Mitochondrion最新文献_第2页

Sex-dependent adaptations in heart mitochondria from transgenic mice overexpressing cytochrome b5 reductase-3 过表达细胞色素b5还原酶-3的转基因小鼠心脏线粒体的性别依赖性适应。

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2025-01-09 DOI: 10.1016/j.mito.2025.102004

Luz Marina Sánchez-Mendoza , José A. González-Reyes , Sandra Rodríguez-López , Miguel Calvo-Rubio , Pilar Calero-Rodríguez , Rafael de Cabo , M. Isabel Burón , José M. Villalba

Summary

Cytochrome b₅ reductase 3 (CYB5R3) overexpression upregulates mitochondrial biogenesis, function, and abundance in skeletal muscle and kidneys, and mimics some of the salutary effects of calorie restriction, with the most striking effects being observed in females. We aimed to investigate the mitochondrial adaptations prompted by CYB5R3 overexpression in the heart, an organ surprisingly overlooked in studies focused on this long-lived transgenic model despite the critical role played by CYB5R3 in supporting cardiomyocytes mitochondrial respiration. Given that CYB5R3 effects have been found to be sex-dependent, we focused our research on both males and females. CYB5R3 was efficiently overexpressed in cardiac tissue from transgenic mice, without any difference between sexes. The abundance of electron transport chain complexes markers and cytochrome c was higher in males than in females. CYB5R3 overexpression downregulated the levels of complexes markers in males but not females, without decreasing oxygen consumption capacity. CYB5R3 increased the size and abundance of cardiomyocytes mitochondria, and reduced thickness and preserved the length of mitochondria-endoplasmic reticulum contact sites in heart from males but not females. Metabolic changes were also highlighted in transgenic mice, with an upregulation of fatty acid oxidation markers, particularly in males. Our results support that CYB5R3 overexpression upregulates markers consistent with enhanced mitochondrial function in the heart, producing most of these actions in males, with illustrates the complexity of the CYB5R3-overexpressing transgenic model.

细胞色素b5还原酶3 （CYB5R3）过表达上调骨骼肌和肾脏的线粒体生物发生、功能和丰度，并模仿卡路里限制的一些有益效果，在女性中观察到最显著的效果。我们的目的是研究CYB5R3在心脏中的过表达引发的线粒体适应，尽管CYB5R3在支持心肌细胞线粒体呼吸中发挥着关键作用，但令人惊讶的是，在关注这种长寿转基因模型的研究中，CYB5R3却被忽视了。鉴于CYB5R3的影响是性别依赖的，我们将研究重点放在了男性和女性身上。CYB5R3在转基因小鼠心脏组织中高效过表达，无性别差异。电子传递链复合物、标记物和细胞色素c的丰度在雄性中高于雌性。CYB5R3过表达下调了雄性复合物标记物的水平，而雌性没有，但不降低氧气消耗能力。CYB5R3增加了雄性心肌细胞线粒体的大小和丰度，减少了线粒体-内质网接触点的厚度，保留了线粒体-内质网接触点的长度，而雌性心肌细胞没有。代谢变化在转基因小鼠中也很突出，脂肪酸氧化标记上调，尤其是在雄性小鼠中。我们的研究结果支持CYB5R3过表达上调与心脏线粒体功能增强一致的标记，在男性中产生大部分这些作用，并说明CYB5R3过表达转基因模型的复杂性。

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引用次数: 0

Yeast Dnm1G178R causes altered organelle dynamics and sheds light on the human DRP1G149R disease mechanism 酵母Dnm1G178R引起细胞器动力学改变，揭示了人类DRP1G149R疾病机制。

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2025-01-07 DOI: 10.1016/j.mito.2025.102006

Ankita Adhikary, Vivian Francis Joseph, Riddhi Banerjee , Shirisha Nagotu

Mitochondrial morphology is a result of regulated opposite events called fission and fusion and requires the GTPase, dynamin-related protein 1 (DRP1/Dnm1), or its homologs. A recent clinical report identified a heterozygous missense mutation in the human DRP1 that replaces Glycine (G) 149 with Arginine (R) and results in debilitating conditions in the patient. In this study, we mimicked this mutation in yeast Dnm1 (G178R) and investigated the impact of the pathogenic mutation on the protein’s function. We provide evidence that the substitution of G with R in the G3 motif of the GTPase domain, renders the protein non-functional and in a dominant-negative way. The mutation hampers the distribution, localization, and function of the protein. Cells expressing the mutant variant exhibit a block in mitochondrial fission and altered peroxisome morphology and number.

