Mitosis Vs. Meiosis
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Mobile Genetic Elements in Streptococci
Curr. Issues Mol. Biol. (2019) 32: 123-166. DOI: https://dx.doi.org/10.21775/cimb.032.123 Mobile Genetic Elements in Streptococci Miao Lu#, Tao Gong#, Anqi Zhang, Boyu Tang, Jiamin Chen, Zhong Zhang, Yuqing Li*, Xuedong Zhou* State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, PR China. #Miao Lu and Tao Gong contributed equally to this work. *Address correspondence to: [email protected], [email protected] Abstract Streptococci are a group of Gram-positive bacteria belonging to the family Streptococcaceae, which are responsible of multiple diseases. Some of these species can cause invasive infection that may result in life-threatening illness. Moreover, antibiotic-resistant bacteria are considerably increasing, thus imposing a global consideration. One of the main causes of this resistance is the horizontal gene transfer (HGT), associated to gene transfer agents including transposons, integrons, plasmids and bacteriophages. These agents, which are called mobile genetic elements (MGEs), encode proteins able to mediate DNA movements. This review briefly describes MGEs in streptococci, focusing on their structure and properties related to HGT and antibiotic resistance. caister.com/cimb 123 Curr. Issues Mol. Biol. (2019) Vol. 32 Mobile Genetic Elements Lu et al Introduction Streptococci are a group of Gram-positive bacteria widely distributed across human and animals. Unlike the Staphylococcus species, streptococci are catalase negative and are subclassified into the three subspecies alpha, beta and gamma according to the partial, complete or absent hemolysis induced, respectively. The beta hemolytic streptococci species are further classified by the cell wall carbohydrate composition (Lancefield, 1933) and according to human diseases in Lancefield groups A, B, C and G. -
Transposable Elements Drive Reorganisation of 3D Chromatin
bioRxiv preprint doi: https://doi.org/10.1101/523712; this version posted January 17, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. Transposable elements drive reorganisation of 3D chromatin during early embryogenesis Kai Kruse1, Noelia Díaz1, §, Rocio Enriquez-Gasca1, §, Xavier Gaume2, 4, Maria-Elena Torres-Padilla2, 3 and Juan M. Vaquerizas1, * 1. Max Planck Institute for Molecular Biomedicine, Roentgenstrasse 20, 48149 Muenster, Germany. 2. Institute of Epigenetics and Stem Cells (IES), Helmholtz Zentrum München, Marchioninistraße 25, 81377 Munich, Germany. 3. Faculty of Biology, Ludwig Maximilians Universität, Großhaderner Str. 2, 82152 Planegg-Martinsried, Germany. 4. Present address: Cancer Research Center of Lyon, 28 Rue Laennec, Lyon 69008, France. §. These authors have contributed equally to this work. *. Correspondence to J.M.V. ([email protected], @vaquerizasjm) Keywords: Chromosome conformation capture; low-input Hi-C; early embryonic development; totipotency; transposable elements; MERVL; TAds; 2-cell embryo; 2-cell-like cells; zygotic genome activation; CAF-1; dux. Transposable elements are abundant genetic components of eukaryotic genomes with important regulatory features affecting transcription, splicing, and recombination, among others. Here we demonstrate that the Murine Endogenous Retroviral Element (MuERV-L/MERVL) family of transposable elements drives the 3D reorganisation of the genome in the early mouse embryo. By generating Hi-C data in 2-cell-like cells, we show that MERLV elements promote the formation of insulating domain boundaries through- out the genome in vivo and in vitro. -
DNA Damage Checkpoint Dynamics Drive Cell Cycle Phase Transitions
bioRxiv preprint doi: https://doi.org/10.1101/137307; this version posted August 4, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. DNA damage checkpoint dynamics drive cell cycle phase transitions Hui Xiao Chao1,2, Cere E. Poovey1, Ashley A. Privette1, Gavin D. Grant3,4, Hui Yan Chao1, Jeanette G. Cook3,4, and Jeremy E. Purvis1,2,4,† 1Department of Genetics 2Curriculum for Bioinformatics and Computational Biology 3Department of Biochemistry and Biophysics 4Lineberger Comprehensive Cancer Center University of North Carolina, Chapel Hill 120 Mason Farm Road Chapel Hill, NC 27599-7264 †Corresponding Author: Jeremy Purvis Genetic Medicine Building 5061, CB#7264 120 Mason Farm Road Chapel Hill, NC 