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Free long-chain fatty acids trigger early postembryonic development in starved Caenorhabditis elegans by suppressing mTORC1. 游离长链脂肪酸通过抑制 mTORC1 触发饥饿的秀丽隐杆线虫胚后早期发育。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-22 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002841
Meiyu Ruan, Fan Xu, Na Li, Jing Yu, Fukang Teng, Jiawei Tang, Cheng Huang, Huanhu Zhu

Postembryonic development of animals has long been considered an internally predetermined program, while macronutrients were believed to be essential solely for providing biomatters and energy to support this process. However, in this study, by using a nematode Caenorhabditis elegans (abbreviated as C. elegans hereafter) model, we surprisingly discovered that dietary supplementation of palmitic acid alone, rather than other abundant essential nutrients such as glucose or amino acid mixture, was sufficient to initiate early postembryonic development even under complete macronutrient deprivation. Such a development was evidenced by changes in morphology, cellular markers in multiple tissues, behaviors, and the global transcription pattern and it occurred earlier than the well-known early L1 nutrient checkpoint. Mechanistically, palmitic acid did not function as a biomatter/energy provider, but rather as a ligand to activate the nuclear hormone receptor NHR-49/80, leading to the production of an unknown peroxisome-derived secretive hormone in the intestine. This hormonal signal was received by chemosensory neurons in the head, regulating the insulin-like neuropeptide secretion and its downstream nuclear receptor to orchestrate global development. Additionally, the nutrient-sensing hub mTORC1 played a negative role in this process. In conclusion, our data indicate that free fatty acids act as a primary nutrient signal to launch the early development in C. elegans, which suggests that specific nutrients, rather than the internal genetic program, serve as the first impetus for postembryonic development.

长期以来,动物的胚后发育一直被认为是一个内部预定的程序,而宏量营养素被认为仅仅是为支持这一过程提供生物物质和能量所必需的。然而,在本研究中,通过使用线虫秀丽隐杆线虫(以下简称秀丽隐杆线虫)模型,我们惊奇地发现,即使在完全缺乏宏量营养素的情况下,仅从食物中补充棕榈酸,而不是其他丰富的必需营养素(如葡萄糖或氨基酸混合物),就足以启动胚后早期发育。这种发育可以通过形态、多种组织的细胞标记、行为和全球转录模式的变化得到证明,而且比众所周知的早期 L1 营养检查点发生得更早。从机理上讲,棕榈酸并不是生物物质/能量的提供者,而是激活核激素受体 NHR-49/80 的配体,从而在肠道中产生一种未知的过氧化物酶分泌激素。这种激素信号被头部的化感神经元接收,调节胰岛素样神经肽的分泌及其下游核受体,从而协调整体发育。此外,营养传感中枢 mTORC1 在这一过程中发挥了负面作用。总之,我们的数据表明,游离脂肪酸是启动秀丽隐杆线虫早期发育的主要营养信号,这表明特定营养物质而非内部遗传程序是胚后发育的第一推动力。
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引用次数: 0
Decoding reveals the neural representation of perceived and imagined musical sounds. 解码揭示了感知和想象的音乐声音的神经表征。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-21 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002858
David R Quiroga-Martinez, Gemma Fernández Rubio, Leonardo Bonetti, Kriti G Achyutuni, Athina Tzovara, Robert T Knight, Peter Vuust

Vividly imagining a song or a melody is a skill that many people accomplish with relatively little effort. However, we are only beginning to understand how the brain represents, holds, and manipulates these musical "thoughts." Here, we decoded perceived and imagined melodies from magnetoencephalography (MEG) brain data (N = 71) to characterize their neural representation. We found that, during perception, auditory regions represent the sensory properties of individual sounds. In contrast, a widespread network including fronto-parietal cortex, hippocampus, basal nuclei, and sensorimotor regions hold the melody as an abstract unit during both perception and imagination. Furthermore, the mental manipulation of a melody systematically changes its neural representation, reflecting volitional control of auditory images. Our work sheds light on the nature and dynamics of auditory representations, informing future research on neural decoding of auditory imagination.