线粒体形态是被称为裂变和融合的调控相反事件的结果，需要GTPase，动力蛋白相关蛋白1 （DRP1/Dnm1）或其同源物。最近的一份临床报告发现，人类DRP1中存在杂合错义突变，该突变将甘氨酸(G) 149替换为精氨酸(R)，并导致患者身体虚弱。在这项研究中，我们在酵母Dnm1 （G178R）中模拟了这种突变，并研究了致病性突变对蛋白质功能的影响。我们提供的证据表明，GTPase结构域G3基序中的R取代G，使蛋白质以显性负性方式无功能。突变阻碍了蛋白质的分布、定位和功能。表达突变变体的细胞在线粒体裂变中受阻，并表现出过氧化物酶体形态和数量的改变。

引用次数: 0

Reactive oxygen species favors Varicellovirus bovinealpha 5 (BoAHV-5) replication in neural cells 活性氧有利于牛痘病毒5 （BoAHV-5）在神经细胞中的复制。

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2025-01-06 DOI: 10.1016/j.mito.2025.102005

Juan José Rosales , María Belén Brunner , Marcelo Rodríguez , Maia Marin , Eduardo Néstor Maldonado , Sandra Pérez

Varicellovirus bovinealpha (BoAHV) 1 and 5 are closely related neurotropic alphaherpesviruses with distinct neuropathogenic potential. BoAHV-5 causes meningoencephalitis in calves whereas encephalitis by BoAHV-1 infection is sporadic. the mechanisms underlying the differences in tropism and clinical outcomes of the infections are not yet completely understood. Here, we used neuroblastoma SH-SY5Y cells as non-differentiated in comparison with the SH-SY5Y neuronal-like cells obtained after exposing SH-SY5Y undifferentiated cells to trans-retinoic acid. We aimed to establish whether there was a relationship between the production of reactive oxygen species (ROS) and the kinetics of virus replication. We demonstrated that ROS production after BoAHV infection was higher in differentiated cells. Generation of ROS was also dependent on the infecting BoAHV strain. Higher ROS levels were produced during BoAHV-5 infection concomitantly with enhanced viral replication. We propose that increased ROS production mechanistically contributes to the tissue damage and neuroinflammation induced by BoAHV-5 infection. Future studies will determine specific targets of ROS that mediate the effects on viral replication.

牛α水痘病毒（BoAHV） 1和5是密切相关的嗜神经型α疱疹病毒，具有明显的神经致病性。BoAHV-5引起小牛脑膜脑炎，而由BoAHV-1感染的脑炎是散发的。感染的倾向和临床结果差异的机制尚不完全清楚。在这里，我们使用未分化的神经母细胞瘤SH-SY5Y细胞与将未分化的SH-SY5Y细胞暴露于反式维甲酸后获得的SH-SY5Y神经元样细胞进行比较。我们的目的是确定活性氧（ROS）的产生与病毒复制动力学之间是否存在关系。我们证明了BoAHV感染后分化细胞中ROS的产生更高。ROS的产生也依赖于感染BoAHV菌株。BoAHV-5感染期间ROS水平升高，同时病毒复制增强。我们认为活性氧的增加在机制上有助于BoAHV-5感染引起的组织损伤和神经炎症。未来的研究将确定ROS介导病毒复制的具体靶标。

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引用次数: 0

Pyridoxal-5-phosphate mitigates age-related metabolic imbalances in the rat heart through the H2S/AKT/GSK3β signaling axis 吡哆醛-5-磷酸通过H2S/AKT/GSK3β信号轴减轻大鼠心脏年龄相关的代谢失衡。

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2025-01-02 DOI: 10.1016/j.mito.2024.102001

Nataliia A. Strutynska , Volodymyr V. Balatskyi , Ruslan B. Strutynskyi , Yulia V. Goshovska , Lidiia A. Mys , Alina Yu. Luchkova , Maiia V. Denysova , Yuliia P. Korkach , Vladyslav R. Strutynskyi , Oksana O. Piven , Pawel Dobrzyn , Vadym F. Sagach

Pyridoxal-5-phosphate (PLP) enhances the synthesis of endogenous hydrogen sulfide, a potent regulator of cell metabolism. We used 24-month-old rats to investigate the PLP mitoprotective function in the aging heart. We demonstrated improvement of mitochondrial bioenergetic functions, inhibition of mPTP opening after PLP administration. Moreover, PLP treatment increased glucose consumption and utilization, decreased lipid transport into the cells, but increased fatty acid β-oxidation, providing sufficient energy. An ECG study showed a significant improvement in cardiac function in PLP-treated old rats. Our data suggest that PLP may exert its effect through the H₂S/AKT/GSK3β axis with further targeting of the Sirt1/PGC-1α signaling pathway.

