Talk:Cell Division - Mitosis

From Embryology
About Discussion Pages  
Mark Hill.jpg
On this website the Discussion Tab or "talk pages" for a topic has been used for several purposes:
  1. References - recent and historic that relates to the topic
  2. Additional topic information - currently prepared in draft format
  3. Links - to related webpages
  4. Topic page - an edit history as used on other Wiki sites
  5. Lecture/Practical - student feedback
  6. Student Projects - online project discussions.
Links: Pubmed Most Recent | Reference Tutorial | Journal Searches

Glossary Links

Glossary: A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | Numbers | Symbols | Term Link

Cite this page: Hill, M.A. (2019, August 18) Embryology Cell Division - Mitosis. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Cell_Division_-_Mitosis


10 Most Recent Papers

Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)


Mitosis

<pubmed limit=10>Mitosis</pubmed>

2017

Mosaicism in Preimplantation Human Embryos: When Chromosomal Abnormalities Are the Norm

Trends Genet. 2017 Apr 27. pii: S0168-9525(17)30054-9. doi: 10.1016/j.tig.2017.04.001. [Epub ahead of print]

McCoy RC.

Abstract

Along with errors in meiosis, mitotic errors during post-zygotic cell division contribute to pervasive aneuploidy in human embryos. Relatively little is known, however, about the genesis of these errors or their fitness consequences. Rapid technological advances are helping to close this gap, revealing diverse molecular mechanisms contributing to mitotic error. These include altered cell cycle checkpoints, aberrations of the centrosome, and failed chromatid cohesion, mirroring findings from cancer biology. Recent studies are challenging the idea that mitotic error is abnormal, emphasizing that the fitness impacts of mosaicism depend on its scope and severity. In light of these findings, technical and philosophical limitations of various screening approaches are discussed, along with avenues for future research. Copyright © 2017 Elsevier Ltd. All rights reserved. KEYWORDS: aneuploidy; fertility; mitosis; preimplantation genetic screening

PMID 28457629 DOI: 10.1016/j.tig.2017.04.001

Golgi apparatus self-organizes into the characteristic shape via postmitotic reassembly dynamics

Proc Natl Acad Sci U S A. 2017 May 1. pii: 201619264. doi: 10.1073/pnas.1619264114. [Epub ahead of print]

Tachikawa M1,2, Mochizuki A3,2,4,5.

Abstract

The Golgi apparatus is a membrane-bounded organelle with the characteristic shape of a series of stacked flat cisternae. During mitosis in mammalian cells, the Golgi apparatus is once fragmented into small vesicles and then reassembled to form the characteristic shape again in each daughter cell. The mechanism and details of the reassembly process remain elusive. Here, by the physical simulation of a coarse-grained membrane model, we reconstructed the three-dimensional morphological dynamics of the Golgi reassembly process. Considering the stability of the interphase Golgi shape, we introduce two hypothetical mechanisms-the Golgi rim stabilizer protein and curvature-dependent restriction on membrane fusion-into the general biomembrane model. We show that the characteristic Golgi shape is spontaneously organized from the assembly of vesicles by proper tuning of the two additional mechanisms, i.e., the Golgi reassembly process is modeled as self-organization. We also demonstrate that the fine Golgi shape forms via a balance of three reaction speeds: vesicle aggregation, membrane fusion, and shape relaxation. Moreover, the membrane fusion activity decreases thickness and the number of stacked cisternae of the emerging shapes.

KEYWORDS: Golgi apparatus; computer simulation; physical biology modeling; self-organization

PMID 28461510 DOI: 10.1073/pnas.1619264114

2014

Stressing mitosis to death

Front Oncol. 2014 Jun 4;4:140. doi: 10.3389/fonc.2014.00140. eCollection 2014.

Burgess A, Rasouli M, Rogers S.

