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Axon demyelination and degeneration in a zebrafish spastizin model of hereditary spastic paraplegia. 遗传性痉挛性截瘫斑马鱼痉挛素模型中的轴突脱髓鞘和退化。
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-06 DOI: 10.1098/rsob.240100
Vranda Garg, Selina André, Luisa Heyer, Gudrun Kracht, Torben Ruhwedel, Patricia Scholz, Till Ischebeck, Hauke B Werner, Christian Dullin, Jacob Engelmann, Wiebke Möbius, Martin C Göpfert, Roland Dosch, Bart R H Geurten

Hereditary spastic paraplegias (HSPs) are a diverse set of neurological disorders characterized by progressive spasticity and weakness in the lower limbs caused by damage to the axons of the corticospinal tract. More than 88 genetic mutations have been associated with HSP, yet the mechanisms underlying these disorders are not well understood. We replicated the pathophysiology of one form of HSP known as spastic paraplegia 15 (SPG15) in zebrafish. This disorder is caused in humans by mutations in the ZFYVE26 gene, which codes for a protein called SPASTIZIN. We show that, in zebrafish, the significant reduction of Spastizin caused degeneration of large motor neurons. Motor neuron degeneration is associated with axon demyelination in the spinal cord and impaired locomotion in the spastizin mutants. Our findings reveal that the reduction in Spastizin compromises axonal integrity and affects the myelin sheath, ultimately recapitulating the pathophysiology of HSPs.

遗传性痉挛性截瘫(HSP)是一种多种神经系统疾病,其特征是由于皮质脊髓束轴突受损而导致下肢进行性痉挛和无力。与 HSP 相关的基因突变超过 88 种,但这些疾病的发病机制尚不十分清楚。我们在斑马鱼身上复制了一种被称为痉挛性截瘫 15(SPG15)的 HSP 的病理生理学。这种疾病是由 ZFYVE26 基因突变引起的,该基因编码一种名为 SPASTIZIN 的蛋白质。我们的研究表明,在斑马鱼体内,Spastizin 的显著减少会导致大运动神经元退化。运动神经元变性与脊髓轴突脱髓鞘和 spastizin 突变体的运动障碍有关。我们的研究结果表明,Spastizin的减少会损害轴突的完整性并影响髓鞘,最终重现HSPs的病理生理学。
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引用次数: 0
Correction to: 'The telomeric protein AKTIP interacts with A- and B-type lamins and is involved in regulation of cellular senescence' (2016), by Burla et al. 更正:端粒蛋白 AKTIP 与 A 型和 B 型薄片蛋白相互作用并参与细胞衰老的调控》(2016 年),作者 Burla 等人。
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-13 DOI: 10.1098/rsob.240314
Romina Burla, Mariateresa Carcuro, Mattia La Torre, Federica Fratini, Marco Crescenzi, Maria Rosaria D'Apice, Paola Spitalieri, Grazia Daniela Raffa, Letizia Astrologo, Giovanna Lattanzi, Enrico Cundari, Domenico Raimondo, Annamaria Biroccio, Maurizio Gatti, Isabella Saggio
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引用次数: 0
Mathematical model of RNA-directed DNA methylation predicts tuning of negative feedback required for stable maintenance. RNA 引导的 DNA 甲基化数学模型预测了稳定维持所需的负反馈调整。
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-13 DOI: 10.1098/rsob.240159
Renee Dale, Rebecca Mosher