27599-7264 [email protected] ABSTRACT DNA damage checkpoints are cellular mechanisms that protect the integrity of the genome during cell cycle progression. In response to genotoxic stress, these checkpoints halt cell cycle progression until the damage is repaired, allowing cells enough time to recover from damage before resuming normal proliferation. Here, we investigate the temporal dynamics of DNA damage checkpoints in individual proliferating cells by observing cell cycle phase transitions following acute DNA damage. We find that in gap phases (G1 and G2), DNA damage triggers an abrupt halt to cell cycle progression in which the duration of arrest correlates with the severity of damage. However, cells that have already progressed beyond a proposed “commitment point” within a given cell cycle phase readily transition to the next phase, revealing a relaxation of checkpoint stringency during later stages of certain cell cycle phases. -
Review Cell Division from a Genetic Perspective
REVIEW CELL DIVISION FROM A GENETIC PERSPECTIVE LELAND H. HARTWELL From the Department of Genetics, University of Washington, Seattle, Washington 98195 Recently, a number of laboratories have begun to incubation at the restrictive condition for that study mutant cells that are defective in specific mutation, whereas mutants with defects in one of stages of the eukaryotic cell cycle. The long-range the continuously required functions will arrest at goals of this work are to identify the genes that the restrictive temperature with cells at a variety code for division-related proteins, to define the of positions in the cell cycle. roles that these gene products play and to investi- Classes of mutants may be distinguished from gate the hierarchies of order that assure their one another and the roles of their products delim- coordinated activity. It is my intent in this brief ited by determining the stage-specific event at review to discuss the strategies employed in this which they arrest. It is convenient to have a genetic approach and to enumerate some of the designation for the first landmark of the cell cycle new conclusions that have come to light. A recent that is blocked in a particular mutant, and I shall review on the genetics of meiosis (2) complements call it the diagnostic landmark for that mutant. this review on mitosis. Mutants of Saccharomyces cerevisiae have been identified that have diagnostic landmarks at spin- MUTANTS dle pole body (SPB) duplication, SPB separation, Mutations that inactivate gene products essential initiation of DNA synthesis, DNA replication, for division would be lethal. -
Clinical Genetics: Mitochondrial Replacement Techniques Under the Spotlight
RESEARCH HIGHLIGHTS Nature Reviews Genetics | AOP, published online 1 July 2014; doi:10.1038/nrg3784 BRAND X PICTURES CLINICAL GENETICS Mitochondrial replacement techniques under the spotlight Mutations in the mitochondrial genome have and quantitative PCR showed that PBs contain been associated with diverse forms of human dis- fewer mitochondria than pronuclei in zygotes and ease, such as Leber’s hereditary optic neuropathy than spindle–chromosome complexes in oocytes. and Leigh’s syndrome, a neurometabolic disorder. The researchers then evaluated the feasibility A preclinical mouse model now demonstrates the of PB1 or PB2 transfer in mice and compared feasibility of using polar body (PB) genomes as their efficacies with that of MST or PNT. Genetic donor genomes in a new type of mitochondrial analysis showed that oocytes generated by PB1 replacement technique aimed at preventing the genome transfer were fertilized at rates that are inheritance of mitochondrial diseases. comparable to those obtained for oocytes ferti- 2014 has seen a surge in interest from both lized after MST (89.5% and 87.5%, respectively). the UK Human Fertilisation and Embryology Moreover, 87.5% of PB1–oocytes and 85.7% Authority (HFEA) and the US Food and Drug of MST–oocytes developed into blastocysts. Administration (FDA) in evaluating methods By contrast, PNT–embryos developed into designed to prevent the transmission of mito- blastocysts more frequently than PB2–oocytes chondrial diseases. One approach that is currently (81.3% and 55.5%, respectively), despite similar under investigation is mitochondrial replacement cleavage rates. by pronuclear transfer (PNT), in which the paren- Normal live progeny were obtained with all of tal pronuclei of a fertilized egg containing the these techniques at birth rates similar to those mother’s mutated mitochondrial DNA (mtDNA) of an intact control group. -