Abstract The final stage of cell division (mitosis), involves the compaction of the duplicated genome into chromatid pairs. Each pair is captured by microtubules emanating from opposite spindle poles, aligned at the metaphase plate, and then faithfully segregated to form two identical daughter cells. Chromatids that are not correctly attached to the spindle are detected by the constitutively active spindle assembly checkpoint (SAC). Any stress that prevents correct bipolar spindle attachment, blocks the satisfaction of the SAC, and induces a prolonged mitotic arrest, providing the cell time to obtain attachment and complete segregation correctly. Unfortunately, during mitosis repairing damage is not generally possible due to the compaction of DNA into chromosomes, and subsequent suppression of gene transcription and translation. Therefore, in the presence of significant damage cell death is instigated to ensure that genomic stability is maintained. While most stresses lead to an arrest in mitosis, some promote premature mitotic exit, allowing cells to bypass mitotic cell death. This mini-review will focus on the effects and outcomes that common stresses have on mitosis, and how this impacts on the efficacy of mitotic chemotherapies. KEYWORDS: Cdk1; DNA damage; SAC; checkpoint; kinetochore; metaphase; mitosis; spindle

PMID 24926440

2013

An estimation of the number of cells in the human body

Ann Hum Biol. 2013 Jul 5.

Bianconi E, Piovesan A, Facchin F, Beraudi A, Casadei R, Frabetti F, Vitale L, Pelleri MC, Tassani S, Piva F, Perez-Amodio S, Strippoli P, Canaider S. Source Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna , Bologna , Italy .

Abstract

Abstract Background: All living organisms are made of individual and identifiable cells, whose number, together with their size and type, ultimately defines the structure and functions of an organism. While the total cell number of lower organisms is often known, it has not yet been defined in higher organisms. In particular, the reported total cell number of a human being ranges between 1012 and 1016 and it is widely mentioned without a proper reference. Aim: To study and discuss the theoretical issue of the total number of cells that compose the standard human adult organism. Subjects and methods: A systematic calculation of the total cell number of the whole human body and of the single organs was carried out using bibliographical and/or mathematical approaches. Results: A current estimation of human total cell number calculated for a variety of organs and cell types is presented. These partial data correspond to a total number of 3.72 × 1013. Conclusions: Knowing the total cell number of the human body as well as of individual organs is important from a cultural, biological, medical and comparative modelling point of view. The presented cell count could be a starting point for a common effort to complete the total calculation.

PMID 23829164


2012

The nucleoporin ELYS/Mel28 regulates nuclear envelope subdomain formation in HeLa cells

Nucleus. 2012 Mar 1;3(2). [Epub ahead of print]

Clever M, Funakoshi T, Mimura Y, Takagi M, Imamoto N. Source Cellular Dynamics Laboratory; Riken Advanced Science Institute; Saitama, Japan.

Abstract

In open mitosis, the nuclear envelope (NE) reassembles at the end of each mitosis. This process involves the reformation of the nuclear pore complex (NPC), the inner and outer nuclear membranes, and the nuclear lamina. In human cells, cell cycle-dependent NE subdomains exist, characterized as A-type lamin-rich/NPC-free or B-type lamin-rich/NPC-rich, which are initially formed as core or noncore regions on mitotic chromosomes, respectively. Although postmitotic NE formation has been extensively studied, little is known about the coordination of NPC and NE assembly. Here, we report that the nucleoporin ELYS/Mel28, which is crucial for postmitotic NPC formation, is essential for recruiting the lamin B receptor (LBR) to the chromosomal noncore region. Furthermore, ELYS/Mel28 is responsible for focusing of A-type lamin-binding proteins like emerin, Lap2α and the barrier-to-autointegration factor (BAF) at the chromosomal core region. ELYS/Mel28 biochemically interacts with the LBR in a phosphorylation-dependent manner. Recruitment of the LBR depends on the nucleoporin Nup107, which interacts with ELYS/Mel28, but not on nucleoporin Pom121, suggesting that the specific molecular interactions with ELYS/Mel28 are involved in the NE assembly at the noncore region. The depletion of the LBR affected neither the behavior of emerin nor Lap2α indicating that the recruitment of the LBR to mitotic chromosomes is not involved in formation of the core region. The depletion of ELYS/Mel28 also accelerates the entry into cytokinesis after recruitment of emerin to chromosomes. Our data show, that ELYS/Mel28 plays a role in NE subdomain formation in late mitosis.