RNA-directed DNA methylation (RdDM) is a plant-specific de novo methylation pathway that is responsible for maintenance of asymmetric methylation (CHH, H = A, T or G) in euchromatin. Loci with CHH methylation produce 24 nucleotide (nt) short interfering (si) RNAs. These siRNAs direct additional CHH methylation to the locus, maintaining methylation states through DNA replication. To understand the necessary conditions to produce stable methylation, we developed a stochastic mathematical model of RdDM. The model describes DNA target search by siRNAs derived from CHH methylated loci bound by an Argonaute. Methylation reinforcement occurs either throughout the cell cycle (steady) or immediately following replication (bursty). We compare initial and final methylation distributions to determine simulation conditions that produce stable methylation. We apply this method to the low CHH methylation case. The resulting model predicts that siRNA production must be linearly proportional to methylation levels, that bursty reinforcement is more stable and that slightly higher levels of siRNA production are required for searching DNA, compared to RNA. Unlike CG methylation, which typically exhibits bi-modality with loci having either 100% or 0% methylation, CHH methylation exists across a range. Our model predicts that careful tuning of the negative feedback in the system is required to enable stable maintenance.

RNA 引导的 DNA 甲基化(RdDM)是一种植物特异的从头甲基化途径,负责维持外染色质中的不对称甲基化(CHH,H = A、T 或 G)。具有 CHH 甲基化的基因座会产生 24 个核苷酸(nt)的短干扰(si)RNA。这些 siRNA 将额外的 CHH 甲基化引导至基因座,通过 DNA 复制维持甲基化状态。为了了解产生稳定甲基化的必要条件,我们建立了一个 RdDM 随机数学模型。该模型描述了由 Argonaute 结合的来自 CHH 甲基化基因座的 siRNA 的 DNA 目标搜索。甲基化强化发生在整个细胞周期(稳定)或复制后立即发生(突发性)。我们比较了初始和最终甲基化分布,以确定产生稳定甲基化的模拟条件。我们将这种方法应用于低 CHH 甲基化情况。由此得出的模型预测,siRNA 的产生必须与甲基化水平成线性比例,突发性强化更为稳定,与 RNA 相比,搜索 DNA 所需的 siRNA 产生水平略高。CG 甲基化通常表现为双模式,即基因位点的甲基化程度要么为 100%,要么为 0%,而 CHH 甲基化则不同,存在一定的范围。我们的模型预测,需要对系统中的负反馈进行仔细调整,以实现稳定的维持。
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引用次数: 0
Cebpa is required for haematopoietic stem and progenitor cell generation and maintenance in zebrafish. 斑马鱼造血干细胞和祖细胞的生成和维持需要 Cebpa。
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-06 DOI: 10.1098/rsob.240215
Kemin Chen, Jieyi Wu, Yuxian Zhang, Wei Liu, Xiaohui Chen, Wenqing Zhang, Zhibin Huang

The CCAAT enhancer binding protein alpha (CEBPA) is crucial for myeloid differentiation and the balance of haematopoietic stem and progenitor cell (HSPC) quiescence and self-renewal, and its dysfunction can drive leukemogenesis. However, its role in HSPC generation has not been fully elucidated. Here, we utilized various zebrafish cebpa mutants to investigate the function of Cebpa in the HSPC compartment. Co-localization analysis showed that cebpa expression is enriched in nascent HSPCs. Complete loss of Cebpa function resulted in a significant reduction in early HSPC generation and the overall HSPC pool during embryonic haematopoiesis. Interestingly, while myeloid differentiation was impaired in cebpa N-terminal mutants expressing the truncated zP30 protein, the number of HSPCs was not affected, indicating a redundant role of Cebpa P42 and P30 isoforms in HSPC development. Additionally, epistasis experiments confirmed that Cebpa functions downstream of Runx1 to regulate HSPC emergence. Our findings uncover a novel role of Cebpa isoforms in HSPC generation and maintenance, and provide new insights into HSPC development.