吡哆醛-5-磷酸（PLP）促进内源性硫化氢的合成，硫化氢是细胞代谢的有效调节剂。我们用24月龄大鼠研究PLP对衰老心脏的有丝分裂保护作用。我们证明了PLP给药后线粒体生物能量功能的改善，mPTP开放的抑制。此外，PLP处理增加了葡萄糖的消耗和利用，减少了脂质向细胞的转运，但增加了脂肪酸β-氧化，提供了足够的能量。心电图研究显示，plp治疗的老年大鼠心功能有显著改善。我们的数据表明，PLP可能通过H2S/AKT/GSK3β轴发挥作用，并进一步靶向Sirt1/PGC-1α信号通路。

引用次数: 0

The role of mitochondrial DNA variants and dysfunction in the pathogenesis and progression of multiple sclerosis 线粒体DNA变异和功能障碍在多发性硬化症发病和进展中的作用。

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2024-12-26 DOI: 10.1016/j.mito.2024.102002

Ramyar Rahimi Darehbagh , Shaghayegh Khanmohammadi , Nima Rezaei

Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS). The etiology of MS remains elusive, with a complex interplay of genetic and environmental factors contributing to its pathogenesis. Recent studies showed mitochondrial DNA (mtDNA) as a potential player in the development and progression of MS. These studies encompassed mtDNA variants, copy number variations, and haplogroups. This narrative review aims to synthesize the current understanding of the role of mtDNA’s in MS. The findings of this review suggest that mtDNA may indeed play a role in the development and progression of MS. Several studies have reported an association between mtDNA variants and increased susceptibility to MS, while others have found a link between mtDNA copy number variations and disease severity. Furthermore, specific mtDNA haplogroups have been demonstrated to confer protection against MS. MtDNA alterations may make neurons and oligodendrocytes more susceptible to inflammatory and oxidative stress, causing demyelination and axonal degeneration in MS patients. In conclusion, this review underscores the potential significance of mtDNA in the pathogenesis of MS and highlights the need for further research to fully elucidate its role. A deeper understanding of mtDNA’s involvement in MS may pave the way for the development of novel therapeutic strategies to combat this debilitating disease.

多发性硬化症（MS）是一种影响中枢神经系统（CNS）的慢性自身免疫性疾病。多发性硬化症的病因仍然难以捉摸，遗传和环境因素的复杂相互作用有助于其发病机制。最近的研究表明，线粒体DNA （mtDNA）在ms的发生和发展中起着潜在的作用，这些研究包括mtDNA变异、拷贝数变异和单倍群。本综述的研究结果表明，mtDNA可能确实在MS的发生和进展中发挥作用。一些研究报道了mtDNA变异与MS易感性增加之间的关联，而其他研究发现mtDNA拷贝数变异与疾病严重程度之间的联系。此外，特定的mtDNA单倍群已被证明对MS具有保护作用。mtDNA的改变可能使神经元和少突胶质细胞更容易受到炎症和氧化应激的影响，导致MS患者脱髓鞘和轴突变性。总之，本综述强调了mtDNA在MS发病机制中的潜在意义，并强调了进一步研究以充分阐明其作用的必要性。对mtDNA在多发性硬化症中的作用的更深入的了解可能为开发新的治疗策略来对抗这种使人衰弱的疾病铺平道路。

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引用次数: 0

Autologous mitochondrial transplantation enhances the bioenergetics of auditory cells and mitigates cell loss induced by H2O2

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2024-12-25 DOI: 10.1016/j.mito.2024.102003