Cyclin-Dependent Kinase 5 Decreases in Gastric Cancer and Its
Published OnlineFirst January 21, 2015; DOI: 10.1158/1078-0432.CCR-14-1950 Biology of Human Tumors Clinical Cancer Research Cyclin-Dependent Kinase 5 Decreases in Gastric Cancer and Its Nuclear Accumulation Suppresses Gastric Tumorigenesis Longlong Cao1,2, Jiechao Zhou2, Junrong Zhang1,2, Sijin Wu3, Xintao Yang1,2, Xin Zhao2, Huifang Li2, Ming Luo1, Qian Yu1, Guangtan Lin1, Huizhong Lin1, Jianwei Xie1, Ping Li1, Xiaoqing Hu3, Chaohui Zheng1, Guojun Bu2, Yun-wu Zhang2,4, Huaxi Xu2,4,5, Yongliang Yang3, Changming Huang1, and Jie Zhang2,4 Abstract Purpose: As a cyclin-independent atypical CDK, the role of correlated with the severity of gastric cancer based on tumor CDK5 in regulating cell proliferation in gastric cancer remains and lymph node metastasis and patient 5-year fatality rate. unknown. Nuclear localization of CDK5 was found to be significantly Experimental Design: Expression of CDK5 in gastric tumor decreased in tumor tissues and gastric cancer cell lines, and paired adjacent noncancerous tissues from 437 patients was whereas exogenously expression of nucleus-targeted CDK5 measured by Western blotting, immunohistochemistry, and real- inhibited the proliferation and xenograft implantation of time PCR. The subcellular translocation of CDK5 was monitored gastric cancer cells. Treatment with the small molecule during gastric cancer cell proliferation. The role of nuclear CDK5 NS-0011, which increases CDK5 accumulation in the nucleus, in gastric cancer tumorigenic proliferation and ex vivo xenografts suppressed both cancer cell proliferation and xenograft was explored. Furthermore, by screening for compounds in the tumorigenesis. PubChem database that disrupt CDK5 association with its nu- Conclusions: Our results suggest that low CDK5 expression is clear export facilitator, we identified a small molecular (NS-0011) associated with poor overall survival in patients with gastric that inhibits gastric cancer cell growth. -
Investigating the Role of Cdk11in Animal Cytokinesis
Investigating the Role of CDK11 in Animal Cytokinesis by Thomas Clifford Panagiotou A thesis submitted in conformity with the requirements for the degree of Master of Science Department of Molecular Genetics University of Toronto © Copyright by Thomas Clifford Panagiotou (2020) Investigating the Role of CDK11 in Animal Cytokinesis Thomas Clifford Panagiotou Master of Science Department of Molecular Genetics University of Toronto 2020 Abstract Finely tuned spatio-temporal regulation of cell division is required for genome stability. Cytokinesis constitutes the final stages of cell division, from chromosome segregation to the physical separation of cells, abscission. Abscission is tightly regulated to ensure it occurs after earlier cytokinetic events, like the maturation of the stem body, the regulatory platform for abscission. Active Aurora B kinase enforces the abscission checkpoint, which blocks abscission until chromosomes have been cleared from the cytokinetic machinery. Currently, it is unclear how this checkpoint is overcome. Here, I demonstrate that the cyclin-dependent kinase CDK11 is required for cytokinesis. Both inhibition and depletion of CDK11 block abscission. Furthermore, the mitosis-specific CDK11p58 kinase localizes to the stem body, where its kinase activity rescues the defects of CDK11 depletion and inhibition. These results suggest a model whereby CDK11p58 antagonizes Aurora B kinase to overcome the abscission checkpoint to allow for successful completion of cytokinesis. ii Acknowledgments I am very grateful for the support of my family and friends throughout my studies. I would also like to express my deep gratitude to Wilde Lab members, both past and present, for their advice and collaboration. In particular, I am very grateful to Matthew Renshaw, whose work comprises part of this thesis. -
Chromatid Cohesion During Mitosis: Lessons from Meiosis