CCAAT增强子结合蛋白α(CEBPA)对于髓系分化以及造血干细胞和祖细胞(HSPC)的静止和自我更新的平衡至关重要,其功能障碍可导致白血病的发生。然而,它在 HSPC 生成中的作用尚未完全阐明。在这里,我们利用各种斑马鱼 cebpa 突变体来研究 Cebpa 在 HSPC 区系中的功能。共定位分析表明,cebpa的表达富集在新生的HSPC中。Cebpa 功能的完全丧失导致胚胎造血过程中早期 HSPC 的生成和整个 HSPC 池的显著减少。有趣的是,在表达截短的 zP30 蛋白的 cebpa N 端突变体中,虽然髓系分化受损,但 HSPC 的数量却不受影响,这表明 Cebpa P42 和 P30 同工酶在 HSPC 发育中起着多余的作用。此外,外显子实验证实,Cebpa 在 Runx1 的下游发挥作用,调控 HSPC 的出现。我们的发现揭示了 Cebpa 同工酶在 HSPC 生成和维持中的新作用,并为 HSPC 的发育提供了新的见解。
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引用次数: 0
Linking planar polarity signalling to actomyosin contractility during vertebrate neurulation. 将脊椎动物神经形成过程中的平面极性信号与肌动蛋白收缩性联系起来
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-20 DOI: 10.1098/rsob.240251
Sarka Novotna, Lorena Agostini Maia, Katarzyna Anna Radaszkiewicz, Pavel Roudnicky, Jakub Harnos

Actomyosin contractility represents an ancient feature of eukaryotic cells participating in many developmental and homeostasis events, including tissue morphogenesis, muscle contraction and cell migration, with dysregulation implicated in various pathological conditions, such as cancer. At the molecular level, actomyosin comprises actin bundles and myosin motor proteins that are sensitive to posttranslational modifications like phosphorylation. While the molecular components of actomyosin are well understood, the coordination of contractility by extracellular and intracellular signals, particularly from cellular signalling pathways, remains incompletely elucidated. This study focuses on WNT/planar cell polarity (PCP) signalling, previously associated with actomyosin contractility during vertebrate neurulation. Our investigation reveals that the main cytoplasmic PCP proteins, Prickle and Dishevelled, interact with key actomyosin components such as myosin light chain 9 (MLC9), leading to its phosphorylation and localized activation. Using proteomics and microscopy approaches, we demonstrate that both PCP proteins actively control actomyosin contractility through Rap1 small GTPases in relevant in vitro and in vivo models. These findings unveil a novel mechanism of how PCP signalling regulates actomyosin contractility through MLC9 and Rap1 that is relevant to vertebrate neurulation.

肌动蛋白收缩性是真核细胞的一个古老特征,它参与了许多发育和稳态事件,包括组织形态发生、肌肉收缩和细胞迁移,其失调与癌症等各种病理状况有关。在分子水平上,肌动蛋白由肌动蛋白束和肌动蛋白马达蛋白组成,这些蛋白对磷酸化等翻译后修饰非常敏感。虽然人们对肌动蛋白的分子成分有了很好的了解,但细胞外和细胞内信号,特别是来自细胞信号通路的信号对收缩力的协调作用仍未完全阐明。本研究的重点是 WNT/平面细胞极性(PCP)信号传导,它以前与脊椎动物神经形成过程中的肌动蛋白收缩性有关。我们的研究发现,主要的细胞质 PCP 蛋白 Prickle 和 Dishevelled 与肌球蛋白的关键成分(如肌球蛋白轻链 9 (MLC9))相互作用,导致其磷酸化和定位激活。我们利用蛋白质组学和显微镜方法证明,在相关的体外和体内模型中,这两种 PCP 蛋白通过 Rap1 小 GTP 酶积极控制肌动蛋白的收缩性。这些发现揭示了 PCP 信号如何通过 MLC9 和 Rap1 调控肌动蛋白收缩性的新机制,该机制与脊椎动物的神经调节有关。
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引用次数: 0
Learning-induced remodelling of inhibitory synapses in the motor cortex. 学习诱导的运动皮层抑制性突触重塑
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-13 DOI: 10.1098/rsob.240109
Nishita Bhembre, Annalisa Paolino, Sooraj S Das, Sumasri Guntupalli, Laura R Fenlon, Victor Anggono