Mustafa Nazir Okur , Adam Ratajczak , Arash Kheradvar , Hamid R Djalilian

Hearing loss is a widespread and disabling condition with no current cure, underscoring the urgent need for new therapeutic approaches for treatment and prevention. A recent mitochondrial therapy approach by introducing exogenous mitochondria to the cells has shown promising results in mitigating mitochondria-related disorders. Despite the essential role of mitochondria in hearing, this novel strategy has not yet been tested for the treatment of hearing loss. More importantly, whether cochlear cells take up exogenous mitochondria and its consequence on cell bioenergetics has never been tested before. Here, we showed that exogenous mitochondria from HEI-OC1 auditory cells internalize into a new set of HEI-OC1 cells through co-incubation in a dose-dependent manner without inducing toxicity. We observed that auditory cells that received exogenous mitochondria exhibited increased bioenergetics compared to the controls that received none. Furthermore, we found that mitochondrial transplantation protects cells from oxidative stress and H₂O₂-induced apoptosis, while partially restoring bioenergetics diminished by H₂O₂ exposure. These findings support initial evidence for the feasibility and potential advantages of mitochondrial therapy in auditory cells. If successful in animal models and ultimately in humans, this novel therapy offers prominent potential for the treatment of sensorineural hearing loss.

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引用次数: 0

Substitution of leucine by glutamate perturbs VopE localization to mitochondria: Lessons from yeast model system 用谷氨酸取代亮氨酸会扰乱 VopE 在线粒体的定位：酵母模型系统的启示

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2024-12-13 DOI: 10.1016/j.mito.2024.101999

Nandita Sharma , Kiran Heer , Saumya Raychaudhuri

VopE, a type III effector protein of Vibrio cholerae, modulates host mitochondrial function. Mitochondrial entry of VopE is directly linked with an N-terminal precursor sequence known as the mitochondrial targeting sequence or MTS. MTS of VopE is constituted with 23 amino acids. Earlier studies have shown the importance of leucine residue at position 4 in VopE translocation to mitochondria. In the present study, we have identified another leucine residue at position 15 contributing to the mitochondrial uptake of VopE in the yeast model system. Substitution of leucine¹⁵ with glutamate decreases mitochondrial localization and toxicity of the mutants.

VopE 是霍乱弧菌的 III 型效应蛋白，可调节宿主线粒体的功能。VopE 进入线粒体与 N 端前体序列（称为线粒体靶向序列或 MTS）直接相关。VopE 的 MTS 由 23 个氨基酸组成。早期的研究表明，位于第 4 位的亮氨酸残基在 VopE 转位至线粒体的过程中起着重要作用。在本研究中，我们在酵母模型系统中发现了另一个位于第 15 位的亮氨酸残基有助于线粒体吸收 VopE。用谷氨酸取代亮氨酸 15 会降低突变体的线粒体定位和毒性。

引用次数: 0

Mitochondria-targeted nanotherapeutics: A new frontier in neurodegenerative disease treatment 线粒体靶向纳米疗法：神经退行性疾病治疗的新前沿。

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2024-12-09 DOI: 10.1016/j.mito.2024.102000

Nishad Keethedeth, Rajesh Anantha Shenoi

Mitochondria are the seat of cellular energy and play key roles in regulating several cellular processes such as oxidative phosphorylation, respiration, calcium homeostasis and apoptotic pathways. Mitochondrial dysfunction results in error in oxidative phosphorylation, redox imbalance, mitochondrial DNA mutations, and disturbances in mitochondrial dynamics, all of which can lead to several metabolic and degenerative diseases. A plethora of studies have provided evidence for the involvement of mitochondrial dysfunction in the pathogenesis of neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. Hence mitochondria have been used as possible therapeutic targets in the regulation of neurodegenerative diseases. However, the double membranous structure of mitochondria poses an additional barrier to most drugs even if they are able to cross the plasma membrane. Most of the drugs acting on mitochondria also required very high doses to exhibit the desired mitochondrial accumulation and therapeutic effect which in-turn result in toxic effects. Mitochondrial targeting has been improved by direct conjugation of drugs to mitochondriotropic molecules like dequalinium (DQA) and triphenyl phosphonium (TPP) cations. But being cationic in nature, these molecules also exhibit toxicity at higher doses. In order to further improve the mitochondrial localization with minimal toxicity, TPP was conjugated with various nanomaterials like liposomes. inorganic nanoparticles, polymeric nanoparticles, micelles and dendrimers. This review provides an overview of the role of mitochondrial dysfunction in neurodegenerative diseases and various nanotherapeutic strategies for efficient targeting of mitochondria-acting drugs in these diseases.

