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The structural role of Skp1 in the synaptonemal complex is conserved in nematodes. Skp1在突触神经复合体中的结构作用在线虫中是保守的。
IF 3.3 3区 生物学 Pub Date : 2024-09-18 DOI: 10.1093/genetics/iyae153
Lisa E Kursel,Kaan Goktepe,Ofer Rog
The synaptonemal complex (SC) is a meiotic interface that assembles between parental chromosomes and is essential for gamete formation. While the dimensions and ultrastructure of the SC are conserved across eukaryotes, its protein components are highly divergent. Recently, an unexpected component of the SC has been described in the nematode C. elegans: the Skp1-related proteins SKR-1/2, which are components of the Skp1, Cullin, F-box (SCF) ubiquitin ligase. Here, we find that the role of SKR-1 in the SC is conserved in P. pacificus. The P. pacificus Skp1 ortholog, Ppa-SKR-1, colocalizes with other SC proteins throughout meiotic prophase, where it occupies the middle of the SC. Like in C. elegans, the dimerization interface of Ppa-SKR-1 is required for its SC function. A dimerization mutant, ppa-skr-1F105E, fails to assemble SC and produces almost no progeny. Interestingly, the evolutionary trajectory of SKR-1 contrasts with other SC proteins. Unlike most SC proteins, SKR-1 is highly conserved in nematodes. Our results suggest that the structural role of SKR-1 in the SC has been conserved since the common ancestor of C. elegans and P. pacificus, and that rapidly evolving SC proteins have maintained the ability to interact with SKR-1 for at least 100 million years.
突触复合体(SC)是在亲本染色体之间组装的减数分裂界面,对配子的形成至关重要。虽然SC的尺寸和超微结构在真核生物中是保守的,但其蛋白质成分却有很大差异。最近,在线虫秀丽隐杆线虫(C. elegans)中发现了一种意想不到的 SC 组成成分:Skp1 相关蛋白 SKR-1/2,它们是 Skp1、Cullin、F-box(SCF)泛素连接酶的组成成分。在这里,我们发现 SKR-1 在 SC 中的作用在太平洋鼠中是保守的。太平洋鼠的 Skp1 同源物 Ppa-SKR-1 在整个减数分裂前期与其他 SC 蛋白共定位,占据 SC 的中间位置。与优雅子一样,Ppa-SKR-1 的二聚化界面也是其 SC 功能所必需的。二聚化突变体 ppa-skr-1F105E 无法组装 SC,几乎不产生后代。有趣的是,SKR-1 的进化轨迹与其他 SC 蛋白形成了鲜明对比。与大多数 SC 蛋白不同,SKR-1 在线虫中高度保守。我们的研究结果表明,自线虫和太平洋鼠的共同祖先以来,SKR-1在SC中的结构作用一直保持不变,而且快速进化的SC蛋白至少在一亿年中一直保持着与SKR-1相互作用的能力。
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引用次数: 0
Interaction between ESCRT-III proteins and the yeast SERINC homolog Tms1. ESCRT-III 蛋白与酵母 SERINC 同源物 Tms1 之间的相互作用。
IF 3.3 3区 生物学 Pub Date : 2024-09-13 DOI: 10.1093/genetics/iyae132
Ralf Kölling
The endosomal sorting complex required for transport (ESCRT)-III is involved in membrane remodeling and abscission during intraluminal vesicle (ILV) formation at endosomes. Our data now suggest that ESCRT-III function could be connected to lipid remodeling of the endosomal membrane. This notion is based on our finding that ESCRT-III proteins bind to the yeast serine incorporator (SERINC) homolog Tms1. Human SERINC3 and SERINC5 are HIV-1 restriction factors and have been shown to act as scramblases, flipping phospholipids between membrane leaflets. Due to the extraordinarily high sequence conservation between Tms1 and human SERINCs, it is likely that Tms1 is also a scramblase. While deletion of TMS1 had only a moderate effect on the sorting of multivesicular body (MVB) cargo proteins, the simultaneous deletion of a component of the Vps55/Vps68 complex led to a strong synergistic phenotype. This pronounced synergism suggests that Tms1 and Vps55/Vps68 perform a parallel function at endosomes. Vps55/Vps68 loosely resembles Tms1 in its overall structure. Thus, it is possible that Vps55/Vps68 is also a scramblase. Since both Vps55 and Tms1 physically interact with ESCRT-III proteins, we propose that the recruitment of a scramblase plays a crucial role in ESCRT-III-dependent membrane remodeling at endosomes.