PMID 22555603


The Abbreviated Pluripotent Cell Cycle

J Cell Physiol. 2012 May 2. doi: 10.1002/jcp.24104. [Epub ahead of print]

Kapinas K, Grandy R, Ghule P, Medina R, Becker K, Pardee A, Zaidi SK, Lian J, Stein J, van Wijnen A, Stein G. Source Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655.

Abstract

Human embryonic stem cells and induced pluripotent stem cells proliferate rapidly and divide symmetrically producing equivalent progeny cells. In contrast, lineage committed cells acquire an extended symmetrical cell cycle. Self-renewal of tissue-specific stem cells is sustained by asymmetric cell division where one progeny cell remains a progenitor while the partner progeny cell exits the cell cycle and differentiates. There are three principal contexts for considering the operation and regulation of the pluripotent cell cycle: temporal, regulatory andstructural. The primary temporal context that the pluripotent self-renewal cell cycle of human embryonic stem cells (hESCs) is a short G1 period without reducing periods of time allocated to S phase, G2, and mitosis. The rules that govern proliferation in hESCs remain to be comprehensively established. However, several lines of evidence suggest a key role for the naïve transcriptome of hESCs, which is competent to stringently regulate the ESC cell cycle. This supports the requirements of pluripotent cells to self propagate while suppressing expression of genes that confer lineage commitment and/or tissue specificity. However, for the first time, we consider unique dimensions to the architectural organization and assembly of regulatory machinery for gene expression in nuclear microenviornments that define parameters of pluripotency. From both fundamental biological and clinical perspectives, understanding control of the abbreviated embryonic stem cell cycle can provide options to coordinate control of proliferation versus differentiation. Wound healing, tissue engineering, and cell-based therapy to mitigate developmental aberrations illustrate applications that benefit from knowledge of the biology of the pluripotent cell cycle. J. Cell. Physiol. © 2012 Wiley Periodicals, Inc. Copyright © 2012 Wiley Periodicals, Inc.

PMID 22552993


The anaphase-promoting complex or cyclosome supports cell survival in response to endoplasmic reticulum stress

PLoS One. 2012;7(4):e35520. Epub 2012 Apr 23.

Chen M, Gutierrez GJ, Ronai ZA. Source Signal Transduction Program, Sanford-Burnham Medical Research Institute, La Jolla, California, United States of America.

Abstract

The anaphase-promoting complex or cyclosome (APC/C) is a multi-subunit ubiquitin ligase that regulates exit from mitosis and G1 phase of the cell cycle. Although the regulation and function of APC/C(Cdh1) in the unperturbed cell cycle is well studied, little is known of its role in non-genotoxic stress responses. Here, we demonstrate the role of APC/C(Cdh1) (APC/C activated by Cdh1 protein) in cellular protection from endoplasmic reticulum (ER) stress. Activation of APC/C(Cdh1) under ER stress conditions is evidenced by Cdh1-dependent degradation of its substrates. Importantly, the activity of APC/C(Cdh1) maintains the ER stress checkpoint, as depletion of Cdh1 by RNAi impairs cell cycle arrest and accelerates cell death following ER stress. Our findings identify APC/C(Cdh1) as a regulator of cell cycle checkpoint and cell survival in response to proteotoxic insults.

PMID 22539978


Visualizing the high curvature regions of post-mitotic nascent nuclear envelope membrane

Commun Integr Biol. 2012 Jan 1;5(1):16-8.

Lu L, Kirchhausen T.

Abstract

We previously reported that mitotic endoplasmic reticulum (ER) membrane cisternae or sheets directly assemble mammalian nuclear envelope (NE) at the end of mitosis. In this study, we investigated the dynamics of the high curvature regions of partially assembled nuclear envelope membrane using reticulon4a as a probe. We found that, after sorting out reticulon4a from the nascent NE membrane sheets, reticulon4a is specifically localized to the leading edges. Our 3D time lapse images suggested that ER tubules could be incompetent in assembling the NE membrane. Our findings suggest a possible role of reticulons at the leading edges during the NE re-assembly and provide further evidences that the mitotic assembly of NE is by ER cisternae rather than tubules. PMID 22482003


The Structure of the Mitotic Spindle and Nucleolus during Mitosis in the Amebo-Flagellate Naegleria

PLoS One. 2012;7(4):e34763. Epub 2012 Apr 6.

