Cell structure and function最新文献_第8页

Expansão Maxilar Apoiada em Mini-implantes (MARPE) – guia prático para planejamento e instalação 微型种植体支持的上颌扩张(MARPE) -规划和安装实用指南

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2020-01-01 DOI: 10.24077/2020;1352-csf1024

L. Fernandes, Jonas Capelli Júnior, J. A. M. Miguel

Rapid maxillary expansion (RME) is an orthodontic treatment alternative that aims to increase the transverse direction of the maxilla by separating the median palatine suture (MPS). miniscrew-assisted rapid palatal expansion (MARPE) aims to enhance the orthopedic effects of RME through skeletal anchorage. Thus, the aim of this article is to provide a guide for MARPE planning in cone beam computed tomography (CBCT) and for installation of the expander device with this technique. In addition, a case report of a Caucasian male patient, 16 years and 3 months old with Class II malocclusion, division 1 right subdivision, posterior crossbite of the right side and atresic upper arch in the post-pubertal growth spurt phase will be presented. The patient was treated with MARPE for a period of 5 weeks, when overcorrection of crossbite, correction of maxillary atresia, opening of MPS and creation of a transient diastema between the upper incisors were achieved, evidencing the success of the MARPE technique in a post-pubertal growth spurt patient.

快速上颌扩张(RME)是一种正畸治疗方案，旨在通过分离腭正中缝合线(MPS)来增加上颌的横向。微型辅助快速腭扩张术(MARPE)旨在通过骨骼锚固来增强RME的矫形效果。因此，本文的目的是为锥形束计算机断层扫描(CBCT)中的MARPE规划和使用该技术安装膨胀装置提供指导。另外，我们将报告一例16岁零3个月的白人男性患者，患有II类错牙合，1区右细分，右侧后牙合，上弓闭锁，处于青春期后生长突增期。患者接受MARPE治疗5周，实现了交叉咬合过矫、上颌闭锁矫正、MPS开放和上门牙间短暂间隙的建立，证明MARPE技术在青春期后生长突增患者中的成功。

引用次数: 0

p18/Lamtor1-mTORC1 Signaling Controls Development of Mucin-producing Goblet Cells in the Intestine. p18/Lamtor1-mTORC1信号传导控制着肠道中产生黏蛋白的上皮细胞的发育。

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2020-01-01 DOI: 10.1247/csf.20018

Shizuka Ito, Shigeyuki Nada, Daisuke Yamazaki, Tetsuya Kimura, Kentaro Kajiwara, Hiroaki Miki, Masato Okada

Mechanistic target of rapamycin complex 1 (mTORC1) plays a pivotal role in controlling cell growth and metabolism in response to nutrients and growth factors. The activity of mTORC1 is dually regulated by amino acids and growth factor signaling, and amino acid-dependent mTORC1 activity is regulated by mTORC1 interaction with the Ragulator-Rag GTPase complex, which is localized to the surface of lysosomes via a membrane-anchored protein, p18/Lamtor1. However, the physiological function of p18-Ragulator-dependent mTORC1 signaling remains elusive. The present study evaluated the function of p18-mediated mTORC1 signaling in the intestinal epithelia using p18 conditional knockout mice. In p18 knockout colonic crypts, mTORC1 was delocalized from lysosomes, and in vivo mTORC1 activity was markedly decreased. Histologically, p18 knockout crypts exhibited significantly increased proliferating cells and dramatically decreased mucin-producing goblet cells, while overall crypt architecture and enteroendocrine cell differentiation were unaffected. Furthermore, p18 knockout crypts normally expressed transcription factors implicated in crypt differentiation, such as Cdx2 and Klf4, indicating that p18 ablation did not affect the genetic program of cell differentiation. Analysis of colon crypt organoid cultures revealed that both p18 ablation and rapamycin treatment robustly suppressed development of mucin-producing goblet cells. Hence, p18-mediated mTORC1 signaling could promote the anabolic metabolism required for robust mucin production in goblet cells to protect the intestinal epithelia from various external stressors.Key words: mTORC1, p18/lamtor1, intestinal epithelium, goblet cells, mucin.