生动地想象一首歌或一段旋律是许多人不费吹灰之力就能做到的技能。然而,我们才刚刚开始了解大脑是如何表现、保持和操纵这些音乐 "思想 "的。在这里,我们通过脑磁图(MEG)大脑数据(71 人)对感知和想象的旋律进行解码,以描述它们的神经表征。我们发现,在感知过程中,听觉区域代表了单个声音的感觉特性。与此相反,在感知和想象过程中,包括前顶叶皮层、海马、基底核和感觉运动区在内的广泛网络将旋律作为一个抽象单元。此外,对旋律的心理操作会系统地改变其神经表征,这反映了对听觉图像的意志控制。我们的研究揭示了听觉表征的本质和动态变化,为未来听觉想象的神经解码研究提供了参考。
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引用次数: 0
Activation of plant immunity through conversion of a helper NLR homodimer into a resistosome. 通过将辅助 NLR 同源二聚体转化为抗原体激活植物免疫。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-18 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002868
Muniyandi Selvaraj, AmirAli Toghani, Hsuan Pai, Yu Sugihara, Jiorgos Kourelis, Enoch Lok Him Yuen, Tarhan Ibrahim, He Zhao, Rongrong Xie, Abbas Maqbool, Juan Carlos De la Concepcion, Mark J Banfield, Lida Derevnina, Benjamin Petre, David M Lawson, Tolga O Bozkurt, Chih-Hang Wu, Sophien Kamoun, Mauricio P Contreras

Nucleotide-binding domain and leucine-rich repeat (NLR) proteins can engage in complex interactions to detect pathogens and execute a robust immune response via downstream helper NLRs. However, the biochemical mechanisms of helper NLR activation by upstream sensor NLRs remain poorly understood. Here, we show that the coiled-coil helper NLR NRC2 from Nicotiana benthamiana accumulates in vivo as a homodimer that converts into a higher-order oligomer upon activation by its upstream virus disease resistance protein Rx. The cryo-EM structure of NbNRC2 in its resting state revealed intermolecular interactions that mediate homodimer formation and contribute to immune receptor autoinhibition. These dimerization interfaces have diverged between paralogous NRC proteins to insulate critical network nodes and enable redundant immune pathways, possibly to minimise undesired cross-activation and evade pathogen suppression of immunity. Our results expand the molecular mechanisms of NLR activation pointing to transition from homodimers to higher-order oligomeric resistosomes.

核苷酸结合域和富含亮氨酸的重复(NLR)蛋白可进行复杂的相互作用,以检测病原体,并通过下游辅助 NLR 执行强有力的免疫反应。然而,人们对上游传感器 NLR 激活辅助 NLR 的生化机制仍然知之甚少。在这里,我们发现来自烟草的盘卷辅助 NLR NRC2 在体内以同源二聚体的形式积累,在被其上游病毒抗病蛋白 Rx 激活后转化为高阶寡聚体。NbNRC2静止状态下的低温电子显微镜结构揭示了分子间相互作用,这些相互作用介导了同源二聚体的形成,并有助于免疫受体的自动抑制。这些二聚化界面在同源的 NRC 蛋白之间发生了分化,从而隔离了关键的网络节点,实现了冗余的免疫途径,这可能是为了最大限度地减少不必要的交叉激活,逃避病原体对免疫的抑制。我们的研究结果拓展了 NLR 激活的分子机制,指出了从同源二聚体到高阶寡聚体的转变。
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引用次数: 0
Structures of the mycobacterial MmpL4 and MmpL5 transporters provide insights into their role in siderophore export and iron acquisition. 霉菌 MmpL4 和 MmpL5 转运体的结构揭示了它们在苷酸输出和铁获取中的作用。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-18 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002874
Rakesh Maharjan, Zhemin Zhang, Philip A Klenotic, William D Gregor, Marios L Tringides, Meng Cui, Georgiana E Purdy, Edward W Yu

The Mycobacterium tuberculosis (Mtb) pathogen, the causative agent of the airborne infection tuberculosis (TB), harbors a number of mycobacterial membrane protein large (MmpL) transporters. These membrane proteins can be separated into 2 distinct subclasses, where they perform important functional roles, and thus, are considered potential drug targets to combat TB. Previously, we reported both X-ray and cryo-EM structures of the MmpL3 transporter, providing high-resolution structural information for this subclass of the MmpL proteins. Currently, there is no structural information available for the subclass associated with MmpL4 and MmpL5, transporters that play a critical role in iron homeostasis of the bacterium. Here, we report cryo-EM structures of the M. smegmatis MmpL4 and MmpL5 transporters to resolutions of 2.95 Å and 3.00 Å, respectively. These structures allow us to propose a plausible pathway for siderophore translocation via these 2 transporters, an essential step for iron acquisition that enables the survival and replication of the mycobacterium.