运输所需的内体分选复合体(ESCRT)-III 参与了内体形成腔内囊泡(ILV)过程中的膜重塑和脱落。我们现在的数据表明,ESCRT-III 的功能可能与内体膜的脂质重塑有关。这一观点的依据是我们发现 ESCRT-III 蛋白与酵母丝氨酸整合子(SERINC)同源物 Tms1 结合。人类 SERINC3 和 SERINC5 是 HIV-1 限制因子,已被证明可作为扰乱酶,在膜小叶之间翻转磷脂。由于 Tms1 与人类 SERINCs 之间的序列保守性极高,因此 Tms1 很可能也是一种扰乱酶。虽然 TMS1 的缺失对多囊体(MVB)货物蛋白的分拣只有适度的影响,但同时缺失 Vps55/Vps68 复合物的一个成分会导致强烈的协同表型。这种明显的协同作用表明,Tms1 和 Vps55/Vps68 在内质体中发挥着平行的功能。Vps55/Vps68 的整体结构与 Tms1 非常相似。因此,Vps55/Vps68 也可能是一种扰乱酶。由于 Vps55 和 Tms1 都与 ESCRT-III 蛋白发生物理相互作用,我们认为扰乱酶的招募在 ESCRT-III 依赖性内体膜重塑中起着关键作用。
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引用次数: 0
Role of male gonad-enriched microRNAs in sperm production in C. elegans. 雄性性腺富集的 microRNA 在秀丽隐杆线虫精子生成中的作用
IF 3.3 3区 生物学 Pub Date : 2024-09-11 DOI: 10.1093/genetics/iyae147
Lu Lu,Allison L Abbott
Germ cell development and gamete production in animals require small RNA pathways. While studies indicate that microRNAs (miRNAs) are necessary for normal sperm production and function, the specific roles for individual miRNAs are largely unknown. Here, we use small RNA sequencing of dissected gonads and functional analysis of new loss of function alleles to identify functions for miRNAs in the control of fecundity and sperm production in Caenorhabditis elegans (C. elegans) males and hermaphrodites. We describe a set of 29 male gonad-enriched miRNAs and identify a set of individual miRNAs (mir-58.1 and mir-235) and a miRNA cluster (mir-4807-4810.1) that are required for optimal sperm production at 20°C and a set of miRNAs (mir-49, mir-57, mir-83, mir-261, and mir-357/358) that are required for sperm production at 25°C. We observed defects in meiotic progression in mutants missing mir-58.1, mir-83, mir-235, and mir-4807-4810.1, which may contribute to the observed defects in sperm production. Further, analysis of multiple mutants of these miRNAs suggested genetic interactions between these miRNAs. This study provides insights on the regulatory roles of miRNAs that promote optimal sperm production and fecundity in males and hermaphrodites.