rapamycin复合体1 (Mechanistic target of rapamycin complex 1, mTORC1)在细胞对营养物质和生长因子的反应中，在控制细胞生长和代谢中起关键作用。mTORC1的活性受到氨基酸和生长因子信号的双重调节，氨基酸依赖性的mTORC1活性受到mTORC1与调节因子- rag GTPase复合物相互作用的调节，该复合物通过膜锚定蛋白p18/Lamtor1定位于溶酶体表面。然而，p18-调节因子依赖的mTORC1信号的生理功能仍然难以捉摸。本研究利用p18条件敲除小鼠，评估了p18介导的mTORC1信号在肠上皮中的功能。在p18基因敲除的结肠隐窝中，mTORC1从溶酶体中脱位，体内mTORC1活性明显降低。组织学上，p18基因敲除后的隐窝增殖细胞显著增加，产生黏液的杯状细胞显著减少，而整体隐窝结构和肠内分泌细胞分化未受影响。此外，p18敲除隐窝正常表达与隐窝分化相关的转录因子，如Cdx2和Klf4，这表明p18敲除不影响细胞分化的遗传程序。结肠隐窝类器官培养分析显示，p18消融和雷帕霉素治疗均可有效抑制产生黏液的杯状细胞的发育。因此，p18介导的mTORC1信号传导可以促进杯状细胞中强大的粘蛋白产生所需的合成代谢，以保护肠上皮免受各种外部应激源的影响。关键词:mTORC1, p18/lamtor1，肠上皮，杯状细胞，粘蛋白

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引用次数: 3

Determinando diâmetro mésio-distal de dentes anteriores em paciente com agenesia dentária 确定牙齿发育不全患者前牙近端-远端直径

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2020-01-01 DOI: 10.24077/2020;1351-csf1019

Diego Ramires Silva Santos, J. A. M. Miguel

引用次数: 0

Folding Latency of Fluorescent Proteins Affects the Mitochondrial Localization of Fusion Proteins. 荧光蛋白的折叠潜伏期影响融合蛋白的线粒体定位。

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2019-11-15 DOI: 10.1247/csf.19028

Sayaka Kashiwagi,Yoichiro Fujioka,Aya O Satoh,Aiko Yoshida,Mari Fujioka,Prabha Nepal,Atsushi Tsuzuki,Ozora Aoki,Sarad Paudel,Hitoshi Sasajima,Yusuke Ohba

The discovery of fluorescent proteins (FPs) has revolutionized cell biology. The fusion of targeting sequences to FPs enables the investigation of cellular organelles and their dynamics; however, occasionally, such fluorescent fusion proteins (FFPs) exhibit behavior different from that of the native proteins. Here, we constructed a color pallet comprising different organelle markers and found that FFPs targeted to the mitochondria were mislocalized when fused to certain types of FPs. Such FPs included several variants of Aequorea victoria green FP (avGFP) and a monomeric variant of the red FP. Because the FFPs that are mislocalized include FPs with faster maturing or folding mutations, the increase in the maturation rate is likely to prevent their expected localization. Indeed, when we reintroduced amino acid substitutions so that the FP sequences were equivalent to that of wild-type avGFP, FFP localization to the mitochondria was significantly enhanced. Moreover, similar amino acid substitutions improved the localization of mitochondria-targeted pHluorin, which is a pH-sensitive variant of GFP, and its capability to monitor pH changes in the mitochondrial matrix. Our findings demonstrate the importance of selecting FPs that maximize FFP function.Key words: fluorescent protein, organelle, fusion protein, mitochondria.

荧光蛋白(FPs)的发现彻底改变了细胞生物学。目标序列与FPs的融合使研究细胞器及其动力学成为可能;然而，偶尔，这种荧光融合蛋白(FFPs)表现出与天然蛋白不同的行为。在这里，我们构建了一个包含不同细胞器标记的色板，发现靶向线粒体的FFPs在与某些类型的FPs融合时定位错误。这类FP包括维多利亚水梨绿色FP (avGFP)的几个变体和红色FP的一个单体变体。由于错误定位的FFPs包括成熟更快或折叠突变更快的FPs，成熟率的增加可能会阻止它们预期的定位。事实上，当我们重新引入氨基酸替换，使FP序列与野生型avGFP相当时，FFP在线粒体中的定位显著增强。此外，类似的氨基酸替换改善了线粒体靶向pHluorin的定位，它是GFP的pH敏感变体，并具有监测线粒体基质pH变化的能力。我们的研究结果证明了选择能够最大化FFP功能的FPs的重要性。关键词:荧光蛋白，细胞器，融合蛋白，线粒体。

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引用次数: 0

Localization of BCR-ABL to Stress Granules Contributes to Its Oncogenic Function. BCR-ABL对应激颗粒的定位有助于其致癌功能。

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2019-11-15 DOI: 10.1247/csf.19033

