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Possible applications of X-ray lasers in biology: X-ray microscopy and X-ray lasers
Published in S Svanberg, C-G Wahlström, X-ray Lasers 1996, 2020
In situ structures of chromatin and chromosome fibers were examined in the present study, and provide an excellent example of biological structures whose fine structure is of great interest to biologists. Chromosomes are assembled at the stage in the cell division cycle called mitosis. The other portion of the cell division cycle is called interphase. The cell spends most of its time between divisions in interphase which can be subdivided into several phases. In interphase, DNA, the main component of the chromosome, is replicated during a period called S phase, and then the DNA and its associated proteins are subsequently assembled into the visible structures called chromosomes during mitosis. Thus, the cellular chromosomes are unfolded or opened, their component parts are replicated, and then subsequently assembled again into visible chromosomes for the subsequent mitosis during a single cycle of cell division (Alberts et al, 1983). Knowledge of the structure of the chromosome is important in understanding its behavior in interphase and mitosis, and in the replication and regulation of genes in the cell. In addition, in situ observations of the chromosomes in undisrupted cells or samples are of the most importance in order to learn as much as possible about biological samples in their native form.
Cell Cycle
Published in Mihai V. Putz, New Frontiers in Nanochemistry, 2020
Grdisa Mira, Ana-Matea Mikecin
The cell cycle (CC) or cell-division cycle is a series of events that take place in a cell leading to its division and duplication (replication) what results with the production of two daughter cells. In prokaryotes, which lack a cell nucleus, the CC occurs via a process termed binary fission. In eukaryotic cells, which have a nucleus, the CC is divided into three parts: interphase, the mitotic (M) phase, and cytokinesis. During interphase, the cells growth, accumulate the nutrients necessary for mitosis, and prepare for DNA duplication as well as cell division. Within the mitotic phase, the cell splits itself into two assigned daughter cells. In the course of the final stage, cytokinesis, the new cell is completely divided. To provide the correct division of the cell, there are control mechanisms known as CC checkpoints. After cell division, each of the daughter cells begins the interphase of a new cycle. Although the various stages of interphase are usually not morphologically discernible, each phase of the CC has a defined set of specialized biochemical processes that prepare the cell for initiation of cell division. Cell division is a vital process by which skin, hair, blood cells and certain internal organs are renewed. With that process also fertilized egg develops into mature organisms.
Illuminating the cycle of life
Published in Raquel Seruca, Jasjit S. Suri, João M. Sanches, Fluorescence Imaging and Biological Quantification, 2017
Anabela Ferro, Patrícia Carneiro, Maria Sofia Fernandes, Tânia Mestre, Ivan Sahumbaiev, João M. Sanches, Raquel Seruca
The cell cycle consists of three gap phases, G0, G1, and G2, which are interspersed between the DNA synthesis phase (S phase) and the mitosis phase (M phase). The G0/G1, S, and G2 phases are collectively known as interphase. The cell cycle is a coordinated network of genes and proteins, cyclically regulated by transcription, posttranslational modifications, as well as dynamic genetic and protein interactions [8,9]. Key regulatory molecules include the cyclin-dependent kinases (CDK), a family of serine/threonine kinases that are specifically activated at different phases of the cell cycle by cyclins. Cell-cycle progression is driven by the periodic oscillation of CDK/cyclin activities, which are in turn regulated by a number of mechanisms, including (1) cyclin synthesis; (2) activation of CDKs by CDK activating kinases (CAKs); (3) inhibition of CDKs by CDK inhibitors (CKIs); and (4) ubiquitin-mediated proteasomal degradation of cyclins [9]. Indeed, protein degradation plays a key role in driving cell-cycle transitions through two major E3 ubiquitin ligases, the Skp1–Cul1-F box protein (SCF) complex and the anaphase-promoting complex/cyclosome (APC/C), which ubiquitinate G1 cyclins from late G1 to early M phase and mitotic cyclins from anaphase till the end of G1 phase, respectively [9,10]. Further regulation is accomplished by a myriad of cell-cycle checkpoints that induce cell-cycle arrest on detection of defects and ensure the progression of the cycle in an orderly fashion while minimizing genomic instability [11,12]. Briefly, the G1/S checkpoint induces an arrest induced by DNA damage in a p53-dependent manner, whereas the S phase checkpoint delays initiation or elongation of DNA replication to minimize replications errors. The G2/M checkpoint restricts entry into mitosis minimizing chromosome missegregation, whereas the spindle assembly checkpoint (SAC) detects improper alignment of chromosomes on the mitotic spindle thus ensuring fidelity of chromosome segregation. Finally, postmitotic arrest prevents abnormal daughter cells from entering the next interphase [2,12]. A schematic representation of the cell cycle is displayed in Figure 12.1.