Walsh CJ. Source Department of Biological Science, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.

Abstract

Mitosis in the amebo-flagellate Naegleria pringsheimi is acentrosomal and closed (the nuclear membrane does not break down). The large central nucleolus, which occupies about 20% of the nuclear volume, persists throughout the cell cycle. At mitosis, the nucleolus divides and moves to the poles in association with the chromosomes. The structure of the mitotic spindle and its relationship to the nucleolus are unknown. To identify the origin and structure of the mitotic spindle, its relationship to the nucleolus and to further understand the influence of persistent nucleoli on cellular division in acentriolar organisms like Naegleria, three-dimensional reconstructions of the mitotic spindle and nucleolus were carried out using confocal microscopy. Monoclonal antibodies against three different nucleolar regions and α-tubulin were used to image the nucleolus and mitotic spindle. Microtubules were restricted to the nucleolus beginning with the earliest prophase spindle microtubules. Early spindle microtubules were seen as short rods on the surface of the nucleolus. Elongation of the spindle microtubules resulted in a rough cage of microtubules surrounding the nucleolus. At metaphase, the mitotic spindle formed a broad band completely embedded within the nucleolus. The nucleolus separated into two discreet masses connected by a dense band of microtubules as the spindle elongated. At telophase, the distal ends of the mitotic spindle were still completely embedded within the daughter nucleoli. Pixel by pixel comparison of tubulin and nucleolar protein fluorescence showed 70% or more of tubulin co-localized with nucleolar proteins by early prophase. These observations suggest a model in which specific nucleolar binding sites for microtubules allow mitotic spindle formation and attachment. The fact that a significant mass of nucleolar material precedes the chromosomes as the mitotic spindle elongates suggests that spindle elongation drives nucleolar division.

PMID 22493714


Bipolar metaphase spindle formation in a fucoid alga cell. Normal spindle formation is disrupted by treatment with the Kinesin-5 inhibitor monastrol. Treated zygotes arrest at the spindle assembly check point and produce monasters, multipolar spindles, and numerous cytasters. Spindle microtubules are shown in green and condensed chromatin is shown in red. This month features a guest image which was recently published in BMC Plant Biology.

http://www.biomedcentral.com/bmccellbiol/imageofthemonth/archive/2006/10

Deciphering protein function during mitosis in PtK cells using RNAi

Knockdown of the kinesin Eg5 leads to mitotic defects. Knockdown of Eg5 levels by treatment with siRNA results in cells with monopolar spindles and a mitotic delay (right hand cell). Microtubule staining is shown in green, Eg5 in red and DNA in blue.

http://www.biomedcentral.com/browse/browse.asp?abbrev=bmccellbiol&imageofthemonth=y&imageoftheyear=y=y&year=2006

http://www.biomedcentral.com/content/pdf/1471-2121-7-26.pdf

Adult Human Tissue Cell Division

Cell turnover and adult tissue homeostasis: from humans to planarians

Annu Rev Genet. 2007;41:83-105.

Pellettieri J, Sánchez Alvarado A. Source Department of Neurobiology and Anatomy, Howard Hughes Medical Institute, University of Utah School of Medicine, Salt Lake City, UT 84132-3401, USA. jpellett@neuro.utah.edu

Abstract

Many fully developed metazoan tissues remain in a state of flux throughout life. During physiological cell turnover, older differentiated cells are typically eliminated by apoptosis and replaced by the division progeny of adult stem cells. Independently, each of these processes has been researched extensively, yet we know very little about how cell death and stem cell division are coordinated in adult organs. Freshwater planarians are an attractive model organism for research in this area. Not only do they undergo a very high rate of somatic cell turnover throughout life, but experimental tools are now available to study this process in vivo. Together, these attributes provide an opportunity to investigate the mechanisms, functions, and regulation of cell turnover in adult tissues.

PMID 18076325

  • Stomach - surface epithelium is renewed approximately every third day.