Sayaka Kashiwagi,Yoichiro Fujioka,Takeshi Kondo,Aya O Satoh,Aiko Yoshida,Mari Fujioka,Hitoshi Sasajima,Maho Amano,Takanori Teshima,Yusuke Ohba

The oncogenic tyrosine kinase BCR-ABL activates a variety of signaling pathways and plays a causative role in the pathogenesis of chronic myelogenous leukemia (CML); however, the subcellular distribution of this chimeric protein remains controversial. Here, we report that BCR-ABL is localized to stress granules and that its granular localization contributes to BCR-ABL-dependent leukemogenesis. BCR-ABL-positive granules were not colocalized with any markers for membrane-bound organelles but were colocalized with HSP90a, a component of RNA granules. The number of such granules increased with thapsigargin treatment, confirming that the granules were stress granules. Given that treatment with the ABL kinase inhibitor imatinib and elimination of the N-terminal region of BCR-ABL abolished granule formation, kinase activity and the coiled-coil domain are required for granule formation. Whereas wild-type BCR-ABL rescued the growth defect in IL-3-depleted Ba/F3 cells, mutant BCR-ABL lacking the N-terminal region failed to do so. Moreover, forced tetramerization of the N-terminus-deleted mutant could not restore the growth defect, indicating that granule formation, but not tetramerization, through its N-terminus is critical for BCR-ABL-dependent oncogenicity. Our findings together provide new insights into the pathogenesis of CML by BCR-ABL and open a window for developing novel therapeutic strategies for this disease.Key words: BCR-ABL, subcellular localization, stress granule.

致癌性酪氨酸激酶BCR-ABL激活多种信号通路，在慢性髓性白血病(CML)的发病机制中起致病作用;然而，这种嵌合蛋白的亚细胞分布仍然存在争议。在这里，我们报道BCR-ABL定位于应激颗粒，其颗粒定位有助于BCR-ABL依赖性白血病的发生。bcr - abl阳性颗粒不与任何膜结合细胞器标记物共定位，但与RNA颗粒成分HSP90a共定位。这些颗粒的数量随着thapsigargin的处理而增加，证实了这些颗粒是应激颗粒。鉴于用ABL激酶抑制剂伊马替尼治疗和消除BCR-ABL的n端区域可消除颗粒形成，因此颗粒形成需要激酶活性和卷曲-卷曲结构域。野生型BCR-ABL修复了il -3缺失的Ba/F3细胞的生长缺陷，而缺乏n端区域的突变型BCR-ABL则无法修复。此外，n端缺失突变体的强制四聚化不能恢复生长缺陷，这表明通过其n端形成颗粒，而不是四聚化，对bcr - abl依赖性的致癌性至关重要。我们的研究结果共同为BCR-ABL的CML发病机制提供了新的见解，并为开发新的治疗策略打开了一扇窗。关键词:BCR-ABL，亚细胞定位，应力颗粒。

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引用次数: 0

MGSE Regulates Crosstalk from the Mucin Pathway to the TFE3 Pathway of the Golgi Stress Response. MGSE调控高尔基应激反应中从粘蛋白途径到TFE3途径的串扰。

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2019-10-19 DOI: 10.1247/csf.19009

Mohamad Ikhwan Jamaludin,Sadao Wakabayashi,Mai Taniguchi,Kanae Sasaki,Ryota Komori,Hirotada Kawamura,Hayataka Takase,Miyu Sakamoto,Hiderou Yoshida

The Golgi apparatus is an organelle where membrane or secretory proteins receive post-translational modifications such as glycosylation and sulfation, after which the proteins are selectively transported to their final destinations through vesicular transport. When the synthesis of secretory or membrane proteins is increased and overwhelms the capacity of the Golgi (Golgi stress), eukaryotic cells activate a homeostatic mechanism called the Golgi stress response to augment the capacity of the Golgi. Four response pathways of the Golgi stress response have been identified, namely the TFE3, CREB3, HSP47, and proteoglycan pathways, which regulate the general function of the Golgi, apoptosis, cell survival, and proteoglycan glycosylation, respectively. Here, we identified a novel response pathway that augments the expression of glycosylation enzymes for mucins in response to insufficiency in mucin-type glycosylation in the Golgi (mucin-type Golgi stress), and we found that expression of glycosylation enzymes for mucins such as GALNT5, GALNT8, and GALNT18 was increased upon mucin-type-Golgi stress. We named this pathway the mucin pathway. Unexpectedly, mucin-type Golgi stress induced the expression and activation of TFE3, a key transcription factor regulating the TFE3 pathway, suggesting that the activated mucin pathway sends a crosstalk signal to the TFE3 pathway. We identified an enhancer element regulating transcriptional induction of TFE3 upon mucin-type Golgi stress, and named it the mucin-type Golgi stress response element, of which consensus was ACTTCC(N9)TCCCCA. These results suggested that crosstalk from the mucin pathway to the TFE3 pathway has an important role in the regulation of the mammalian Golgi stress response.Key words: Golgi stress, mucin, TFE3, organelle autoregulation, organelle zone.

