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Activation of the PGC-1α-mediated mitochondrial glutamine metabolism pathway attenuates female offspring osteoarthritis induced by prenatal excessive prednisone. 激活 PGC-1α 介导的线粒体谷氨酰胺代谢途径可减轻产前过量泼尼松诱导的雌性后代骨关节炎。
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-08-21 DOI: 10.1007/s11427-023-2593-4
Qingxian Li, Fan Zhang, Yongguo Dai, Liang Liu, Liaobin Chen, Hui Wang

Osteoarthritis is a chronic, age-related joint disease. Previous studies have shown that osteoarthritis develops during intrauterine development. Prednisone is frequently used to treat pregnancies complicated by autoimmune diseases. However, limited research has been conducted on the enduring effects of prednisone use during pregnancy on the offspring. In this study, we investigated the effect of excessive prednisone exposure on cartilage development and susceptibility to osteoarthritis in the offspring. We found that prenatal prednisone exposure (PPE) impaired cartilage extracellular matrix (ECM) synthesis, resulting in poor cartilage pathology in female offspring during the adult period, which was further exacerbated after long-distance running stimulation. Additionally, PPE suppressed cartilage development during the intrauterine period. Tracing back to the intrauterine period, we found that Pred, rather than prednisone, decreased glutamine metabolic flux, which resulted in increased oxidative stress, and decreased histone acetylation, and expression of cartilage phenotypic genes. Further, PGC-1α-mediated mitochondrial biogenesis, while PPE caused hypermethylation in the promoter region of PGC-1α and decreased its expression in fetal cartilage by activating the glucocorticoid receptor, resulting in a reduction of glutamine flux controlled by mitochondrial biogenesis. Additionally, overexpression of PGC-1α (either pharmacological or through lentiviral transfection) reversed PPE- and Pred-induced cartilage ECM synthesis impairment. In summary, this study demonstrated that PPE causes chondrodysplasia in female offspring and increases their susceptibility to postnatal osteoarthritis. Hence, targeting PGC-1α early on could be a potential intervention strategy for PPE-induced osteoarthritis susceptibility.

骨关节炎是一种与年龄有关的慢性关节疾病。以往的研究表明,骨关节炎是在宫内发育过程中形成的。泼尼松常用于治疗妊娠合并自身免疫性疾病。然而,关于孕期使用泼尼松对后代的持久影响的研究却很有限。在这项研究中,我们调查了过量泼尼松暴露对后代软骨发育和骨关节炎易感性的影响。我们发现,产前泼尼松暴露(PPE)会损害软骨细胞外基质(ECM)的合成,从而导致雌性后代成年后软骨病理状况不佳,而长跑刺激会进一步加剧这种状况。此外,PPE 还会抑制宫内软骨的发育。追溯到宫内期,我们发现Pred而不是泼尼松降低了谷氨酰胺代谢通量,从而导致氧化应激增加、组蛋白乙酰化减少以及软骨表型基因的表达。此外,PGC-1α 介导线粒体生物生成,而 PPE 通过激活糖皮质激素受体,导致 PGC-1α 启动子区域甲基化过度,并降低其在胎儿软骨中的表达,从而导致线粒体生物生成控制的谷氨酰胺通量减少。此外,过表达 PGC-1α(药理或通过慢病毒转染)可逆转 PPE 和 Pred 诱导的软骨 ECM 合成障碍。总之,本研究证明,PPE 会导致雌性后代软骨发育不良,并增加其对出生后骨关节炎的易感性。因此,早期靶向 PGC-1α 可能是干预 PPE 诱导的骨关节炎易感性的一种潜在策略。
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引用次数: 0
Innovative genome editing in plants: a transposase and CRISPR combination approach. 创新的植物基因组编辑:转座酶和 CRISPR 组合方法。
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 DOI: 10.1007/s11427-024-2729-2
Hamza Sohail, Iqra Noor, Xuehao Chen, Xiaodong Yang
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引用次数: 0
Zika virus infection induces glycometabolic disorder in northern pig-tailed macaques. 寨卡病毒感染会诱发北方猪尾猕猴糖代谢紊乱。
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-08-30 DOI: 10.1007/s11427-024-2663-6
Qing Li, Ren-Hua Yang, Yan Hu, Bei-Bei Tang, Ying-Jie Jiang, Chang-Bo Zheng, Tian-Zhang Song
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引用次数: 0
Androgens exert multifaceted functions in sex differences analyzed through single-cell transcriptome. 通过单细胞转录组分析雄激素在性别差异中发挥的多方面功能
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-06-26 DOI: 10.1007/s11427-024-2652-y
Xinxin Tang, Yinkun Fu, Zhihui Zou, Yue Li, Ming He
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引用次数: 0
Temperature regulates negative supercoils to modulate meiotic crossovers and chromosome organization. 温度调节负超螺旋,从而调节减数分裂交叉和染色体组织。
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-07-23 DOI: 10.1007/s11427-024-2671-1
Yingjin Tan, Taicong Tan, Shuxian Zhang, Bo Li, Beiyi Chen, Xu Zhou, Ying Wang, Xiao Yang, Binyuan Zhai, Qilai Huang, Liangran Zhang, Shunxin Wang