Robust structural and functional plasticity occurs at excitatory synapses in the motor cortex in response to learning. It is well established that local spinogenesis and the subsequent maintenance of newly formed spines are crucial for motor learning. However, despite local synaptic inhibition being essential for shaping excitatory synaptic input, less is known about the structural rearrangement of inhibitory synapses following learning. In this study, we co-expressed the structural marker tdTomato and a mEmerald-tagged intrabody against gephyrin to visualize inhibitory synapses in layer 2/3 cortical neurons of wild-type CD1 mice. We found that a 1-day accelerated rotarod paradigm induced robust motor learning in male and female adult CD1 mice. Histological analyses revealed a significant increase in the surface area of gephyrin puncta in neurons within the motor cortex but not in the somatosensory cortex upon motor learning. Furthermore, this learning-induced reorganization of inhibitory synapses only occurred in dendritic shafts and not in the spines. These data suggest that learning induces experience-dependent remodelling of existing inhibitory synapses to fine-tune intrinsic plasticity and input-specific modulation of excitatory connections in the motor cortex.

运动皮层中的兴奋性突触在学习过程中会产生强大的结构和功能可塑性。局部棘突生成和随后新形成棘突的维持对运动学习至关重要,这一点已得到公认。然而,尽管局部突触抑制对形成兴奋性突触输入至关重要,但人们对学习后抑制性突触的结构重排却知之甚少。在这项研究中,我们共同表达了结构标记物tdTomato和mEmerald标记的抗ephyrin内体,以观察野生型CD1小鼠2/3层皮层神经元的抑制性突触。我们发现,为期1天的加速转体范式能诱导雄性和雌性成年CD1小鼠进行强健的运动学习。组织学分析表明,在运动学习过程中,运动皮层神经元的ephyrin点表面积显著增加,而体感皮层神经元的ephyrin点表面积则没有增加。此外,这种学习诱导的抑制性突触重组只发生在树突轴而不是棘突上。这些数据表明,学习会诱导对现有抑制性突触进行经验依赖性重塑,以微调运动皮层中兴奋性连接的内在可塑性和输入特异性调节。
{"title":"Learning-induced remodelling of inhibitory synapses in the motor cortex.","authors":"Nishita Bhembre, Annalisa Paolino, Sooraj S Das, Sumasri Guntupalli, Laura R Fenlon, Victor Anggono","doi":"10.1098/rsob.240109","DOIUrl":"10.1098/rsob.240109","url":null,"abstract":"<p><p>Robust structural and functional plasticity occurs at excitatory synapses in the motor cortex in response to learning. It is well established that local spinogenesis and the subsequent maintenance of newly formed spines are crucial for motor learning. However, despite local synaptic inhibition being essential for shaping excitatory synaptic input, less is known about the structural rearrangement of inhibitory synapses following learning. In this study, we co-expressed the structural marker tdTomato and a mEmerald-tagged intrabody against gephyrin to visualize inhibitory synapses in layer 2/3 cortical neurons of wild-type CD1 mice. We found that a 1-day accelerated rotarod paradigm induced robust motor learning in male and female adult CD1 mice. Histological analyses revealed a significant increase in the surface area of gephyrin puncta in neurons within the motor cortex but not in the somatosensory cortex upon motor learning. Furthermore, this learning-induced reorganization of inhibitory synapses only occurred in dendritic shafts and not in the spines. These data suggest that learning induces experience-dependent remodelling of existing inhibitory synapses to fine-tune intrinsic plasticity and input-specific modulation of excitatory connections in the motor cortex.</p>","PeriodicalId":19629,"journal":{"name":"Open Biology","volume":"14 11","pages":"240109"},"PeriodicalIF":4.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142623536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Pck2 association with the plasma membrane and efficient response of the cell integrity pathway require regulation of PI4P homeostasis by exomer. Pck2 与质膜的结合以及细胞完整性途径的高效响应需要外显子对 PI4P 平衡的调节。
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-13 DOI: 10.1098/rsob.240101
Esteban Moscoso-Romero, Sandra Moro, Alicia Duque, Francisco Yanguas, M-Henar Valdivieso