高尔基体是一种细胞器，膜或分泌蛋白在其中接受翻译后修饰，如糖基化和硫酸化，之后蛋白质通过囊泡运输选择性地转运到最终目的地。当分泌蛋白或膜蛋白的合成增加并超过高尔基体的能力(高尔基应激)时，真核细胞激活一种称为高尔基应激反应的稳态机制来增强高尔基体的能力。目前鉴定出高尔基体应激反应的4条应答通路，分别是TFE3、CREB3、HSP47和蛋白多糖通路，它们分别调控高尔基体的一般功能、细胞凋亡、细胞存活和蛋白多糖糖基化。在这里，我们发现了一种新的反应途径，在高尔基体中，当粘蛋白型糖基化不足时，增加粘蛋白糖基化酶的表达(粘蛋白型高尔基应激)，我们发现粘蛋白糖基化酶如GALNT5、GALNT8和GALNT18的表达在粘蛋白型高尔基应激下增加。我们将这一途径命名为粘蛋白途径。出乎意料的是，粘蛋白型高尔基应激诱导了调控TFE3通路的关键转录因子TFE3的表达和激活，表明被激活的粘蛋白通路向TFE3通路发送了串扰信号。我们鉴定出一个调节TFE3在黏素型高尔基胁迫下转录诱导的增强元件，并将其命名为黏素型高尔基胁迫应答元件，一致命名为actcc (N9)TCCCCA。这些结果表明，从粘蛋白途径到TFE3途径的串扰在哺乳动物高尔基应激反应的调控中具有重要作用。关键词:高尔基应激，粘蛋白，TFE3，细胞器自调节，细胞器区

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引用次数: 0

Dispersion of endoplasmic reticulum-associated compartments by 4-phenyl butyric acid in yeast cells. 酵母细胞中4-苯基丁酸对内质网相关室的分散作用。

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2019-10-17 DOI: 10.1247/csf.19023

T. Mai, Yuki Ishiwata‐Kimata, Q. Le, Hiroyuki Kido, Y. Kimata

In yeast Saccharomyces cerevisiae cells, some aberrant multimembrane-spanning proteins are not transported to the cell surface but form and are accumulated in endoplasmic reticulum (ER)-derived subcompartments, known as the ER-associated compartments (ERACs), which are observed as puncta under fluorescence microscopy. Here we show that a mutant of the cell surface protein Pma1, Pma1-2308, was accumulated in the ERACs, as well as the heterologously expressed mammalian cystic fibrosis transmembrane conductance regulator (CFTR), in yeast cells. Pma1-2308 and CFTR were located on the same ERACs. We also note that treatment of cells with 4-phenyl butyric acid (4-PBA) compromised the ERAC formation by Pma1-2308 and CFTR, suggesting that 4-PBA exerts a chaperone-like function in yeast cells. Intriguingly, unlike ER stress induced by the canonical ER stressor tunicamycin, ER stress that was induced by Pma1-2308 was aggravated by 4-PBA. We assume that this observation demonstrates a beneficial aspect of ERACs, and thus propose that the ERACs are formed through aggregation of aberrant transmembrane proteins and work as the accumulation sites of multiple ERAC-forming proteins for their sequestration. Key words: protein aggregation, organelle, unfolded protein response, ER stress, 4-PBA.