Crossover recombination is a hallmark of meiosis that holds the paternal and maternal chromosomes (homologs) together for their faithful segregation, while promoting genetic diversity of the progeny. The pattern of crossover is mainly controlled by the architecture of the meiotic chromosomes. Environmental factors, especially temperature, also play an important role in modulating crossovers. However, it is unclear how temperature affects crossovers. Here, we examined the distribution of budding yeast axis components (Red1, Hop1, and Rec8) and the crossover-associated Zip3 foci in detail at different temperatures, and found that both increased and decreased temperatures result in shorter meiotic chromosome axes and more crossovers. Further investigations showed that temperature changes coordinately enhanced the hyperabundant accumulation of Hop1 and Red1 on chromosomes and the number of Zip3 foci. Most importantly, temperature-induced changes in the distribution of axis proteins and Zip3 foci depend on changes in DNA negative supercoils. These results suggest that yeast meiosis senses temperature changes by increasing the level of negative supercoils to increase crossovers and modulate chromosome organization. These findings provide a new perspective on understanding the effect and mechanism of temperature on meiotic recombination and chromosome organization, with important implications for evolution and breeding.

交叉重组是减数分裂的一个标志,它将父源染色体和母源染色体(同源染色体)结合在一起,使其忠实分离,同时促进后代的遗传多样性。交叉模式主要受减数分裂染色体结构的控制。环境因素,尤其是温度,在调节交叉方面也起着重要作用。然而,目前还不清楚温度是如何影响交叉的。在这里,我们详细研究了不同温度下芽殖酵母轴成分(Red1、Hop1和Rec8)和与交叉相关的Zip3病灶的分布,发现温度升高和降低都会导致减数分裂染色体轴变短和交叉增多。进一步的研究表明,温度变化会协调增强染色体上Hop1和Red1的超量积累以及Zip3病灶的数量。最重要的是,温度诱导的轴蛋白和Zip3病灶分布变化取决于DNA负超螺旋的变化。这些结果表明,酵母减数分裂通过增加负超螺水平来感知温度变化,从而增加交叉和调节染色体组织。这些发现为理解温度对减数分裂重组和染色体组织的影响和机制提供了一个新的视角,对进化和育种具有重要意义。
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引用次数: 0
Whole-genome sequencing identifies novel genes for autism in Chinese trios. 全基因组测序发现中国三胞胎中的自闭症新基因
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-08-07 DOI: 10.1007/s11427-023-2564-8
Suhua Chang, Jia Jia Liu, Yilu Zhao, Tao Pang, Xiangyu Zheng, Zhirui Song, Anyi Zhang, Xuping Gao, Lingxue Luo, Yanqing Guo, Jing Liu, Li Yang, Lin Lu