动物生殖细胞的发育和配子的产生需要小 RNA 途径。虽然研究表明微小 RNA(miRNA)是正常精子生成和功能所必需的,但个体 miRNA 的具体作用在很大程度上是未知的。在这里,我们利用对解剖性腺的小 RNA 测序和对新的功能缺失等位基因的功能分析,来确定 miRNA 在控制秀丽隐杆线虫(C. elegans)雄性和雌雄同体的繁殖力和精子生成中的功能。我们描述了一组 29 个雄性性腺富集的 miRNAs,并鉴定出一组单个 miRNAs(mir-58.1 和 mir-235)和一个 miRNA 簇(mir-4807-4810.1),这些 miRNAs 是 20°C 最佳精子生产所必需的,以及一组 miRNAs(mir-49、mir-57、mir-83、mir-261 和 mir-357/358),这些 miRNAs 是 25°C 精子生产所必需的。我们观察到缺失 mir-58.1、mir-83、mir-235 和 mir-4807-4810.1 的突变体在减数分裂过程中存在缺陷,这可能是造成所观察到的精子生成缺陷的原因。此外,对这些 miRNAs 多个突变体的分析表明,这些 miRNAs 之间存在遗传相互作用。这项研究深入揭示了促进雄性和雌雄同体动物精子生产和繁殖力优化的 miRNA 的调控作用。
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引用次数: 0
Trait Imputation Enhances Nonlinear Genetic Prediction for Some Traits. 性状置换增强了某些性状的非线性遗传预测能力
IF 3.3 3区 生物学 Pub Date : 2024-09-10 DOI: 10.1093/genetics/iyae148
Ruoyu He,Jinwen Fu,Jingchen Ren,Wei Pan
The expansive collection of genetic and phenotypic data within biobanks offers an unprecedented opportunity for biomedical research. However, the frequent occurrence of missing phenotypes presents a significant barrier to fully leveraging this potential. In our target application, on one hand, we have only a small and complete dataset with both genotypes and phenotypes to build a genetic prediction model, commonly called a polygenic (risk) score (PGS or PRS); on the other hand, we have a large dataset of genotypes (e.g. from a biobank) without the phenotype of interest. Our goal is to leverage the large dataset of genotypes (but without the phenotype) and a separate GWAS summary dataset of the phenotype to impute the phenotypes, which are then used as an individual-level dataset, along with the small complete dataset, to build a nonlinear model as PGS. More specifically, we trained some nonlinear models to 7 imputed and observed phenotypes from the UK Biobank data. We then trained an ensemble model to integrate these models for each trait, resulting in higher R2 values in prediction than using only the small complete (observed) dataset. Additionally, for 2 of the 7 traits, we observed that the nonlinear model trained with the imputed traits had higher R2 than using the imputed traits directly as the PGS, while for the remaining 5 traits, no improvement was found. These findings demonstrates the potential of leveraging existing genetic data and accounting for nonlinear genetic relationships to improve prediction accuracy for some traits.
生物库中广泛收集的基因和表型数据为生物医学研究提供了前所未有的机遇。然而,经常出现的表型缺失是充分发挥这一潜力的重大障碍。在我们的目标应用中,一方面,我们只有一个包含基因型和表型的小型完整数据集来建立遗传预测模型,即通常所说的多基因(风险)评分(PGS 或 PRS);另一方面,我们有一个包含基因型的大型数据集(如来自生物库的数据集),却没有感兴趣的表型。我们的目标是利用大型基因型数据集(但不含表型)和单独的表型 GWAS 摘要数据集来估算表型,然后将其作为个体级数据集,与小型完整数据集一起,建立一个非线性模型作为 PGS。更具体地说,我们对英国生物库数据中的 7 个估算表型和观察表型进行了非线性模型训练。然后,我们训练了一个集合模型来整合每个性状的这些模型,结果预测的 R2 值高于仅使用小型完整(观测)数据集的预测值。此外,对于 7 个性状中的 2 个性状,我们观察到使用估算性状训练的非线性模型比直接使用估算性状作为 PGS 的 R2 值更高,而对于其余 5 个性状,没有发现任何改进。这些发现表明,利用现有遗传数据和非线性遗传关系来提高某些性状的预测准确性是有潜力的。
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引用次数: 0
Robust and heritable knockdown of gene expression using a self-cleaving ribozyme in Drosophila. 在果蝇中使用自裂解核糖酶稳健并可遗传地敲除基因表达。
IF 3.3 3区 生物学 Pub Date : 2024-05-03 DOI: 10.1093/genetics/iyae067
Kevin G Nyberg, Fritz Gerald Navales, Eren Keles, Joseph Q Nguyen, Laura M Hertz, Richard W Carthew
The current toolkit for genetic manipulation in the model animal Drosophila melanogaster is extensive and versatile but not without its limitations. Here, we report a powerful and heritable method to knockdown gene expression in D. melanogaster using the self-cleaving N79 hammerhead ribozyme, a modification of a naturally occurring ribozyme found in the parasite Schistosoma mansoni. A 111 bp ribozyme cassette, consisting of the N79 ribozyme surrounded by insulating spacer sequences, was inserted into four independent long noncoding RNA genes as well as the male-specific splice variant of doublesex using scarless CRISPR/Cas9-mediated genome editing. Ribozyme-induced RNA cleavage resulted in robust destruction of 3' fragments typically exceeding 90%. Single molecule RNA fluorescence in situ hybridization results suggest that cleavage and destruction can even occur for nascent transcribing RNAs. Knockdown was highly specific to the targeted RNA, with no adverse effects observed in neighboring genes or the other splice variants. To control for potential effects produced by the simple insertion of 111 nucleotides into genes, we tested multiple catalytically inactive ribozyme variants and found that a variant with scrambled N79 sequence best recapitulated natural RNA levels. Thus, self-cleaving ribozymes offer a novel approach for powerful gene knockdown in Drosophila, with potential applications for the study of noncoding RNAs, nuclear-localized RNAs, and specific splice variants of protein-coding genes.