线粒体是细胞能量的所在地，在调节氧化磷酸化、呼吸、钙稳态和凋亡途径等细胞过程中发挥关键作用。线粒体功能障碍导致氧化磷酸化错误、氧化还原失衡、线粒体DNA突变和线粒体动力学紊乱，所有这些都可导致多种代谢和退行性疾病。大量的研究已经为线粒体功能障碍参与神经退行性疾病的发病机制提供了证据，如帕金森病、阿尔茨海默病、亨廷顿病和肌萎缩侧索硬化症。因此，线粒体已被用作调节神经退行性疾病的可能治疗靶点。然而，线粒体的双膜结构对大多数药物构成了额外的屏障，即使它们能够穿过质膜。大多数作用于线粒体的药物也需要非常高的剂量才能表现出所需的线粒体积累和治疗效果，而这反过来又会导致毒性作用。通过将药物直接偶联到去qualinium （DQA）和triphenyl phospium （TPP）阳离子等线粒体性分子，线粒体靶向性得到了改善。但这些分子本质上是阳离子的，在高剂量下也会表现出毒性。为了进一步改善线粒体定位，降低毒性，TPP与各种纳米材料如脂质体偶联。无机纳米粒子，聚合纳米粒子，胶束和树状大分子。本文综述了线粒体功能障碍在神经退行性疾病中的作用，以及在这些疾病中有效靶向线粒体作用药物的各种纳米治疗策略。

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引用次数: 0

Mitochondrial DNA (mtDNA) accelerates oxygen-glucose deprivation-induced injury of proximal tubule epithelia cell via inhibiting NLRC5 线粒体DNA（mtDNA）通过抑制NLRC5加速氧-葡萄糖剥夺诱导的近端肾小管上皮细胞损伤。

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2024-11-24 DOI: 10.1016/j.mito.2024.101989

Guojun Ge , Bocheng Zhu , Xiaofeng Zhu , Zhenfei Yu , Keqing Zhu , Mengshi Cheng

The high morbidity and mortality associated with acute kidney injury (AKI) are global health concerns. AKI is commonly attributed to ischemia/reperfusion injury (IRI), a condition characterized by activation of inflammatory responses and mitochondrial dysfunction. Nonetheless, mitochondrial DNA (mtDNA) has the potential to induce renal IRI. This study aimed to elucidate the mechanism and function of mtDNA in HK-2 cells that had been exposed to oxygen-glucose deprivation/reperfusion (OGD/R) and in renal IRI mice. OGD/R was discovered to induce an increase in the amount of mtDNA in HK-2 cells. Moreover, our study demonstrated that mtDNA facilitated cellular apoptosis and inflammation in vivo and in vitro. Given the potential role of inflammation in OGD/R, we investigated the effect of mtDNA on various signaling pathways associated with inflammation. Western blot analysis demonstrated that mtDNA significantly upregulated NLRC5/TAP1 signaling. Furthermore, the upregulation of NLRC5 and TAP1 expression induced by mtDNA was reversed when NLRC5 was inhibited. It is worth mentioning that the loss of NLRC5 effectively nullified the beneficial effects of mtDNA on inflammation and cell apoptosis induced by OGD/R. In addition, in renal IRI mice, mtDNA treatment also aggravated inflammation and kidney damage, and increased the NLRC5 levels in kidney tissues. These results suggested that NLRC5 acts as an intermediary between mtDNA and the pathogenicity of renal IRI. In summary, this study provides evidence that mtDNA promotes apoptosis and inflammation in OGD/R treated HK-2 cells and renal IRI mice through upregulating NLRC5 levels.

与急性肾损伤（AKI）相关的高发病率和高死亡率是全球关注的健康问题。急性肾损伤通常归因于缺血/再灌注损伤（IRI），这是一种以炎症反应激活和线粒体功能障碍为特征的疾病。然而，线粒体 DNA（mtDNA）有可能诱发肾脏 IRI。本研究旨在阐明氧-葡萄糖剥夺/再灌注（OGD/R）HK-2细胞和肾脏IRI小鼠中线粒体DNA的机制和功能。研究发现，OGD/R 可诱导 HK-2 细胞中的 mtDNA 数量增加。此外，我们的研究还证明，mtDNA 在体内和体外都能促进细胞凋亡和炎症。鉴于炎症在 OGD/R 中的潜在作用，我们研究了 mtDNA 对与炎症相关的各种信号通路的影响。Western 印迹分析表明，mtDNA 能显著上调 NLRC5/TAP1 信号传导。此外，当抑制 NLRC5 时，mtDNA 诱导的 NLRC5 和 TAP1 表达上调被逆转。值得一提的是，NLRC5的缺失有效地抵消了mtDNA对OGD/R诱导的炎症和细胞凋亡的有益影响。此外，在肾脏 IRI 小鼠中，mtDNA 处理也加重了炎症和肾脏损伤，并增加了肾脏组织中的 NLRC5 水平。这些结果表明，NLRC5是mtDNA与肾脏IRI致病性之间的中介。总之，本研究提供了证据，证明mtDNA通过上调NLRC5水平促进了经OGD/R处理的HK-2细胞和肾脏IRI小鼠的细胞凋亡和炎症。