结核分枝杆菌(Mtb)病原体是通过空气传播的结核病(TB)的致病菌,它携带有许多分枝杆菌膜蛋白大(MmpL)转运体。这些膜蛋白可分为两个不同的亚类,它们在其中发挥着重要的功能作用,因此被认为是抗击结核病的潜在药物靶标。此前,我们报道了 MmpL3 转运体的 X 射线和低温电子显微镜结构,为该亚类 MmpL 蛋白提供了高分辨率的结构信息。目前,还没有与 MmpL4 和 MmpL5 相关的亚类的结构信息,这些转运体在细菌的铁平衡中发挥着关键作用。在此,我们报告了 M. smegmatis MmpL4 和 MmpL5 转运体的低温电子显微镜结构,其分辨率分别为 2.95 Å 和 3.00 Å。通过这些结构,我们提出了通过这两个转运体进行苷酸转运的合理途径,而苷酸转运是获得铁的一个重要步骤,可使分枝杆菌得以生存和复制。
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引用次数: 0
Chromatin remodeller Chd7 is developmentally regulated in the neural crest by tissue-specific transcription factors. 染色质重塑因子 Chd7 在神经嵴中受组织特异性转录因子的发育调控。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-17 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002786
Ruth M Williams, Guneş Taylor, Irving T C Ling, Ivan Candido-Ferreira, Daniel M Fountain, Sarah Mayes, Perihan Seda Ateş-Kalkan, Julianna O Haug, Andrew J Price, Sean A McKinney, Yavor K Bozhilovh, Richard C V Tyser, Shankar Srinivas, Jim R Hughes, Tatjana Sauka-Spengler

Neurocristopathies such as CHARGE syndrome result from aberrant neural crest development. A large proportion of CHARGE cases are attributed to pathogenic variants in the gene encoding CHD7, chromodomain helicase DNA binding protein 7, which remodels chromatin. While the role for CHD7 in neural crest development is well documented, how this factor is specifically up-regulated in neural crest cells is not understood. Here, we use epigenomic profiling of chick and human neural crest to identify a cohort of enhancers regulating Chd7 expression in neural crest cells and other tissues. We functionally validate upstream transcription factor binding at candidate enhancers, revealing novel epistatic relationships between neural crest master regulators and Chd7, showing tissue-specific regulation of a globally acting chromatin remodeller. Furthermore, we find conserved enhancer features in human embryonic epigenomic data and validate the activity of the human equivalent CHD7 enhancers in the chick embryo. Our findings embed Chd7 in the neural crest gene regulatory network and offer potentially clinically relevant elements for interpreting CHARGE syndrome cases without causative allocation.

神经嵴发育异常会导致神经嵴病,如 CHARGE 综合征。很大一部分 CHARGE 病例是由于编码 CHD7(染色质域螺旋酶 DNA 结合蛋白 7)的基因中的致病变体造成的,该基因可重塑染色质。虽然CHD7在神经嵴发育过程中的作用已得到充分证实,但该因子是如何在神经嵴细胞中特异性上调的还不清楚。在这里,我们利用雏鸡和人类神经嵴的表观基因组图谱鉴定了一组调控神经嵴细胞和其他组织中 Chd7 表达的增强子。我们从功能上验证了上游转录因子与候选增强子的结合,揭示了神经嵴主调控因子与 Chd7 之间新的表观关系,显示了全球作用的染色质重塑因子对组织的特异性调控。此外,我们还发现了人类胚胎表观基因组数据中保守的增强子特征,并验证了人类等效的 CHD7 增强子在小鸡胚胎中的活性。我们的研究结果将 Chd7 嵌入了神经嵴基因调控网络,并为解释无因果关系分配的 CHARGE 综合征病例提供了潜在的临床相关因素。
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引用次数: 0
Mice employ a bait-and-switch escape mechanism to de-escalate social conflict. 小鼠采用诱饵-开关逃脱机制来缓和社会冲突。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-15 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002496
Rachel S Clein, Megan R Warren, Joshua P Neunuebel

Intraspecies aggression has profound ecological and evolutionary consequences, as recipients can suffer injuries, decreases in fitness, and become outcasts from social groups. Although animals implement diverse strategies to avoid hostile confrontations, the extent to which social influences affect escape tactics is unclear. Here, we used computational and machine-learning approaches to analyze complex behavioral interactions as mixed-sex groups of mice, Mus musculus, freely interacted. Mice displayed a rich repertoire of behaviors marked by changes in behavioral state, aggressive encounters, and mixed-sex interactions. A distinctive behavioral sequence consistently occurred after aggressive encounters, where males in submissive states quickly approached and transiently interacted with females immediately before the aggressor engaged with the same female. The behavioral sequences were also associated with substantially fewer physical altercations. Furthermore, the male's behavioral state could be predicted by distinct features of the behavioral sequence, such as kinematics and the latency to and duration of male-female interactions. More broadly, our work revealed an ethologically relevant escape strategy influenced by the presence of females that may serve as a mechanism for de-escalating social conflict and preventing consequential reductions in fitness.