Exomer is a protein complex that facilitates trafficking between the Golgi and the plasma membrane (PM). Schizosaccharomyces pombe exomer is composed of Cfr1 and Bch1, and we have found that full activation of the cell integrity pathway (CIP) in response to osmotic stress requires exomer. In the wild-type, the CIP activators Rgf1 (Rho1 GEF) and Pck2 (PKC homologue) and the MEK kinase Mkh1 localize in the PM, internalize after osmotic shock and re-localize after adaptation. This re-localization is inefficient in exomer mutants. Overexpression of the PM-associated 1-phosphatidylinositol 4-kinase stt4+, and deletion of the nem1+ phosphatase suppress the defects in Pck2 dynamics in exomer mutants, but not their defect in CIP activation, demonstrating that exomer regulates CIP in additional ways. Exomer mutants accumulate PI4P in the TGN, and increasing the expression of the Golgi-associated 1-phosphatidylinositol 4-kinase pik1+ suppresses their defect in Pck2 dynamics. These findings suggest that efficient PI4P transport from the Golgi to the PM requires exomer. Mutants lacking clathrin adaptors are defective in CIP activation, but not in Pck2 dynamics or in PI4P accumulation in the Golgi. Hence, traffic from the Golgi regulates CIP activation, and exomer participates in this regulation through an exclusive mechanism.

Exomer是一种蛋白质复合物,可促进高尔基体和质膜(PM)之间的转运。我们发现,细胞完整性通路(CIP)在应对渗透压时的完全激活需要外泌体。在野生型中,CIP 激活因子 Rgf1(Rho1 GEF)和 Pck2(PKC 同源物)以及 MEK 激酶 Mkh1 定位于 PM 中,在受到渗透压冲击后内化,并在适应后重新定位。在外显子突变体中,这种重新定位的效率很低。PM 相关的 1-磷脂酰肌醇 4- 激酶 stt4+ 的过表达和 nem1+ 磷酸酶的缺失抑制了外显子突变体中 Pck2 动态的缺陷,但没有抑制其 CIP 激活的缺陷,这表明外显子以其他方式调节 CIP。外显子突变体在 TGN 中积累 PI4P,增加与高尔基相关的 1-磷脂酰肌醇 4- 激酶 pik1+ 的表达可抑制其 Pck2 动力学缺陷。这些发现表明,PI4P 从高尔基体向 PM 的高效运输需要外泌体。缺乏凝集素适配体的突变体在 CIP 激活方面存在缺陷,但在高尔基体中的 Pck2 动态或 PI4P 积累方面没有缺陷。因此,来自高尔基体的运输调节了CIP的激活,而外泌体通过一种排他性机制参与了这种调节。
{"title":"Pck2 association with the plasma membrane and efficient response of the cell integrity pathway require regulation of PI4P homeostasis by exomer.","authors":"Esteban Moscoso-Romero, Sandra Moro, Alicia Duque, Francisco Yanguas, M-Henar Valdivieso","doi":"10.1098/rsob.240101","DOIUrl":"10.1098/rsob.240101","url":null,"abstract":"<p><p>Exomer is a protein complex that facilitates trafficking between the Golgi and the plasma membrane (PM). <i>Schizosaccharomyces pombe</i> exomer is composed of Cfr1 and Bch1, and we have found that full activation of the cell integrity pathway (CIP) in response to osmotic stress requires exomer. In the wild-type, the CIP activators Rgf1 (Rho1 GEF) and Pck2 (PKC homologue) and the MEK kinase Mkh1 localize in the PM, internalize after osmotic shock and re-localize after adaptation. This re-localization is inefficient in exomer mutants. Overexpression of the PM-associated 1-phosphatidylinositol 4-kinase <i>stt4+</i>, and deletion of the <i>nem1+</i> phosphatase suppress the defects in Pck2 dynamics in exomer mutants, but not their defect in CIP activation, demonstrating that exomer regulates CIP in additional ways. Exomer mutants accumulate PI4P in the TGN, and increasing the expression of the Golgi-associated 1-phosphatidylinositol 4-kinase <i>pik1+</i> suppresses their defect in Pck2 dynamics. These findings suggest that efficient PI4P transport from the Golgi to the PM requires exomer. Mutants lacking clathrin adaptors are defective in CIP activation, but not in Pck2 dynamics or in PI4P accumulation in the Golgi. Hence, traffic from the Golgi regulates CIP activation, and exomer participates in this regulation through an exclusive mechanism.</p>","PeriodicalId":19629,"journal":{"name":"Open Biology","volume":"14 11","pages":"240101"},"PeriodicalIF":4.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142623669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SID-2 is a conserved extracellular vesicle protein that is not associated with environmental RNAi in parasitic nematodes. SID-2 是一种保守的细胞外囊泡蛋白,与寄生线虫的环境 RNAi 无关。
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-06 DOI: 10.1098/rsob.240190
Frances Blow, Kate Jeffrey, Franklin Wang-Ngai Chow, Inna A Nikonorova, Maureen M Barr, Atlanta G Cook, Bram Prevo, Dhanya K Cheerambathur, Amy H Buck