在酵母细胞中，一些异常的多膜跨越蛋白不会被运输到细胞表面，而是形成并积聚在内质网(ER)衍生的亚室中，称为内质网相关室(ERACs)，荧光显微镜下可以观察到这些小点。在这里，我们发现细胞表面蛋白Pma1的突变体Pma1-2308在erac中积累，以及在酵母细胞中异源表达的哺乳动物囊性纤维化跨膜传导调节因子(CFTR)。Pma1-2308和CFTR位于同一erac上。我们还注意到，用4-苯基丁酸(4-PBA)处理细胞会破坏Pma1-2308和CFTR形成的ERAC，这表明4-PBA在酵母细胞中发挥了类似伴侣的功能。有趣的是，与典型内质网应激源tunicamycin诱导的内质网应激不同，Pma1-2308诱导的内质网应激被4-PBA加重。我们假设这一观察结果表明了erac的有益方面，因此提出erac是通过异常跨膜蛋白的聚集形成的，并作为多种erac形成蛋白的积累位点进行隔离。关键词:蛋白聚集，细胞器，未折叠蛋白反应，内质网应激，4-PBA

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引用次数: 3

Identification of 15 New Bypassable Essential Genes of Fission Yeast. 裂变酵母15个新的可绕过必需基因的鉴定。

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2019-09-27 DOI: 10.1247/csf.19025

Aoi Takeda, Shigeaki Saitoh, Hiroyuki Ohkura, Kenneth E Sawin, Gohta Goshima

Every organism has a different set of genes essential for its viability. This indicates that an organism can become tolerant to the loss of an essential gene under certain circumstances during evolution, via the manifestation of 'masked' alternative mechanisms. In our quest to systematically uncover masked mechanisms in eukaryotic cells, we developed an extragenic suppressor screening method using haploid spores deleted of an essential gene in the fission yeast Schizosaccharomyces pombe. We screened for the 'bypass' suppressors of lethality of 92 randomly selected genes that are essential for viability in standard laboratory culture conditions. Remarkably, extragenic mutations bypassed the essentiality of as many as 20 genes (22%), 15 of which have not been previously reported. Half of the bypass-suppressible genes were involved in mitochondria function; we also identified multiple genes regulating RNA processing. 18 suppressible genes were conserved in the budding yeast Saccharomyces cerevisiae, but 13 of them were non-essential in that species. These trends suggest that essentiality bypass is not a rare event and that each organism may be endowed with secondary or backup mechanisms that can substitute for primary mechanisms in various biological processes. Furthermore, the robustness of our simple spore-based methodology paves the way for genome-scale screening.Key words: Schizosaccharomyces pombe, extragenic suppressor screening, bypass of essentiality (BOE), cut7 (kinesin-5), hul5 (E3 ubiquitin ligase).

每一种生物都有一套不同的对其生存至关重要的基因。这表明，在进化过程中，生物体可以通过“隐藏”替代机制的表现，在某些情况下耐受基本基因的缺失。为了系统地揭示真核细胞中的隐藏机制，我们利用分裂酵母Schizosaccharomyces pombe中缺失一个重要基因的单倍体孢子，开发了一种外基因抑制筛选方法。我们筛选了92个随机选择的基因的“旁路”致命抑制因子，这些基因对标准实验室培养条件下的生存能力至关重要。值得注意的是，基因外突变绕过了多达20个基因(22%)的必要性，其中15个以前没有报道过。一半的旁路抑制基因参与线粒体功能;我们还发现了多个调控RNA加工的基因。在出芽酵母中保守的抑制基因有18个，其中13个为非必需基因。这些趋势表明，本质绕过并非罕见事件，每个生物体都可能被赋予次要或备用机制，可以替代各种生物过程中的主要机制。此外，我们简单的基于孢子的方法的稳健性为基因组规模的筛选铺平了道路。关键词:裂糖酵母，基因外抑制因子筛选，必要性旁路(BOE)， cut7(激酶-5)，hul5 (E3泛素连接酶)。

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引用次数: 0

Mutations in mxc Tumor-Suppressor Gene Induce Chromosome Instability in Drosophila Male Meiosis. mxc抑癌基因突变诱导果蝇雄性减数分裂染色体不稳定。

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2019-09-05 DOI: 10.1247/csf.19022