物种间的攻击会对生态和进化产生深远的影响,因为受攻击者可能会受伤、体能下降,并成为社会群体的弃儿。虽然动物会采取多种策略来避免敌对对抗,但社会影响对逃避策略的影响程度尚不清楚。在这里,我们使用计算和机器学习方法分析了小鼠(Mus musculus)混性群体自由互动时的复杂行为互动。小鼠在行为状态变化、攻击性相遇和混性互动中表现出丰富的行为。在攻击性相遇后会持续出现一个独特的行为序列,即处于顺从状态的雄性小鼠会迅速接近雌性小鼠并与之短暂互动,紧接着攻击者会与同一雌性小鼠互动。这种行为序列还与较少的肢体冲突有关。此外,雄性的行为状态可以通过行为序列的不同特征来预测,如运动学、雄性与雌性互动的潜伏期和持续时间。更广泛地说,我们的研究揭示了一种受雌性存在影响的与伦理学相关的逃避策略,它可以作为一种缓和社会冲突和防止由此导致的适应能力下降的机制。
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引用次数: 0
The human olfactory bulb communicates perceived odor valence to the piriform cortex in the gamma band and receives a refined representation back in the beta band. 人的嗅球通过伽马波段将感知到的气味价位传递给梨状皮层,并通过贝塔波段接收回馈的精细表征。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-14 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002849
Frans Nordén, Behzad Iravani, Martin Schaefer, Anja L Winter, Mikael Lundqvist, Artin Arshamian, Johan N Lundström

A core function of the olfactory system is to determine the valence of odors. In humans, central processing of odor valence perception has been shown to take form already within the olfactory bulb (OB), but the neural mechanisms by which this important information is communicated to, and from, the olfactory cortex (piriform cortex, PC) are not known. To assess communication between the 2 nodes, we simultaneously measured odor-dependent neural activity in the OB and PC from human participants while obtaining trial-by-trial valence ratings. By doing so, we could determine when subjective valence information was communicated, what kind of information was transferred, and how the information was transferred (i.e., in which frequency band). Support vector machine (SVM) learning was used on the coherence spectrum and frequency-resolved Granger causality to identify valence-dependent differences in functional and effective connectivity between the OB and PC. We found that the OB communicates subjective odor valence to the PC in the gamma band shortly after odor onset, while the PC subsequently feeds broader valence-related information back to the OB in the beta band. Decoding accuracy was better for negative than positive valence, suggesting a focus on negative valence. Critically, we replicated these findings in an independent data set using additional odors across a larger perceived valence range. Combined, these results demonstrate that the OB and PC communicate levels of subjective odor pleasantness across multiple frequencies, at specific time points, in a direction-dependent pattern in accordance with a two-stage model of odor processing.

嗅觉系统的一个核心功能是确定气味的价值。在人类中,对气味价值感知的中枢处理已在嗅球(OB)中形成,但这一重要信息与嗅觉皮层(梨状皮层,PC)之间的神经机制尚不清楚。为了评估这两个节点之间的交流,我们同时测量了人类参与者嗅球和PC中依赖于气味的神经活动,同时获得了逐次试验的价值评级。通过这种方法,我们可以确定主观情绪信息何时被传递、传递了何种信息以及信息是如何传递的(即在哪个频段)。我们使用支持向量机(SVM)学习相干频谱和频率分辨格兰杰因果关系,以识别主观情感与主观情感之间的功能和有效连通性的差异。我们发现,在气味开始后不久,嗅觉器官就会在伽马波段将主观气味价值传递给个人计算机,而个人计算机随后会在β波段将与价值相关的信息反馈给嗅觉器官。对负面情绪的解码准确性要好于对正面情绪的解码准确性,这表明负面情绪是解码的重点。重要的是,我们在一个独立的数据集中使用了更多的气味,在更大的感知价位范围内重复了这些发现。综合上述结果,我们发现在特定的时间点,主观气味愉快度的水平会在多个频率上与 OB 和 PC 进行交流,这种交流模式与气味加工的两阶段模型相一致。
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引用次数: 0
Reduction of endocytosis and EGFR signaling is associated with the switch from isolated to clustered apoptosis during epithelial tissue remodeling in Drosophila. 果蝇上皮组织重塑过程中,内吞和表皮生长因子受体信号转导的减少与细胞凋亡从孤立凋亡到集群凋亡的转变有关。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-14 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002823
Kevin Yuswan, Xiaofei Sun, Erina Kuranaga, Daiki Umetsu

