Cell structure and function最新文献_第8页

Reinvestigation of Disulfide-bonded Oligomeric Forms of the Unfolded Protein Response Transducer ATF6. 重新研究未折叠蛋白反应转换器 ATF6 的二硫键寡聚体形式。

IF 1.5 4区生物学

Cell structure and function Pub Date : 2020-01-30 Epub Date: 2019-12-19 DOI: 10.1247/csf.19030

Hibiki Koba, Shengyu Jin, Nanami Imada, Tokiro Ishikawa, Satoshi Ninagawa, Tetsuya Okada, Tetsushi Sakuma, Takashi Yamamoto, Kazutoshi Mori

{"title":"Reinvestigation of Disulfide-bonded Oligomeric Forms of the Unfolded Protein Response Transducer ATF6.","authors":"Hibiki Koba, Shengyu Jin, Nanami Imada, Tokiro Ishikawa, Satoshi Ninagawa, Tetsuya Okada, Tetsushi Sakuma, Takashi Yamamoto, Kazutoshi Mori","doi":"10.1247/csf.19030","DOIUrl":"10.1247/csf.19030","url":null,"abstract":"ATF6α is an endoplasmic reticulum (ER)-embedded transcription factor which is rapidly activated by ER stress, and a major regulator of ER chaperone levels in vertebrates. We previously suggested that ATF6α occurs as a monomer, dimer and oligomer in the unstressed ER of Chinese hamster ovary cells due to the presence of two evolutionarily conserved cysteine residues in its luminal region (C467 and C618), and showed that ATF6α is reduced upon ER stress, such that only reduced monomer ATF6α is translocated to the Golgi apparatus for activation by proteolysis. However, mutagenesis analysis (C467A and C618A) revealed that the C618A mutant behaves in an unexpected manner (monomer and oligomer) during non-reducing SDS-PAGE, for reasons which remained unclear. Here, we used human colorectal carcinoma-derived HCT116 cells deficient in ATF6α and its relevant ATF6β, and found that ATF6α dimer and oligomer are both dimers, which we designated C618-dimer and C467-dimer, respectively. We demonstrated that C467-dimer (previously considered an oligomer) behaved bigger than C618-dimer (previously considered a dimer) during non-reducing SDS-PAGE, based on their disulfide-bonded structures. Furthermore, ATF6α monomer physically associates with another ATF6α monomer in the absence of disulfide bonding, which renders two C467 residues in close proximity so that formation of C467-dimer is much easier than that of C618-dimer. In contrast, C618-dimer is more easily reduced upon ER stress. Thus, our analysis revealed that all forms of ATF6α, namely monomer, C618-dimer and C467-dimer, are activated by single reduction of a disulfide bond in response to ER stress, ensuring the rapidity of ATF6α activation.Key words: disulfide-bonded structure, endoplasmic reticulum, membrane-bound transcription factor, non-reducing SDS-PAGE, unfolded protein response.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"45 1","pages":"9-21"},"PeriodicalIF":1.5,"publicationDate":"2020-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.19030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37470936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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: 11

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

Cell structure and function Pub Date : 2020-01-01 DOI: 10.24077/2020;1352-csf1024

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

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

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

{"title":"p18/Lamtor1-mTORC1 Signaling Controls Development of Mucin-producing Goblet Cells in the Intestine.","authors":"Shizuka Ito, Shigeyuki Nada, Daisuke Yamazaki, Tetsuya Kimura, Kentaro Kajiwara, Hiroaki Miki, Masato Okada","doi":"10.1247/csf.20018","DOIUrl":"10.1247/csf.20018","url":null,"abstract":"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.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"45 2","pages":"93-105"},"PeriodicalIF":1.5,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10511045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38139562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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: 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

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

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

{"title":"Folding Latency of Fluorescent Proteins Affects the Mitochondrial Localization of Fusion Proteins.","authors":"Sayaka Kashiwagi,Yoichiro Fujioka,Aya O Satoh,Aiko Yoshida,Mari Fujioka,Prabha Nepal,Atsushi Tsuzuki,Ozora Aoki,Sarad Paudel,Hitoshi Sasajima,Yusuke Ohba","doi":"10.1247/csf.19028","DOIUrl":"https://doi.org/10.1247/csf.19028","url":null,"abstract":"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.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"1 1","pages":"183-194"},"PeriodicalIF":1.5,"publicationDate":"2019-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138524153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

{"title":"Localization of BCR-ABL to Stress Granules Contributes to Its Oncogenic Function.","authors":"Sayaka Kashiwagi,Yoichiro Fujioka,Takeshi Kondo,Aya O Satoh,Aiko Yoshida,Mari Fujioka,Hitoshi Sasajima,Maho Amano,Takanori Teshima,Yusuke Ohba","doi":"10.1247/csf.19033","DOIUrl":"https://doi.org/10.1247/csf.19033","url":null,"abstract":"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.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"75 4","pages":"195-204"},"PeriodicalIF":1.5,"publicationDate":"2019-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138524158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

{"title":"MGSE Regulates Crosstalk from the Mucin Pathway to the TFE3 Pathway of the Golgi Stress Response.","authors":"Mohamad Ikhwan Jamaludin,Sadao Wakabayashi,Mai Taniguchi,Kanae Sasaki,Ryota Komori,Hirotada Kawamura,Hayataka Takase,Miyu Sakamoto,Hiderou Yoshida","doi":"10.1247/csf.19009","DOIUrl":"https://doi.org/10.1247/csf.19009","url":null,"abstract":"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.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"48 3","pages":"137-151"},"PeriodicalIF":1.5,"publicationDate":"2019-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138524159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

{"title":"Dispersion of endoplasmic reticulum-associated compartments by 4-phenyl butyric acid in yeast cells.","authors":"T. Mai, Yuki Ishiwata‐Kimata, Q. Le, Hiroyuki Kido, Y. Kimata","doi":"10.1247/csf.19023","DOIUrl":"https://doi.org/10.1247/csf.19023","url":null,"abstract":"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.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"1 1","pages":""},"PeriodicalIF":1.5,"publicationDate":"2019-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.19023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42456783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

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

{"title":"Identification of 15 New Bypassable Essential Genes of Fission Yeast.","authors":"Aoi Takeda, Shigeaki Saitoh, Hiroyuki Ohkura, Kenneth E Sawin, Gohta Goshima","doi":"10.1247/csf.19025","DOIUrl":"https://doi.org/10.1247/csf.19025","url":null,"abstract":"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).","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":"44 2","pages":"113-119"},"PeriodicalIF":1.5,"publicationDate":"2019-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.19025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9295691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

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

Cell structure and function Pub Date : 2019-09-05 DOI: 10.1247/csf.19022

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

{"title":"Mutations in mxc Tumor-Suppressor Gene Induce Chromosome Instability in Drosophila Male Meiosis.","authors":"K. Tanabe, Rie Awane, Tsuyoshi Shoda, Kanta Yamazoe, Y. Inoue","doi":"10.1247/csf.19022","DOIUrl":"https://doi.org/10.1247/csf.19022","url":null,"abstract":"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.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2019-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1247/csf.19022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44741624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8