Autism spectrum disorder (ASD) is a neurodevelopmental disorder with high genetic heritability but heterogeneity. Fully understanding its genetics requires whole-genome sequencing (WGS), but the ASD studies utilizing WGS data in Chinese population are limited. In this study, we present a WGS study for 334 individuals, including 112 ASD patients and their non-ASD parents. We identified 146 de novo variants in coding regions in 85 cases and 60 inherited variants in coding regions. By integrating these variants with an association model, we identified 33 potential risk genes (P<0.001) enriched in neuron and regulation related biological process. Besides the well-known ASD genes (SCN2A, NF1, SHANK3, CHD8 etc.), several high confidence genes were highlighted by a series of functional analyses, including CTNND1, DGKZ, LRP1, DDN, ZNF483, NR4A2, SMAD6, INTS1, and MRPL12, with more supported evidence from GO enrichment, expression and network analysis. We also integrated RNA-seq data to analyze the effect of the variants on the gene expression and found 12 genes in the individuals with the related variants had relatively biased expression. We further presented the clinical phenotypes of the proband carrying the risk genes in both our samples and Caucasian samples to show the effect of the risk genes on phenotype. Regarding variants in non-coding regions, a total of 74 de novo variants and 30 inherited variants were predicted as pathogenic with high confidence, which were mapped to specific genes or regulatory features. The number of de novo variants found in patient was significantly associated with the parents' ages at the birth of the child, and gender with trend. We also identified small de novo structural variants in ASD trios. The results in this study provided important evidence for understanding the genetic mechanism of ASD.

自闭症谱系障碍(ASD)是一种神经发育障碍,具有高度遗传性和异质性。要充分了解其遗传学,需要进行全基因组测序(WGS),但在中国人群中利用 WGS 数据进行的 ASD 研究非常有限。在本研究中,我们对 334 人进行了 WGS 研究,其中包括 112 名 ASD 患者及其非 ASD 父母。我们在 85 个病例中发现了 146 个编码区的从头变异和 60 个编码区的遗传变异。通过将这些变异与关联模型相结合,我们发现了 33 个潜在的风险基因(P
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引用次数: 0
Unveiling potential sex-determining genes and sex-specific markers in autotetraploid Carassius auratus. 揭示自交系鲫鱼的潜在性别决定基因和性别特异性标记。
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-08-09 DOI: 10.1007/s11427-023-2694-5
Kun Zhang, Xu Huang, Chongqing Wang, Xidan Xu, Xiaowei Xu, Xiaoping Dong, Qingwen Xiao, Jinhai Bai, Yue Zhou, Zhengkun Liu, Xinyi Deng, Yan Tang, Siyang Li, Enkui Hu, Wanjing Peng, Ling Xiong, Qinbo Qin, Shaojun Liu

Autotetraploid Carassius auratus is a stable hereditary autotetraploid fish resulting from the hybridization of Carassius auratus red var. (RCC, ♀) × Megalobrama amblycephala (BSB, ♂), containing four sets of RCC chromosomes. However, the molecular mechanism underlying the determination of sex in this species remains largely unknown. Currently, there lacks a full understanding of the molecular mechanisms governing sex determination and specific molecular markers to differentiate sex in this species. In this study, 25,801,677 SNPs (Single-nucleotide polymorphism) and 6,210,306 Indels (insertion-deletion) were obtained from whole-genome resequencing of 100 individuals (including 50 female and 50 male). Further identification confirmed the candidate chromosomes as Chr46B, with the sex-determining region located at Chr46B: 22,500,000-22,800,000 bp. Based on the male-specific insertion (26 bp) within the candidate sex-determining region, a pair of sex-specific molecular markers has been identified. In addition, based on the screening of candidate sex-determining region genes and RT-qPCR validation analysis, ADAM10, AQP9 and tc1a were identified as candidate sex-determining genes. These findings provide a robust foundation for investigating sex determination mechanisms in fish, the evolution of sex chromosomes, and the development of monosex populations.

