sav. (Cyperaceae) maintained under interspecific hybridization. 毛茛(Carex podogyna france)后缘群体的遗传纯度。等干腊肠。(苏柏科)维持种间杂交。
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-05-12 DOI: 10.1266/ggs.21-00087
K. Nagasawa, Shigeru Fukumoto, H. Setoguchi, M. Ishihara, Kenjiro Hiratsuka, Kazutoshi Masuda, S. Sakaguchi
Interspecific hybridization is a critical issue in conservation biology because it may drive small populations to extinction through direct or indirect processes. In this study, to develop a conservation strategy for an endangered rear-edge population of Carex podogyna in Ashiu, Kyoto, Japan, we performed a molecular genetic analysis of the wild population and an ex-situ population established from wild seeds. Microsatellite genotypic data revealed a complete loss of genetic diversity in the wild population, suggesting that it has long been prone to genetic drift due to isolation as a small population. In contrast, microsatellite analysis of 13 ex-situ individuals detected multiple alleles that are not harbored in the wild C. podogyna population. Sequence analysis revealed that these individuals are likely natural hybrids between C. podogyna and a co-occurring species, C. curvicollis, although established hybrids have never been found in the natural habitat. Based on our observation of variegated leaves in hybrid individuals, we propose that hybrids have been excluded by natural selection and/or interspecific competition caused by insufficient productivity of photosynthesis, although other genetic and ecological factors may also be influential. Overall, this study indicates that natural mechanisms selectively removing the hybrids have maintained the genetic purity of this rear-edge population of C. podogyna, and also emphasizes the importance of genetic assessment in ex-situ conservation programs.
种间杂交是保护生物学中的一个关键问题,因为它可能通过直接或间接的过程导致小种群灭绝。在这项研究中,为了制定日本京都阿流一个濒危的苔草后缘种群的保护策略,我们对野生种群和从野生种子中建立的迁地种群进行了分子遗传学分析。微卫星基因型数据显示,野生种群的遗传多样性完全丧失,这表明它作为一个小种群,由于与世隔绝,长期以来容易发生遗传漂移。相反,对13个离地个体的微卫星分析检测到了野生足根线虫种群中不存在的多个等位基因。序列分析显示,这些个体很可能是足柄线虫和共生物种弯柄线虫的自然杂交种,尽管从未在自然栖息地发现过已建立的杂交种。基于我们对杂交个体中杂色叶片的观察,我们提出,由于光合作用生产力不足导致的自然选择和/或种间竞争,杂交种被排除在外,尽管其他遗传和生态因素也可能有影响。总的来说,这项研究表明,选择性地去除杂交种的自然机制保持了足根线虫后缘种群的遗传纯度,也强调了基因评估在迁地保护计划中的重要性。
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引用次数: 0
Sperm chromatin condensation: epigenetic mechanisms to compact the genome and spatiotemporal regulation from inside and outside the nucleus. 精子染色质凝聚:从细胞核内外压缩基因组的表观遗传学机制和时空调控。
IF 1.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2022-04-29 DOI: 10.1266/ggs.21-00065
Y. Okada
Sperm chromatin condensation is a critical step in mammalian spermatogenesis to protect the paternal DNA from external damaging factors and to acquire fertility. During chromatin condensation, various events proceed in a chronological order, independently or in sequence, interacting with each other both inside and outside the nucleus to support the dramatic chromatin changes. Among these events, histone-protamine replacement, which is concomitant with acrosome biogenesis and cytoskeletal alteration, is the most critical step associated with nuclear elongation. Failures of not only intranuclear events but also extra-nuclear events severely affect sperm shape and chromatin state and are subsequently linked to infertility. This review focuses on nuclear and non-nuclear factors that affect sperm chromatin condensation and its effects, and further discusses the possible utility of sperm chromatin for clinical applications.
精子染色质凝聚是哺乳动物精子发生过程中保护父系DNA免受外部损伤和获得生育能力的关键步骤。在染色质浓缩过程中,各种事件按时间顺序独立或顺序进行,在细胞核内外相互作用,以支持染色质的剧烈变化。在这些事件中,与顶体生物发生和细胞骨架改变相伴的组蛋白鱼精蛋白置换是与细胞核延伸相关的最关键的步骤。核内事件和核外事件的失败不仅严重影响精子的形状和染色质状态,随后与不孕有关。本文综述了影响精子染色质凝聚的核因子和非核因子及其影响,并进一步讨论了精子染色质在临床应用中的可能用途。
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引用次数: 5
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Genes & genetic systems
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