Synthesis, cytotoxicity, apoptosis and cell cycle arrest of a monoruthenium(II)-substituted Dawson polyoxotungstate
Published in Journal of Coordination Chemistry, 2019
Shi-Fang Jia, Xiu-Li Hao, Yan-Zhen Wen, Yan Zhang
The distribution of C33A cells in various compartments during the cell cycle was analyzed by flow cytometry in cells stained with propidium iodide. The cell cycle is generally divided into two stages, the interphase is mainly the replication of DNA and the M-phase is mainly the average distribution of the replication DNA to two daughter cells. The interphase is divided into three stages, Gl phase, S phase and G2 phase. S phase mainly completes the DNA replication. Entering S phase from Gl phase is the main stage of the cell cycle. Some chemotherapeutic drugs can be specific to the S phase, which interferes with the DNA replication. As shown in Figure 9, treatment of C33A cells with 5, 10, and 25 µM M1 for 48 h cause significant enhancement of 0.19, 0.63, and 3.36% in S phase compared with the control; treatment of C33A cells with 25 µM M1 for 48 h cause decrease of 7.8 in G0/G1 phase compared with the control. These data show that M1 induce S-phase arrest in C33A cells. Ru-adpa as antitumor agent was reported by our group; treatment of AGS cells with 5, 10, 20, and 40 µM Ru-adpa for 12 h cause significant enhancement of 3.1, 4.9, 10.8, and 19.7% in S phase compared with the control [29].
Astral microtubules determine the final division axis of cells confined on anisotropic surface topography
Published in Journal of Experimental Nanoscience, 2020
Kyunghee Lee, Yen Ling Koon, Jaewon Kim, Keng-Hwee Chiam, Sungsu Park
Both cellular geometry [1,10] and adhesion patterns or cortical cues [12] have been separately proposed to regulate mitotic spindle orientation. For cells cultured on 2D substrates, it has previously been shown that cortical cues override cellular geometry in determining spindle orientation [12]. It is however unknown whether such phenomenon persists in cells grown on 3D substrates. In the present study, we showed cellular geometry could be altered by growing cells on different topographic surfaces during interphase. This topographic effect on the cellular geometry was maintained through metaphase as well (Supplementary Figure 2). Measurements of aspect ratio and spindle angle revealed an inverse correlation that exists both in RPE-1 and HeLa cells (Figure 1). This implies that cells on microgratings obey Hertwig’s rule and that cellular geometry controls spindle angle orientation. Modification of cortical cues was performed by using CD to disrupt focal adhesions. RPE-1 and HeLa cells elongate in the presence of CD on 1 µm gratings. Surprisingly, both spindle angles of RPE-1 and HeLa decrease upon CD treatment in accordance to Hertwig’s rule (Figure 2(B,C) and Table 4). This is not to be expected if spindle angle orientation is governed by cortical cues since ablation of cortical cues should lead to a random distribution of spindle angles similar to that observed on 2D flat surfaces. Instead, we observed a more skewed distribution of spindle angles toward the smaller angles upon CD treatment implying that cell shape plays a more critical role in dictating spindle orientation. Thus, determination of the cell division axis on microgratings appears to depend more on cellular geometry that varies with topographic surface rather than on cortical cues.