目前对模式动物黑腹果蝇进行遗传操作的工具包既广泛又通用,但也有其局限性。在这里,我们报告了一种利用自裂解 N79 锤头核糖酶敲除黑腹果蝇基因表达的强大且可遗传的方法,N79 核糖酶是对曼氏血吸虫寄生虫中天然存在的核糖酶的改良。利用无痕 CRISPR/Cas9 介导的基因组编辑技术,将由绝缘间隔序列包围的 N79 核糖酶组成的 111 bp 核糖酶盒插入到四个独立的长非编码 RNA 基因以及双倍体的雄性特异性剪接变体中。核糖酶诱导的 RNA 裂解导致 3' 片段被强力破坏,破坏率通常超过 90%。单分子 RNA 荧光原位杂交结果表明,新生转录 RNA 甚至也会发生裂解和破坏。基因敲除对目标 RNA 具有高度特异性,对邻近基因或其他剪接变体没有不良影响。为了控制简单地在基因中插入 111 个核苷酸可能产生的影响,我们测试了多种催化活性不高的核糖酶变体,结果发现带有乱码 N79 序列的变体最能再现天然 RNA 水平。因此,自裂解核糖酶为果蝇的强效基因敲除提供了一种新方法,有望应用于研究非编码 RNA、核定位 RNA 和蛋白质编码基因的特定剪接变体。
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引用次数: 0
The Dmc1 recombinase physically interacts with and promotes the meiotic crossover functions of the Mlh1-Mlh3 endonuclease. Dmc1 重组酶与 Mlh1-Mlh3 内切酶发生物理作用,并促进减数分裂交叉功能。
IF 3.3 3区 生物学 Pub Date : 2024-04-24 DOI: 10.1093/genetics/iyae066
Gianno Pannafino, Jun Jie Chen, Viraj Mithani, Lisette Payero, Michael Gioia, J. B. Crickard, Eric Alani
The accurate segregation of homologous chromosomes during the Meiosis I reductional division in most sexually reproducing eukaryotes requires crossing over between homologs. In baker's yeast approximately 80 percent of meiotic crossovers result from Mlh1-Mlh3 and Exo1 acting to resolve double-Holliday junction (dHJ) intermediates in a biased manner. Little is known about how Mlh1-Mlh3 is recruited to recombination intermediates to perform its role in crossover resolution. We performed a gene dosage screen in baker's yeast to identify novel genetic interactors with Mlh1-Mlh3. Specifically, we looked for genes whose lowered dosage reduced meiotic crossing over using sensitized mlh3 alleles that disrupt the stability of the Mlh1-Mlh3 complex and confer defects in mismatch repair but do not disrupt meiotic crossing over. To our surprise we identified genetic interactions between MLH3 and DMC1, the recombinase responsible for recombination between homologous chromosomes during meiosis. We then showed that Mlh3 physically interacts with Dmc1 in vitro and in vivo. Partial complementation of Mlh3 crossover functions was observed when MLH3 was expressed under the control of the CLB1 promoter (NDT80 regulon), suggesting that Mlh3 function can be provided late in meiotic prophase at some functional cost. A model for how Dmc1 could facilitate Mlh1-Mlh3's role in crossover resolution is presented.