自四倍体鲫鱼(Carassius auratus)是一种稳定的遗传性自四倍体鱼类,由鲫鱼红变种(Carassius auratus red var., RCC, ♀)×大鳞鲫(Megalobrama amblycephala, BSB, ♂)杂交而成,含有四组RCC染色体。然而,该物种性别决定的分子机制在很大程度上仍然未知。目前,人们对该物种性别决定的分子机制和区分性别的特异性分子标记缺乏全面了解。本研究通过对 100 个个体(包括 50 个雌性个体和 50 个雄性个体)进行全基因组重测序,获得了 25,801,677 个 SNPs(单核苷酸多态性)和 6,210,306 个 Indels(插入缺失)。进一步鉴定确认候选染色体为 Chr46B,性别决定区位于 Chr46B:22,500,000-22,800,000 bp。根据候选性别决定区内的雄性特异性插入(26 bp),确定了一对性别特异性分子标记。此外,根据对候选性别决定区基因的筛选和 RT-qPCR 验证分析,ADAM10、AQP9 和 tc1a 被确定为候选性别决定基因。这些发现为研究鱼类的性别决定机制、性染色体的进化以及单性种群的发展奠定了坚实的基础。
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引用次数: 0
RpL38 modulates germ cell differentiation by controlling Bam expression in Drosophila testis. RpL38通过控制果蝇睾丸中Bam的表达调节生殖细胞分化
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-08-21 DOI: 10.1007/s11427-024-2646-3
Yang Fang, Fengchao Zhang, Fangzhen Zhao, Jiajia Wang, Xinkai Cheng, Fei Ye, Jiayu He, Long Zhao, Ying Su

Switching from mitotic spermatogonia to meiotic spermatocytes is critical to producing haploid sperms during male germ cell differentiation. However, the underlying mechanisms of this switch remain largely unexplored. In Drosophila melanogaster, the gene RpL38 encodes the ribosomal protein L38, one component of the 60S subunit of ribosomes. We found that its depletion in spermatogonia severely diminished the production of mature sperms and thus led to the infertility of male flies. By examining the germ cell differentiation in testes, we found that RpL38-knockdown blocked the transition from spermatogonia to spermatocytes and accumulated spermatogonia in the testis. To understand the intrinsic reason for this blockage, we conducted proteomic analysis for these spermatogonia populations. Differing from the control spermatogonia, the accumulated spermatogonia in RpL38-knockdown testes already expressed many spermatocyte markers but lacked many meiosis-related proteins, suggesting that spermatogonia need to prepare some important proteins for meiosis to complete their switch into spermatocytes. Mechanistically, we found that the expression of bag of marbles (bam), a crucial determinant in the transition from spermatogonia to spermatocytes, was inhibited at both the mRNA and protein levels upon RpL38 depletion. We also confirmed that the bam loss phenocopied RpL38 RNAi in the testis phenotype and transcriptomic profiling. Strikingly, overexpressing bam was able to fully rescue the testis abnormality and infertility of RpL38-knockdown flies, indicating that bam is the key effector downstream of RpL38 to regulate spermatogonia differentiation. Overall, our data suggested that germ cells start to prepare meiosis-related proteins as early as the spermatogonial stage, and RpL38 in spermatogonia is required to regulate their transition toward spermatocytes in a bam-dependent manner, providing new knowledge for our understanding of the transition process from spermatogonia to spermatocytes in Drosophila spermatogenesis.