Journal of Cell Science 112, 2607-2613 (1999) 2607 Printed in Great Britain © The Company of Biologists Limited 1999 JCS0467 COMMENTARY Chromatid cohesion during mitosis: lessons from meiosis Conly L. Rieder1,2,3 and Richard Cole1 1Wadsworth Center, New York State Dept of Health, PO Box 509, Albany, New York 12201-0509, USA 2Department of Biomedical Sciences, State University of New York, Albany, New York 12222, USA 3Marine Biology Laboratory, Woods Hole, MA 02543-1015, USA *Author for correspondence (e-mail: [email protected]) Published on WWW 21 July 1999 SUMMARY The equal distribution of chromosomes during mitosis and temporally separated under various conditions. Finally, we meiosis is dependent on the maintenance of sister demonstrate that in the absence of a centromeric tether, chromatid cohesion. In this commentary we review the arm cohesion is sufficient to maintain chromatid cohesion evidence that, during meiosis, the mechanism underlying during prometaphase of mitosis. This finding provides a the cohesion of chromatids along their arms is different straightforward explanation for why mutants in proteins from that responsible for cohesion in the centromere responsible for centromeric cohesion in Drosophila (e.g. region. We then argue that the chromatids on a mitotic ord, mei-s332) disrupt meiosis but not mitosis. chromosome are also tethered along their arms and in the centromere by different mechanisms, and that the Key words: Sister-chromatid cohesion, Mitosis, Meiosis, Anaphase functional action of these two mechanisms can be onset INTRODUCTION (related to the fission yeast Cut1P; Ciosk et al., 1998). When Pds1 is destroyed Esp1 is liberated, and this event somehow The equal distribution of chromosomes during mitosis is induces a class of ‘glue’ proteins, called cohesins (e.g. -
Meiosis Is a Simple Equation Where the DNA of Two Parents Combines to Form the DNA of One Offspring
6.2 Process of Meiosis Bell Ringer: • Meiosis is a simple equation where the DNA of two parents combines to form the DNA of one offspring. In order to make 1 + 1 = 1, what needs to happen to the DNA of the parents? 6.2 Process of Meiosis KEY CONCEPT During meiosis, diploid cells undergo two cell divisions that result in haploid cells. 6.2 Process of Meiosis Cells go through two rounds of division in meiosis. • Meiosis reduces chromosome number and creates genetic diversity. 6.2 Process of Meiosis Bell Ringer • Draw a venn diagram comparing and contrasting meiosis and mitosis. 6.2 Process of Meiosis • Meiosis I and meiosis II each have four phases, similar to those in mitosis. – Pairs of homologous chromosomes separate in meiosis I. – Homologous chromosomes are similar but not identical. – Sister chromatids divide in meiosis II. – Sister chromatids are copies of the same chromosome. homologous chromosomes sister sister chromatids chromatids 6.2 Process of Meiosis • Meiosis I occurs after DNA has been replicated. • Meiosis I divides homologous chromosomes in four phases. 6.2 Process of Meiosis • Meiosis II divides sister chromatids in four phases. • DNA is not replicated between meiosis I and meiosis II. 6.2 Process of Meiosis • Meiosis differs from mitosis in significant ways. – Meiosis has two cell divisions while mitosis has one. – In mitosis, homologous chromosomes never pair up. – Meiosis results in haploid cells; mitosis results in diploid cells. 6.2 Process of Meiosis Haploid cells develop into mature gametes. • Gametogenesis is the production of gametes. • Gametogenesis differs between females and males. -
Aging Mice Have Increased Chromosome Instability That Is Exacerbated by Elevated Mdm2 Expression
Oncogene (2011) 30, 4622–4631 & 2011 Macmillan Publishers Limited All rights reserved 0950-9232/11 www.nature.com/onc ORIGINAL ARTICLE Aging mice have increased chromosome instability that is exacerbated by elevated Mdm2 expression T Lushnikova1, A Bouska2, J Odvody1, WD Dupont3 and CM Eischen1 1Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN, USA; 2Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA and 3Department of Biostatistics, Vanderbilt University School of Medicine, Nashville, TN, USA Aging is thought to negatively affect multiple cellular Introduction processes including the ability to maintain chromosome stability. Chromosome instability (CIN) is a common Genomic instability refers to the accumulation or property of cancer cells and may be a contributing factor acquisition of numerical and/or structural abnormali- to cellular transformation. The types of DNA aberrations ties in chromosomes. It has