Epithelial tissues undergo cell turnover both during development and for homeostatic maintenance. Removal of cells is coordinated with the increase in number of newly dividing cells to maintain barrier function of the tissue. In Drosophila metamorphosis, larval epidermal cells (LECs) are replaced by adult precursor cells called histoblasts. Removal of LECs must counterbalance the exponentially increasing adult histoblasts. Previous work showed that the LEC removal accelerates as endocytic activity decreases throughout all LECs. Here, we show that the acceleration is accompanied by a mode switching from isolated single-cell apoptosis to clustered ones induced by the endocytic activity reduction. We identify the epidermal growth factor receptor (EGFR) pathway via extracellular-signal regulated kinase (ERK) activity as the main components downstream of endocytic activity in LECs. The reduced ERK activity, caused by the decrease in endocytic activity, is responsible for the apoptotic mode switching. Initially, ERK is transiently activated in normal LECs surrounding a single apoptotic LEC in a ligand-dependent manner, preventing clustered cell death. Following the reduction of endocytic activity, LEC apoptosis events do not provoke these transient ERK up-regulations, resulting in the acceleration of the cell elimination rate by frequent clustered apoptosis. These findings contrasted with the common perspective that clustered apoptosis is disadvantageous. Instead, switching to clustered apoptosis is required to accommodate the growth of neighboring tissues.

上皮组织在生长发育和维持平衡的过程中都会发生细胞更替。细胞的清除与新分裂细胞数量的增加相互协调,以维持组织的屏障功能。在果蝇的变态过程中,幼虫表皮细胞(LEC)被称为组织细胞的成虫前体细胞取代。LEC 的移除必须与呈指数增长的成体组织细胞相平衡。以前的研究表明,随着所有 LEC 内细胞活性的降低,LEC 的移除速度会加快。在这里,我们发现伴随着这种加速的是由内细胞活性降低引起的从孤立的单细胞凋亡到集群凋亡的模式转换。我们确定表皮生长因子受体(EGFR)通路通过细胞外信号调节激酶(ERK)活性是 LECs 内细胞活性下游的主要成分。内细胞活性降低导致的ERK活性降低是凋亡模式转换的原因。最初,在单个凋亡 LEC 周围的正常 LEC 中,ERK 会以配体依赖的方式被短暂激活,从而防止细胞集群死亡。内细胞活性降低后,LEC凋亡事件不会引发这些瞬时的ERK上调,从而导致频繁的集群细胞凋亡加快了细胞淘汰率。这些发现与通常认为集群凋亡不利的观点形成了鲜明对比。相反,切换到集群凋亡是适应邻近组织生长所必需的。
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引用次数: 0
Widespread regulation of the maternal transcriptome by Nanos in Drosophila. 果蝇的母体转录组受到 Nanos 的广泛调控。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-14 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002840
Mohammad Marhabaie, Tammy H Wharton, Sung Yun Kim, Robin P Wharton

The translational repressor Nanos (Nos) regulates a single target, maternal hunchback (hb) mRNA, to govern abdominal segmentation in the early Drosophila embryo. Nos is recruited to sites in the 3' UTR of hb mRNA in collaboration with the sequence-specific RNA-binding protein Pumilio (Pum); on its own, Nos has no binding specificity. Nos is expressed at other stages of development, but very few mRNA targets that might mediate its action at these stages have been described. Nor has it been clear whether Nos is targeted to other mRNAs in concert with Pum or via other mechanisms. In this report, we identify mRNAs targeted by Nos via 2 approaches. First, we identify mRNAs depleted upon expression of a chimera bearing Nos fused to the nonsense mediated decay (NMD) factor Upf1. We find that, in addition to hb, Upf1-Nos depletes approximately 2,600 mRNAs from the maternal transcriptome in early embryos. Virtually all of these appear to be targeted in a canonical, hb-like manner in concert with Pum. In a second, more conventional approach, we identify mRNAs that are stabilized during the maternal zygotic transition (MZT) in embryos from nos- females. Most (86%) of the 1,185 mRNAs regulated by Nos are also targeted by Upf1-Nos, validating use of the chimera. Previous work has shown that 60% of the maternal transcriptome is degraded in early embryos. We find that maternal mRNAs targeted by Upf1-Nos are hypoadenylated and inefficiently translated at the ovary-embryo transition; they are subsequently degraded in the early embryo, accounting for 59% of all destabilized maternal mRNAs. We suggest that the late ovarian burst of Nos represses a large fraction of the maternal transcriptome, priming it for later degradation by other factors in the embryo.