In the free-living nematode Caenorhabditis elegans, the transmembrane protein SID-2 imports double-stranded RNA into intestinal cells to trigger systemic RNA interference (RNAi), allowing organisms to sense and respond to environmental cues such as the presence of pathogens. This process, known as environmental RNAi, has not been observed in the most closely related parasites that are also within clade V. Previous sequence-based searches failed to identify sid-2 orthologues in available clade V parasite genomes. In this study, we identified sid-2 orthologues in these parasites using genome synteny and protein structure-based comparison, following identification of a SID-2 orthologue in extracellular vesicles from the murine intestinal parasitic nematode Heligmosomoides bakeri. Expression of GFP-tagged H. bakeri SID-2 in C. elegans showed similar localization to the intestinal apical membrane as seen for GFP-tagged C. elegans SID-2, and further showed mobility in intestinal cells in vesicle-like structures. We tested the capacity of H. bakeri SID-2 to functionally complement environmental RNAi in a C. elegans SID-2 null mutant and show that H. bakeri SID-2 does not rescue the phenotype in this context. Our work identifies SID-2 as a highly abundant EV protein whose ancestral function may be unrelated to environmental RNAi, and rather highlights an association with extracellular vesicles in nematodes.

在自由生活的线虫秀丽隐杆线虫(Caenorhabditis elegans)中,跨膜蛋白SID-2将双链RNA导入肠细胞,引发系统性RNA干扰(RNAi),使生物体能够感知环境线索(如病原体的存在)并做出反应。这一过程被称为环境 RNAi,但在同属 V 支系的关系最密切的寄生虫中却未观察到这一过程。在本研究中,我们利用基因组同源性和基于蛋白质结构的比较,在小鼠肠道寄生线虫 Heligmosomoides bakeri 的细胞外囊泡中发现了 SID-2 的同源物,从而确定了这些寄生虫中的 sid-2 同源物。在 elegans 中表达 GFP 标记的 H. bakeri SID-2,显示出与 GFP 标记的 C. elegans SID-2 相似的在肠顶端膜的定位,并进一步显示出在肠细胞中囊泡状结构的流动性。我们测试了H. bakeri SID-2对 elegans SID-2缺失突变体中环境RNAi的功能补充能力,结果表明H. bakeri SID-2并不能在这种情况下挽救表型。我们的研究发现,SID-2是一种高含量的EV蛋白,其祖先的功能可能与环境RNAi无关,而是强调了它与线虫细胞外囊泡的联系。
{"title":"SID-2 is a conserved extracellular vesicle protein that is not associated with environmental RNAi in parasitic nematodes.","authors":"Frances Blow, Kate Jeffrey, Franklin Wang-Ngai Chow, Inna A Nikonorova, Maureen M Barr, Atlanta G Cook, Bram Prevo, Dhanya K Cheerambathur, Amy H Buck","doi":"10.1098/rsob.240190","DOIUrl":"10.1098/rsob.240190","url":null,"abstract":"<p><p>In the free-living nematode <i>Caenorhabditis elegans,</i> the transmembrane protein SID-2 imports double-stranded RNA into intestinal cells to trigger systemic RNA interference (RNAi), allowing organisms to sense and respond to environmental cues such as the presence of pathogens. This process, known as environmental RNAi, has not been observed in the most closely related parasites that are also within clade V. Previous sequence-based searches failed to identify <i>sid-2</i> orthologues in available clade V parasite genomes. In this study, we identified <i>sid-2</i> orthologues in these parasites using genome synteny and protein structure-based comparison, following identification of a SID-2 orthologue in extracellular vesicles from the murine intestinal parasitic nematode <i>Heligmosomoides bakeri</i>. Expression of GFP-tagged <i>H. bakeri</i> SID-2 in <i>C. elegans</i> showed similar localization to the intestinal apical membrane as seen for GFP-tagged <i>C. elegans</i> SID-2, and further showed mobility in intestinal cells in vesicle-like structures. We tested the capacity of <i>H. bakeri</i> SID-2 to functionally complement environmental RNAi in a <i>C. elegans</i> SID-2 null mutant and show that <i>H. bakeri</i> SID-2 does not rescue the phenotype in this context. Our work identifies SID-2 as a highly abundant EV protein whose ancestral function may be unrelated to environmental RNAi, and rather highlights an association with extracellular vesicles in nematodes.</p>","PeriodicalId":19629,"journal":{"name":"Open Biology","volume":"14 11","pages":"240190"},"PeriodicalIF":4.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11538922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Ultrastructural features of psychological stress resilience in the brain: a microglial perspective. 大脑心理压力复原力的超微结构特征:小胶质细胞视角。
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-20 DOI: 10.1098/rsob.240079
Fernando González Ibáñez, Jared VanderZwaag, Jessica Deslauriers, Marie-Ève Tremblay

Psychological stress is the major risk factor for major depressive disorder. Sustained stress causes changes in behaviour, brain connectivity and in its cells and organelles. Resilience to stress is understood as the ability to recover from stress in a positive way or the resistance to the negative effects of psychological stress. Microglia, the resident immune cells of the brain, are known players of stress susceptibility, but less is known about their role in stress resilience and the cellular changes involved. Ultrastructural analysis has been a useful tool in the study of microglia and their function across contexts of health and disease. Despite increased access to electron microscopy, the interpretation of electron micrographs remains much less accessible. In this review, we will first present microglia and the concepts of psychological stress susceptibility and resilience. Afterwards, we will describe ultrastructural analysis, notably of microglia, as a readout to study the mechanisms underlying psychological stress resilience. Lastly, we will cover nutritional ketosis as a therapeutic intervention that was shown to be effective in promoting psychological stress resilience as well as modifying microglial function and ultrastructure.