long been observed that that arise during aging before tumor development and that chromosome instability (CIN) is a hallmark of cancer contribute to tumorigenesis are currently unclear. Mdm2, cells and is postulated to be required for tumorigenesis a key regulator of the p53 tumor suppressor and (Lengauer et al., 1998; Negrini et al., 2010). Genomic modulator of DNA break repair, is frequently over- changes, such as chromosome breaks, translocations, expressed in malignancies and contributes to CIN. To genome rearrangements, aneuploidy and telomere short- determine the relationship between aging and CIN and the ening have been observed in aging organisms (Nisitani role of Mdm2, precancerous wild-type C57Bl/6 and et al., 1990; Tucker et al., 1999; Dolle and Vijg, 2002; littermate-matched Mdm2 transgenic mice at various Aubert and Lansdorp, 2008; Zietkiewicz et al., 2009). -
Mitosin/CENP-F in Mitosis, Transcriptional Control, and Differentiation
Journal of Biomedical Science (2006) 13: 205–213 205 DOI 10.1007/s11373-005-9057-3 Mitosin/CENP-F in mitosis, transcriptional control, and differentiation Li Ma1,2, Xiangshan Zhao1 & Xueliang Zhu1,* 1Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China; 2Graduate School of Chinese Academy of Sciences, Beijing, 100039, China Ó 2006 National Science Council, Taipei Key words: differentiation, kinetochore, mitosis, transcription Summary Mitosin/CENP-F is a large nuclear/kinetochore protein containing multiple leucine zipper motifs poten- tially for protein interactions. Its expression levels and subcellular localization patterns are regulated in a cell cycle-dependent manner. Recently, accumulating lines of evidence have suggested it a multifunctional protein involved in mitotic control, microtubule dynamics, transcriptional regulation, and muscle cell differentiation. Consistently, it is shown to interact directly with a variety of proteins including CENP-E, NudE/Nudel, ATF4, and Rb. Here we review the current progress and discuss possible mechanisms through which mitosin may function. Mitosin, also named CENP-F, was initially iden- acid residues (GenBank Accession No. CAH73032) tified as a human autoimmune antigen [1, 2] and [3]. The gene expression is cell cycle-dependent, as an in vitro binding protein of the tumor suppressor the mRNA levels increase following S phase Rb [3, 4]. Its dynamic temporal expression and progression and peak in early M phase [3]. Such modification patterns as well as ever-changing patterns are regulated by the Forkhead transcrip- spatial distributions following the cell cycle pro- tion factor FoxM1 [5]. -
Kinetochores, Microtubules, and Spindle Assembly Checkpoint
Review Joined at the hip: kinetochores, microtubules, and spindle assembly checkpoint signaling 1 1,2,3 Carlos Sacristan and Geert J.P.L. Kops 1 Molecular Cancer Research, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands 2 Center for Molecular Medicine, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands 3 Cancer Genomics Netherlands, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands Error-free chromosome segregation relies on stable and cell division. The messenger is the SAC (also known as connections between kinetochores and spindle microtu- the mitotic checkpoint) (Figure 1). bules. The spindle assembly checkpoint (SAC) monitors The transition to anaphase is triggered by the E3 ubiqui- such connections and relays their absence to the cell tin ligase APC/C, which tags inhibitors of mitotic exit cycle machinery to delay cell division. The molecular (CYCLIN B) and of sister chromatid disjunction (SECURIN) network at kinetochores that is responsible for microtu- for proteasomal degradation [2]. The SAC has a one-track bule binding is integrated with the core components mind, inhibiting APC/C as long as incorrectly attached of the SAC signaling system. Molecular-mechanistic chromosomes persist. It goes about this in the most straight- understanding of how the SAC is coupled to the kineto- forward way possible: it assembles a direct and diffusible chore–microtubule interface has advanced significantly inhibitor of APC/C at kinetochores that are not connected in recent years. The latest insights not only provide a to spindle microtubules. This inhibitor is named the striking view of the dynamics and regulation of SAC mitotic checkpoint complex (MCC) (Figure 1).