翻译抑制因子Nanos(Nos)只调节一个目标,即母体驼背(hb)mRNA,从而控制果蝇早期胚胎的腹部分割。Nos 与序列特异性 RNA 结合蛋白 Pumilio(Pum)合作,被招募到 hb mRNA 的 3' UTR 位点;Nos 本身没有结合特异性。Nos 在发育的其他阶段也有表达,但在这些阶段可能介导其作用的 mRNA 靶点却很少被描述。也不清楚 Nos 是与 Pum 协同作用还是通过其他机制靶向其他 mRNA。在本报告中,我们通过两种方法确定了 Nos 靶向的 mRNA。首先,我们确定了表达 Nos 与无义介导衰变(NMD)因子 Upf1 融合的嵌合体时耗竭的 mRNA。我们发现,除 hb 外,Upf1-Nos 还会从早期胚胎的母体转录组中删除约 2,600 个 mRNA。几乎所有这些mRNA似乎都以类似于hb的典型方式与Pum协同作用。在第二种更传统的方法中,我们识别了在母系子代转换(MZT)过程中,nos-雌性胚胎中稳定的 mRNA。在受 Nos 调控的 1,185 个 mRNA 中,大部分(86%)也是 Upf1-Nos 的靶标,从而验证了嵌合体的有效性。以前的研究表明,60%的母体转录组在早期胚胎中降解。我们发现,Upf1-Nos 靶向的母体 mRNA 在卵巢-胚胎过渡阶段腺苷酸过低,翻译效率低下;随后在早期胚胎中降解,占所有不稳定母体 mRNA 的 59%。我们认为,卵巢晚期的 Nos 爆发抑制了母体转录组的很大一部分,使其在胚胎中被其他因子降解。
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引用次数: 0
Functional networks of inhibitory neurons orchestrate synchrony in the hippocampus. 抑制性神经元的功能网络协调了海马的同步性。
IF 9.8 1区 生物学 Q1 Agricultural and Biological Sciences Pub Date : 2024-10-14 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002837
Marco Bocchio, Artem Vorobyev, Sadra Sadeh, Sophie Brustlein, Robin Dard, Susanne Reichinnek, Valentina Emiliani, Agnes Baude, Claudia Clopath, Rosa Cossart

Inhibitory interneurons are pivotal components of cortical circuits. Beyond providing inhibition, they have been proposed to coordinate the firing of excitatory neurons within cell assemblies. While the roles of specific interneuron subtypes have been extensively studied, their influence on pyramidal cell synchrony in vivo remains elusive. Employing an all-optical approach in mice, we simultaneously recorded hippocampal interneurons and pyramidal cells and probed the network influence of individual interneurons using optogenetics. We demonstrate that CA1 interneurons form a functionally interconnected network that promotes synchrony through disinhibition during awake immobility, while preserving endogenous cell assemblies. Our network model underscores the importance of both cell assemblies and dense, unspecific interneuron connectivity in explaining our experimental findings, suggesting that interneurons may operate not only via division of labor but also through concerted activity.

抑制性中间神经元是大脑皮层回路的关键组成部分。除了提供抑制作用外,它们还被认为能协调细胞集合内兴奋神经元的发射。虽然对特定中间神经元亚型的作用进行了广泛的研究,但它们对锥体细胞体内同步性的影响仍然难以捉摸。我们在小鼠体内采用全光方法,同时记录海马中间神经元和锥体细胞,并利用光遗传学方法探究单个中间神经元对网络的影响。我们证明,CA1 中间神经元形成了一个功能性互连网络,在保持内源性细胞集结的同时,通过在清醒不动状态下解除抑制来促进同步性。我们的网络模型强调了细胞集结和密集的非特异性中间神经元连接在解释我们的实验发现方面的重要性,表明中间神经元可能不仅通过分工而且还通过协同活动来运作。
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引用次数: 0
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