心理压力是导致重度抑郁症的主要风险因素。持续的压力会导致行为、大脑连接及其细胞和细胞器发生变化。对压力的复原力被理解为以积极的方式从压力中恢复的能力或抵抗心理压力负面影响的能力。小胶质细胞是大脑中的常驻免疫细胞,是已知的压力易感性的参与者,但人们对它们在压力恢复能力中的作用以及所涉及的细胞变化却知之甚少。超微结构分析一直是研究小胶质细胞及其在健康和疾病环境中的功能的有用工具。尽管使用电子显微镜的机会越来越多,但对电子显微图像的解读却仍然不那么容易。在这篇综述中,我们将首先介绍小胶质细胞以及心理压力易感性和恢复力的概念。随后,我们将介绍超微结构分析,特别是小胶质细胞的超微结构分析,以此作为研究心理压力复原力的基础机制的一种读出方法。最后,我们将介绍营养酮病作为一种治疗干预措施,在促进心理压力复原力以及改变小胶质细胞功能和超微结构方面的有效性。
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引用次数: 0
An endoplasmic reticulum localized acetyl-CoA transporter is required for efficient fatty acid synthesis in Toxoplasma gondii. 弓形虫体内脂肪酸的高效合成需要内质网定位的乙酰-CoA 转运体。
IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-11-13 DOI: 10.1098/rsob.240184
Biyun Qin, Bolin Fan, Yazhou Li, Yidan Wang, Bang Shen, Ningbo Xia

Toxoplasma gondii is an obligate intracellular parasite that can infect humans and diverse animals. Fatty acids are critical for the growth and proliferation of T. gondii, which has at least two pathways to synthesize fatty acids, including the type II de novo synthesis pathway in the apicoplast and the elongation pathway in the endoplasmic reticulum (ER). Acetyl-CoA is the key substrate for both fatty acid synthesis pathways. In the apicoplast, acetyl-CoA is mainly provided by the pyruvate dehydrogenase complex. However, how the ER acquires acetyl-CoA is not fully understood. Here, we identified a putative acetyl-CoA transporter (TgAT1) that localized to the ER of T. gondii. Deletion of TgAT1 impaired parasite growth and invasion in vitro and attenuated tachyzoite virulence in vivo. Metabolic tracing using 13C-acetate found that loss of TgAT1 reduced the incorporation of 13C into certain fatty acids, suggesting reduced activities of elongation. Truncation of AT1 was previously reported to confer resistance to the antimalarial compound GNF179 in Plasmodium falciparum. Interestingly, GNF179 had much weaker inhibitory effect on Toxoplasma than on Plasmodium. In addition, deletion of AT1 did not affect the susceptibility of Toxoplasma to GNF179, suggesting that this compound might be taken up differently or has different inhibitory mechanisms in these parasites. Together, our data show that TgAT1 has important roles for parasite growth and fatty acid synthesis, but its disruption does not confer GNF179 resistance in T. gondii.

弓形虫是一种可感染人类和各种动物的细胞内寄生虫。脂肪酸对弓形虫的生长和增殖至关重要,弓形虫至少有两条合成脂肪酸的途径,包括在细胞顶质中的 II 型从头合成途径和在内质网(ER)中的延伸途径。乙酰-CoA 是这两种脂肪酸合成途径的关键底物。在细胞质中,乙酰-CoA 主要由丙酮酸脱氢酶复合体提供。然而,人们对 ER 如何获得乙酰-CoA 并不完全清楚。在这里,我们发现了一个定位在淋球菌ER的推定乙酰-CoA转运体(TgAT1)。TgAT1的缺失会影响寄生虫在体外的生长和侵袭,并削弱其在体内的毒力。利用 13C 乙酸进行的代谢追踪发现,TgAT1 的缺失减少了某些脂肪酸中 13C 的掺入,这表明延伸活动减少。以前曾有报道称,AT1的截短会使恶性疟原虫对抗疟化合物GNF179产生抗药性。有趣的是,GNF179 对弓形虫的抑制作用比对疟原虫弱得多。此外,AT1的缺失并不影响弓形虫对GNF179的敏感性,这表明这种化合物在这些寄生虫体内的吸收方式或抑制机制可能不同。总之,我们的数据表明,TgAT1 对寄生虫的生长和脂肪酸合成具有重要作用,但破坏它并不会使弓形虫对 GNF179 产生抗药性。
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