在大多数有性生殖真核生物的减数第一次还原分裂过程中,同源染色体的准确分离需要同源染色体之间的交叉。在面包酵母中,大约 80% 的减数分裂交叉是由 Mlh1-Mlh3 和 Exo1 以偏向的方式作用于双霍利迪连接(dHJ)中间体而产生的。人们对 Mlh1-Mlh3 如何被招募到重组中间体以发挥其解决交叉的作用知之甚少。我们在面包酵母中进行了基因剂量筛选,以确定与 Mlh1-Mlh3 相互作用的新基因。具体来说,我们使用敏化的 mlh3 等位基因来寻找剂量降低会减少减数分裂交叉的基因,这些基因会破坏 Mlh1-Mlh3 复合物的稳定性,导致错配修复缺陷,但不会破坏减数分裂交叉。令我们惊讶的是,我们发现了 MLH3 和 DMC1 之间的遗传相互作用,DMC1 是减数分裂过程中负责同源染色体间重组的重组酶。我们随后发现,Mlh3 与 Dmc1 在体外和体内都有物理相互作用。当MLH3在CLB1启动子(NDT80调控子)的控制下表达时,可观察到Mlh3交叉功能的部分互补,这表明Mlh3的功能可在减数分裂前期的晚期以一定的功能代价提供。本文提出了一个模型,说明 Dmc1 如何促进 Mlh1-Mlh3 在交叉解析中发挥作用。
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引用次数: 0
Osiris gene family defines the cuticle nanopatterns of Drosophila. Osiris 基因家族确定了果蝇角质层的纳米形态。
IF 3.3 3区 生物学 Pub Date : 2024-04-23 DOI: 10.1093/genetics/iyae065
Zhengkuan Sun, Sachi Inagaki, Keita Miyoshi, Kuniaki Saito, Shigeo Hayashi
Nanostructures of pores and protrusions in the insect cuticle modify molecular permeability and surface wetting, and help insects sense various environmental cues. However, the cellular mechanisms that modify cuticle nanostructures are poorly understood. Here, we elucidate how insect-specific Osiris family genes are expressed in various cuticle-secreting cells in the Drosophila head during the early stages of cuticle secretion and cover nearly the entire surface of the head epidermis. Furthermore, we demonstrate how each sense organ cell with various cuticular nanostructures expressed a unique combination of Osiris genes. Osiris gene mutations cause various cuticle defects in the corneal nipples and pores of the chemosensory sensilla. Thus, our study emphasizes on the importance of Osiris genes for elucidating cuticle nanopatterning in insects.
昆虫角质层中的纳米孔隙和突起结构可改变分子渗透性和表面润湿性,并帮助昆虫感知各种环境线索。然而,人们对改变角质层纳米结构的细胞机制知之甚少。在这里,我们阐明了昆虫特异性 Osiris 家族基因如何在果蝇头部分泌角质层的早期阶段在各种分泌角质层的细胞中表达,并覆盖头部表皮的几乎整个表面。此外,我们还展示了具有各种角质层纳米结构的每个感觉器官细胞是如何表达独特的 Osiris 基因组合的。Osiris 基因突变会导致角膜乳头和化学感觉器孔的各种角质层缺陷。因此,我们的研究强调了 Osiris 基因对于阐明昆虫角质层纳米结构的重要性。
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引用次数: 0
Ploidy inference from single-cell data: application to human and mouse cell atlases. 从单细胞数据推断倍性:应用于人类和小鼠细胞图谱。
IF 3.3 3区 生物学 Pub Date : 2024-04-23 DOI: 10.1093/genetics/iyae061
Fumihiko Takeuchi, Norihiro Kato
Ploidy is relevant to numerous biological phenomena, including development, metabolism, and tissue regeneration. Single-cell RNA-seq and other omics studies are revolutionizing our understanding of biology, yet they have largely overlooked ploidy. This is likely due to the additional assay step required for ploidy measurement. Here, we developed a statistical method to infer ploidy from single-cell ATAC-seq data, addressing this gap. When applied to data from human and mouse cell atlases, our method enabled systematic detection of polyploidy across diverse cell types. This method allows for the integration of ploidy analysis into single-cell studies. Additionally, this method can be adapted to detect the proliferating stage in the cell cycle and copy number variations in cancer cells. The software is implemented as the scPloidy package of the R software and is freely available from CRAN.