在雄性生殖细胞分化过程中,从有丝分裂精原细胞到减数分裂精母细胞的转换是产生单倍体精子的关键。然而,这种转换的内在机制在很大程度上仍未得到探索。在黑腹果蝇中,RpL38 基因编码核糖体蛋白 L38,它是核糖体 60S 亚基的一个组成部分。我们发现,精原细胞中该基因的缺失会严重减少成熟精子的产生,从而导致雄蝇不育。通过研究睾丸中生殖细胞的分化,我们发现 RpL38 的敲除阻断了精原细胞向精母细胞的转变,并在睾丸中积累了精原细胞。为了了解这种阻滞的内在原因,我们对这些精原细胞群进行了蛋白质组分析。与对照组精原细胞不同,RpL38敲除后的睾丸中积累的精原细胞已经表达了许多精母细胞标志物,但却缺乏许多减数分裂相关蛋白,这表明精原细胞需要为减数分裂准备一些重要蛋白才能完成向精母细胞的转变。从机理上讲,我们发现精原细胞向精母细胞转变过程中的一个重要决定因素--弹珠袋(bam)的表达在RpL38缺失后的mRNA和蛋白水平上都受到了抑制。我们还证实,在睾丸表型和转录组图谱分析中,bam缺失与RpL38 RNAi表型相同。令人震惊的是,过表达bam能够完全挽救RpL38敲除蝇的睾丸异常和不育,这表明bam是RpL38下游调控精原细胞分化的关键效应物。总之,我们的数据表明,生殖细胞早在精原细胞阶段就开始准备减数分裂相关蛋白,而精原细胞中的RpL38需要以依赖bam的方式调控精原细胞向精母细胞的转变,这为我们了解果蝇精子发生过程中精原细胞向精母细胞的转变过程提供了新的知识。
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引用次数: 0
MSC-mediated mitochondrial transfer restores mitochondrial DNA and function in neural progenitor cells of Leber's hereditary optic neuropathy. 间充质干细胞介导的线粒体转移可恢复勒伯遗传性视神经病变神经祖细胞的线粒体 DNA 和功能。
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-08-08 DOI: 10.1007/s11427-024-2647-8
Rui Wang, Feixiang Bao, Manjiao Lu, Xiaoyun Jia, Jiahui Xiao, Yi Wu, Qingjiong Zhang, Xingguo Liu

Leber's hereditary optic neuropathy (LHON) is a debilitating mitochondrial disease associated with mutations in mitochondrial DNA (mtDNA). Unfortunately, the available treatment options for LHON patients are limited due to challenges in mitochondrial replacement. In our study, we reprogramming LHON urine cells into induced pluripotent stem cells (iPSCs) and differentiating them into neural progenitor cells (NPCs) and neurons for disease modeling. Our research revealed that LHON neurons exhibited significantly higher levels of mtDNA mutations and reduced mitochondrial function, confirming the disease phenotype. However, through co-culturing LHON iPSC-derived NPCs with mesenchymal stem cells (MSCs), we observed a remarkable rescue of mutant mtDNA and a significant improvement in mitochondrial metabolic function in LHON neurons. These findings suggest that co-culturing with MSCs can enhance mitochondrial function in LHON NPCs, even after their differentiation into neurons. This discovery holds promise as a potential therapeutic strategy for LHON patients.

勒伯遗传性视神经病变(LHON)是一种与线粒体 DNA(mtDNA)突变有关的线粒体疾病,会使人衰弱。遗憾的是,由于线粒体替代方面的挑战,LHON 患者的现有治疗方案非常有限。在我们的研究中,我们将LHON尿液细胞重编程为诱导多能干细胞(iPSCs),并将其分化为神经祖细胞(NPCs)和神经元,用于疾病建模。我们的研究发现,LHON神经元的mtDNA突变水平明显较高,线粒体功能降低,证实了疾病的表型。然而,通过将 LHON iPSC 衍生的 NPC 与间充质干细胞(MSCs)共培养,我们观察到 LHON 神经元的突变 mtDNA 得到了明显的挽救,线粒体代谢功能也得到了显著改善。这些研究结果表明,与间充质干细胞共同培养可以增强 LHON 神经元的线粒体功能,即使在它们分化成神经元之后也是如此。这一发现有望成为LHON患者的一种潜在治疗策略。
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引用次数: 0
Huangjing is not only a good medicine but also an affordable healthy diet. 黄精不仅是一味良药,也是一种经济实惠的健康饮食。
IF 8 2区 生物学 Q1 BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-09-27 DOI: 10.1007/s11427-024-2713-1
Donghong Chen, Dun Si, Jingjing Liu, Jinping Si
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引用次数: 0
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