Cell division
Frank J. Dye in Human Life Before Birth, 2019
Like the chromosomes, the spindle plays an important role in mitosis. Unlike the chromosomes, the spindle is a short-lived cellular structure that comes and goes according to the cell's needs. Two microtubule-organizing centers (MTOCs; classically called centrosomes) make the spindle during the earliest stage of mitosis (prophase). The spindle is composed of a protein called tubulin that has been organized into microtubules. As the chromosomes condense during prophase, the centrosome divides, and the two resulting daughter centrosomes move to opposite ends of the nucleus, organizing the spindle as they go (see Figure 3.6). When the nuclear membrane disappears at the end of prophase, initiating prometaphase, the condensed chromosomes are captured by spindle fibers (bundles of microtubules).
Disease Prediction and Drug Development
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam in Introduction to Computational Health Informatics, 2019
Mitosis is a multiphase process. The main stages are: 1) prophase; 2) prometaphase; 3) metaphase; 4) anaphase and 5) telophase. In the prophase, the chromosome-strands called chromatids separate. However, the chromatids remain connected at the constricted region joining the chromatids. After that, chromatids undergo a condensation process on a bipolar fibrous material within a cell. This fibrous material is called mitotic spindle. During prometaphase, the nuclear envelope within a cell is divided into multiple fluid-filled fragments called a vesicle. These vesicles are divided eventually in daughter-cells. In the anaphase, the sister-chromatids separate abruptly. The spindle-poles separate using motor proteins. Mitosis ends with telophase when the separated chromosomes reach the poles of the spindle, and the chromosomes begin to decondense from the spindle. Telophase is followed by cytokinesis – the division of the cytoplasm into identical cells: cells having identical genetic composition.
ENTRIES A–Z
Philip Winn in Dictionary of Biological Psychology, 2003
Mitosis is one part of the CELL CYCLE. During the mitotic phase of the cell cycle (which is further divisible into prophase, prometaphase, metaphase, anaphase and telophase) two essential steps take place: mitosis itself (the division of the cell NUCLEUS) and cytokinesis (the division of the CYTOPLASM). Preparation for these takes place in the second major component of the cell cycle, the interphase. The interphase (accounting for some 90% of the cycle) is divisible into three components: G1 (the first gap) (a period of cell growth), the S phase (during which CHROMOSOMES replicate, in preparation for mitosis each divided cell nucleus must have an exact copy of the GENOME) and finally the G2 phase (second gap, during which further cell growth takes place). Mitosis is regulated by chemical control systems, involving various GROWTH FACTORS external to the cell and a class of kinases known as cyclin- dependent kinases (Cdks) that are found within cells (see KINASE). Mitotic cell division occurs continuously in some cells. Fresh BLOOD cells are, for example, produced in bone marrow throughout an individual's life. Other cells however assume a final form and divide no more: the term POSTMITOTIC indicates a cell that has completed all the mitotic divisions it will go through.
Ultrastructure of colorectal adenocarcinoma and peritumoral tissue in untreated patients
Published in Ultrastructural Pathology, 2018
Hector L. Osorio, Hector J. Finol, L. Roschman Gonzalez, Carlos E. Sardiñas
Different ultrastructural alterations were found in epithelial cells of CAC (tumor). Initially changes were seen in mitochondrial morphology (Figure 1(a,b)). On the contrary, rough endoplasmic reticulum (RER) looked normal (Figure 1(a)). Furthermore, in addition to cells with normal looking RER, other cells appeared with RER alterations consisting of swollen cisternae (Figure 1(b)) and rests of RER participating in the formation of autophagosomes (Figure 1(c)). In relation to the Golgi apparatus, there was a significant cisternae reduction and its presence was observed in areas with autophagosomes (Figure 1(d)). In these cells, nucleus exhibited a normal ultrastructure (Figure 1(a,d)). Nevertheless, other cells showed nuclei with deep invaginations and nucleoli with a very electron dense aspect (Figure 3(c)). In advanced stages of degeneration and necrosis, nuclei presented heterochromatin alteration and loss of nuclear envelope with nuclear matrix extraction (Figure 2(a,b)). Mitochondrial and RER swelling was also seen in the prometaphase of some dividing cells (Figure 2(c)), In this case, a chromosome still covered with rests of nuclear envelope was found. In addition, loss of intercellular desmosomes was detected (Figure 2(d)), the altered cells also presented mitochondrial swelling, abundant polysomes and the disappearance of RER. Note also the presence of multivesicular bodies.
Aurora kinase inhibitors: a patent review (2014-2020)
Published in Expert Opinion on Therapeutic Patents, 2021
Xue-Li Jing, Shi-Wu Chen
Aurora kinase family includes three subtypes: named as Aurora A, B and C. They all possess a highly conserved C-terminal domain and an N-terminal domain but have differences in functionality [4]. In the cell cycle, Aurora A is responsible for mitotic entry, centrosome maturation, and separation, spindle assembly and spindle damage repair [5]. Aurora A is activated by ajuba at the beginning of the S phase and at G2/M transition its activity arrives at a peak to stimulate duplicated centrosomes to separate and initiate the mitotic entry [4]. Aurora A kinase activity depends on the phosphorylation status of a threonine residue (T288) located on the ‘activation loop’ of the enzyme. In prometaphase, Aurora A is targeted to microtubules by phosphorylating TPX2 to contribute to spindle assembly and bipolar spindle microtubule conformation [6]. In addition, Aurora A also has a variety of non-mitotic functions, such as DNA damage response (DDR) [7] and activation of epithelial–mesenchymal transition (EMT) reprograming [8]. Inhibition of Aurora A would result in uneven distribution of chromosomes to daughter cells and abnormal spindle structure, followed by aneuploidy [9].
Retinal dystrophy associated with a Kizuna (KIZ) mutation and a predominantly macular phenotype
Published in Ophthalmic Genetics, 2019
Yue Zhao, Razek Georges Coussa, Meghan J. M. DeBenedictis, Elias I. Traboulsi
Kizuna (KIZ) is a 673 amino acid protein encoded by 12kb on chromosome 20p11.23 and is involved in ciliary structural integrity. Studies in HeLA cell lines have demonstrated its role in maintaining centrosome stability during prometaphase (2). During mitosis, mature centrosomes, consisting of a pair of centrioles surrounded by pericentriolar material, form at each pole of the dividing cell. From the pericentriolar material, microtubules are successively enucleated to form spindle complexes that attach to the centrally aligned chromosomes and form scaffolding for chromatid separation (9,10). Oshimori et al. showed that phosphorylation of Kiz Thr-379 is required for centrosomal maturation and chromosomal movement (2). In the absence of Kiz, dissociation of pericentriolar material from the centrosome results in spindle fragmentation (1). In mice, Kizuna has been shown to be preferentially expressed in the retina, especially in the outer nuclear layer (1). It is hypothesized that the outer retina is predominantly affected by KIZ mutations. In the present case, KIZ c.226 C > T (p.Arg76*) is a nonsense mutation that results in a truncated non-functional protein and hence is pathogenic in a homozygous state.
Related Knowledge Centers
- Eukaryote
- Kinetochore
- Nuclear Envelope
- Spindle Apparatus
- Spindle Checkpoint
- Mitosis
- Metaphase
- Prophase
- Somatic
- Cell