倍性与许多生物现象有关,包括发育、新陈代谢和组织再生。单细胞RNA-seq和其他omics研究正在彻底改变我们对生物学的理解,但它们在很大程度上忽略了倍性。这可能是由于倍性测量需要额外的检测步骤。在这里,我们开发了一种从单细胞 ATAC-seq 数据推断倍性的统计方法,弥补了这一空白。当应用到人类和小鼠细胞图谱的数据时,我们的方法能够系统地检测不同细胞类型的多倍体。这种方法可将多倍体分析整合到单细胞研究中。此外,这种方法还可用于检测细胞周期的增殖阶段和癌细胞的拷贝数变化。该软件作为 R 软件的 scPloidy 软件包实现,可从 CRAN 免费获取。
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引用次数: 0
MAB-5/Hox regulates the Q neuroblast transcriptome, including cwn-1/Wnt, to mediate posterior migration in Caenorhabditis elegans. MAB-5/Hox调节Q神经母细胞转录组,包括cwn-1/Wnt,以介导秀丽隐杆线虫的后向迁移。
IF 3.3 3区 生物学 Pub Date : 2024-04-23 DOI: 10.1093/genetics/iyae045
Vitoria K. Paolillo, Matthew E. Ochs, E. Lundquist
Neurogenesis involves the precisely coordinated action of genetic programs controlling large-scale neuronal fate specification down to terminal events of neuronal differentiation. The Q neuroblasts in Caenorhabditis elegans, QL on the left and QR on the right, divide, differentiate, and migrate in a similar pattern to produce three neurons each. However, QL on the left migrates posteriorly, and QR on the right migrates anteriorly. The MAB-5/Hox transcription factor is necessary and sufficient for posterior Q lineage migration and is normally expressed only in the QL lineage. To define genes controlled by MAB-5 in the Q cells, fluorescence-activated cell sorting was utilized to isolate populations of Q cells at a time in early L1 larvae when MAB-5 first becomes active. Sorted Q cells from wild-type, mab-5 loss-of-function (lof), and mab-5 gain-of-function (gof) mutants were subject to RNA-seq and differential expression analysis. Genes enriched in Q cells included those involved in cell division, DNA replication, and DNA repair, consist with the neuroblast stem cell identity of the Q cells at this stage. Genes affected by mab-5 included those involved in neurogenesis, neural development, and interaction with the extracellular matrix. cwn-1, which encodes a Wnt signaling molecule, showed a paired response to mab-5 in the Q cells: cwn-1 expression was reduced in mab-5(lof) and increased in mab-5(gof), suggesting that MAB-5 is required for cwn-1 expression in Q cells. MAB-5 is required to prevent anterior migration of the Q lineage while it transcriptionally reprograms the Q lineage for posterior migration. Functional genetic analysis revealed that CWN-1 is required downstream of MAB-5 to inhibit anterior migration of the QL lineage, likely in parallel to EGL-20/Wnt in a noncanonical Wnt pathway. In sum, work here describes a Q cell transcriptome, and a set of genes regulated by MAB-5 in the QL lineage. One of these genes, cwn-1, acts downstream of mab-5 in QL migration, indicating that this gene set includes other genes utilized by MAB-5 to facilitate posterior neuroblast migration.