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引用次数: 0

Expression of fragmented ribosomal RNA from the mitochondrial genome of Eimeria tenella 天牛埃默氏菌线粒体基因组片段核糖体 RNA 的表达。

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion

Pub Date : 2024-11-24 DOI: 10.1016/j.mito.2024.101990

Perryn S. Kruth , Chloe MacNeil , John R. Barta

Highly fragmented ribosomal RNA-coding sequences are characteristic of mitogenomes of protozoan parasites of the phylum Apicomplexa. Identification of ribosomal RNA encoding sequences in apicomplexan mitogenomes has largely relied on sequence similarity with several apicomplexan species for which expression of these genes has been demonstrated. The present study applied Next-Gen sequencing to investigate the expression of fragmented putative mitochondrial rRNAs in Eimeria tenella, a coccidian parasite of poultry.

Expression of 18 of 19 putative rDNA fragments included in the original published E. tenella mitogenome was confirmed. Sequence comparison with Plasmodium falciparum and NGS identified 14 additional putative fragments. Two small RNAs were identified that did not share sequence similarities with other known rDNA sequences. Eight sRNAs were identified that represented smaller chunks of putative rDNA fragments and three were observed that represented two putative rDNA fragments (i.e., polycistronic transcripts). Relative abundances of each sRNA species ranged across three orders of magnitude. Twenty-five of the 45 distinct sRNAs expressed from the mitogenome were polyadenylated in more than 50% of instances.

The identification of unique sRNAs without significant homology to known sequences and the observation of polycistronic transcripts highlight the complexity of regulation of expression of the E. tenella mitogenome. The varied relative abundances, presence of shorter RNAs expressed from longer putative rDNA fragments, and variable polyadenylation of these sRNAs highlight additional areas for future work towards better understanding the expression of the mitogenome in this important poultry pathogen. More generally, these findings expand our wider understanding of evolution of apicomplexan mitogenomes.

高度片段化的核糖体 RNA 编码序列是原生动物门（Apicomplexa）寄生虫有丝分裂原体的特征。有丝分裂原体中核糖体 RNA 编码序列的鉴定主要依赖于与已证实表达这些基因的几个有丝分裂原体物种的序列相似性。本研究应用 Next-Gen 测序技术研究了家禽球虫寄生虫 Eimeria tenella 的线粒体 rRNA 片段表达情况。在最初公布的十日龄艾美拉球虫基因组中包含了 19 个假定 rDNA 片段，其中 18 个的表达得到了证实。与恶性疟原虫和 NGS 的序列比较确定了另外 14 个推测片段。发现了两个与其他已知 rDNA 序列不具有序列相似性的小 RNA。鉴定出的 8 条 sRNA 代表了较小块的推定 rDNA 片段，观察到的 3 条 sRNA 代表了两个推定 rDNA 片段（即多聚转录本）。每种 sRNA 的相对丰度在三个数量级之间。在有丝分裂基因组表达的 45 种不同 sRNA 中，有 25 种在 50%以上的情况下具有多腺苷酸化。与已知序列无显著同源性的独特 sRNA 的鉴定以及多聚转录本的观察突出表明了 E.tenell 有丝分裂基因组表达调控的复杂性。这些 sRNAs 的相对丰度不同、存在由较长的推定 rDNA 片段表达的较短 RNAs，以及多聚腺苷酸化程度不同，这些都凸显了未来工作的其他领域，以便更好地了解这一重要家禽病原体的有丝分裂基因组的表达。更广泛地说，这些发现拓展了我们对类病毒有丝分裂基因组进化的理解。

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引用次数: 0