K. Tanabe, Rie Awane, Tsuyoshi Shoda, Kanta Yamazoe, Y. Inoue

Drosophila Mxc protein is a component of the histone locus body (HLB), which is required for the expression of canonical histone genes, and severe mxc mutations generate tumors in larval hematopoietic tissues. A common characteristic of cancer cells is chromosomal instability (CIN), but whether mxc mutants exhibit this feature is unknown. Here, examination of post-meiotic spermatids created after male meiosis revealed that a fraction of the spermatids in hypomorphic mxcG46 mutants contained extra micronuclei or abnormally sized nuclei, corresponding to CIN. Moreover, we observed that the so-called lagging chromosomes retained between chromosomal masses separated toward spindle poles at telophase I. Time-lapse recordings show that micronuclei were generated from lagging chromosomes, and the abnormal chromosomes in mxcG46 mutants lacked centromeres. In normal spermatocyte nuclei, the HLB component FLASH colocalized with Mxc, whereas FLASH was dispersed in mxcG46 spermatocyte nuclei. Furthermore, we observed genetic interactions between Mxc and other HLB components in meiotic chromosome segregation, which suggests that inhibition of HLB formation is responsible for aberrant chromosome segregation in mxcG46. Quantitative real-time PCR revealed that canonical histone mRNA levels were decreased in mxcG46. Lastly, similar meiotic phenotypes appeared in the spermatids of histone H4 mutants and in the spermatids in testes depleted for chromosome-construction factors. Considering these genetic data, we propose that abnormal chromosome segregation leading to CIN development results from a loss of chromosome integrity caused by diminished canonical histone levels in mxc mutants. Key words: Chromosome instability, Drosophila, meiosis, tumor-suppressor gene.

果蝇Mxc蛋白是组蛋白基因座体（HLB）的一种成分，是典型组蛋白基因表达所必需的，严重的Mxc突变会在幼虫造血组织中产生肿瘤。癌症细胞的一个常见特征是染色体不稳定性（CIN），但mxc突变体是否表现出这种特征尚不清楚。在这里，对雄性减数分裂后产生的减数分裂后精子细胞的检查显示，亚形态mxcG46突变体中的一部分精子细胞含有额外的微核或异常大小的细胞核，对应于CIN。此外，我们观察到，在末期I，所谓的滞后染色体保留在向纺锤极分离的染色体团之间。延时记录显示，微核是由滞后染色体产生的，mxcG46突变体中的异常染色体缺乏着丝粒。在正常精母细胞核中，HLB组分FLASH与Mxc共定位，而FLASH分散于mxcG46精母细胞核。此外，我们在减数分裂染色体分离中观察到Mxc和其他HLB成分之间的遗传相互作用，这表明HLB形成的抑制是mxcG46异常染色体分离的原因。定量实时PCR显示mxcG46中典型组蛋白mRNA水平降低。最后，类似的减数分裂表型出现在组蛋白H4突变体的精子细胞和染色体构建因子缺失的睾丸中的精子细胞中。考虑到这些遗传数据，我们认为导致CIN发展的异常染色体分离是由mxc突变体中典型组蛋白水平降低引起的染色体完整性丧失引起的。关键词：染色体不稳定，果蝇，减数分裂，肿瘤抑制基因。

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引用次数: 8

Implication of a novel function of Sar1 in the nucleus. Sar1在细胞核中的新功能。

IF 1.5 4区生物学 Q4 CELL BIOLOGY

Cell structure and function

Pub Date : 2019-08-09 DOI: 10.1247/csf.19019

K. Horikawa, Tomohiro Yorimitsu, C. Kodera, Ken Sato

The coat protein complex II (COPII) generates transport carriers that deliver newly synthesized proteins from the endoplasmic reticulum (ER) to the Golgi apparatus. The small GTPase Sar1 is a well-known regulator of the assembly of the COPII coat. In the present study, we demonstrate that, besides its well-established role in ER-to-Golgi trafficking, the nuclear localization of Sar1 is essential for the viability of Saccharomyces cerevisiae. Inhibition of either the nuclear entry or retention of Sar1 leads to a severe growth defect. Additionally, in vivo deletion of Sar1, by using conditional genetic depletion, further demonstrates that the loss of nuclear localization of Sar1 results in an abnormal nuclear envelope shape. Our findings highlighted a possible novel role of Sar1 within the nucleus, which may relate to the proper formation of the nuclear envelope. Keywords: Sar1, COPII, small GTPase, nuclear envelope, membrane traffic.

外壳蛋白复合体II（COPII）产生运输载体，将新合成的蛋白质从内质网（ER）输送到高尔基体。小型GTPase Sar1是众所周知的COPII涂层组件调节器。在本研究中，我们证明，除了其在内质网至高尔基体运输中的既定作用外，Sar1的核定位对酿酒酵母的生存能力至关重要。抑制Sar1的核进入或保留会导致严重的生长缺陷。此外，通过使用条件遗传耗竭对Sar1进行体内缺失，进一步证明Sar1的核定位缺失导致异常的核膜形状。我们的发现强调了Sar1在细胞核内可能发挥的新作用，这可能与核膜的正确形成有关。关键词：Sar1，COPII，小GTP酶，核包膜，膜交通。

引用次数: 3