神经发生涉及基因程序的精确协调作用,这些程序控制着大范围神经元命运的规范,直至神经元分化的终端事件。秀丽隐杆线虫的 Q 神经母细胞(左侧为 QL,右侧为 QR)以相似的模式分裂、分化和迁移,各自产生三个神经元。不过,左侧的 QL 向后迁移,而右侧的 QR 则向前方迁移。MAB-5/Hox 转录因子是 Q 系向后迁移的必要和充分条件,通常只在 QL 系中表达。为了确定 Q 细胞中受 MAB-5 控制的基因,我们利用荧光激活细胞分选技术,在 L1 幼虫早期 MAB-5 开始活跃时分离 Q 细胞群。对野生型、mab-5 功能缺失(lof)和 mab-5 功能增益(gof)突变体的 Q 细胞进行了 RNA 序列和差异表达分析。Q细胞中富集的基因包括参与细胞分裂、DNA复制和DNA修复的基因,这与此阶段Q细胞的神经母细胞干细胞特征一致。编码Wnt信号分子的cwn-1在Q细胞中显示出与mab-5成对的反应:cwn-1在mab-5(lof)中表达减少,而在mab-5(gof)中表达增加,这表明MAB-5对Q细胞中cwn-1的表达是必需的。MAB-5是防止Q系向前方迁移所必需的,同时它还能转录重编程Q系向后方迁移。功能基因分析表明,CWN-1需要在MAB-5的下游抑制QL系的前向迁移,很可能与EGL-20/Wnt并行于非经典的Wnt通路。总之,本文描述了 Q 细胞转录组和 QL 系中受 MAB-5 调控的一组基因。其中一个基因cwn-1在QL迁移过程中作用于mab-5的下游,这表明该基因组包括MAB-5用于促进后部神经母细胞迁移的其他基因。
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引用次数: 0
Evolutionary graph theory beyond single mutation dynamics: on how network structured populations cross fitness landscapes. 超越单一突变动力学的进化图论:网络结构种群如何跨越适应性景观。
IF 3.3 3区 生物学 Pub Date : 2024-04-18 DOI: 10.1093/genetics/iyae055
Yang Ping Kuo, Oana Carja
Spatially-resolved datasets are revolutionizing knowledge in molecular biology, yet are under-utilized for questions in evolutionary biology. To gain insight from these large-scale datasets of spatial organization, we need mathematical representations and modeling techniques that can both capture their complexity, but also allow for mathematical tractability. Evolutionary graph theory utilizes the mathematical representation of networks as a proxy for heterogeneous population structure and has started to reshape our understanding of how spatial structure can direct evolutionary dynamics. However, previous results are derived for the case of a single new mutation appearing in the population and the role of network structure in shaping fitness landscape crossing is still poorly understood. Here we study how network structured populations cross fitness landscapes and show that even a simple extension to a two-mutational landscape can exhibit complex evolutionary dynamics that cannot be predicted using previous single-mutation results. We show how our results can be intuitively understood through the lens of how the two main evolutionary properties of a network, the amplification and acceleration factors, change the expected fate of the intermediate mutant in the population and further discuss how to link these models to spatially-resolved datasets of cellular organization.
空间分辨数据集正在彻底改变分子生物学知识,但在进化生物学问题上却未得到充分利用。为了从这些大规模的空间组织数据集中获得洞察力,我们需要既能捕捉其复杂性,又具有数学可操作性的数学表征和建模技术。进化图论利用网络的数学表示作为异质种群结构的代表,已经开始重塑我们对空间结构如何引导进化动态的理解。然而,以往的结果都是针对种群中出现单个新突变的情况得出的,人们对网络结构在塑造适应性景观交叉中的作用仍然知之甚少。在这里,我们研究了网络结构种群如何跨越适应性景观,并表明即使是简单扩展到双突变景观,也会表现出复杂的进化动态,而这是以前的单突变结果无法预测的。我们展示了如何通过网络的两个主要进化特性--放大因子和加速因子--如何改变种群中中间突变体的预期命运来直观地理解我们的结果,并进一步讨论了如何将这些模型与细胞组织的空间分辨数据集联系起来。
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引用次数: 0
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