What Would Happen If Sister Chromatids Failed To Separate
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What Would Happen If Sister Chromatids Failed To Separate
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Received: November 10, 2016 / Revised: January 24, 2017 / Received: January 26, 2017 / Published: February 8, 2017
Errors during cell division often alter the chromosome content, resulting in aneuploid or polyploid daughter cells. Polyploid cells can undergo abnormal division and produce aneuploid cells. Chromosome segregation errors can also affect entire pieces of chromosomes. The primary consequence of segregation errors is a change in the relative dosage of products from genes located on abnormally segregated chromosomes. Misexpression of transcriptional regulators can also affect genes on properly segregated chromosomes. The consequences of these disruptions in gene expression depend on the interaction of the aneuploid phenotype with the chromosome involved and the environment. Often, this distribution of new chromosomes is detrimental to the health and survival of the organism. However, in an altered environment, changes in gene copy number can create a more adaptive phenotype. Chromosome segregation errors also have important consequences for human health. They can promote drug resistance of pathogenic microorganisms. They represent a source of genetic and phenotypic variation in neoplastic cells, which can select populations with increased malignancy and resistance to treatment. Finally, errors in chromosome segregation in meiosis during gamete formation are a major cause of human birth defects and infertility. This review describes new concepts and consequences of mitotic and meiotic errors with a focus on human health.
Describe What Occurs During Each Stage Of The Cell Cycle.
Aneuploidy polyploidy microtubule chromosomal instability; tumors birth defects; resistance to fertility drugs; centromere kinetochore aneuploidy; polyploidy microtubule chromosomal instability; tumors birth defects; resistance to fertility drugs; Centromere kinetochore
Other articles in the special issue of “Mechanisms of Mitotic Chromosome Segregation” looked at the events of cell division and how errors can cause errors in chromosome migration in daughter cells. The defects are of various origins, including abnormalities of chromosome structure and function, causing chromosomes to remain in the anaphase phase or show incomplete separation of sister chromatids. Spindle abnormalities, such as multipolar spindles and defects in cytokinesis, are additional sources of abnormal chromosome segregation. Finally, defects in cell cycle regulation, including division delays and cell cycle checkpoint defects, also lead to abnormal segregation. In this final chapter, we deal with the consequences of mitotic and meiotic errors. They can be mild or severe, depending on the severity and nature of the disorder, the genetic makeup of the cell, and the exact role of the cell in question. It should be noted that segregation abnormalities do not always cause aneuploidy. Even for a single chromosome undergoing premature chromatid segregation, random selection results in proper segregation into two daughter cells 50% of the time. The outcome of defect segregation is also affected by stochastic variables, causing cells in apparently the same position to choose different routes to the same defects . Cell cycle checkpoints can sometimes identify impending errors and offer corrective countermeasures that lead to normal distribution. If the checkpoints do not resolve the problem, but division continues, daughter cells are produced with genetic imbalances in one or more entire chromosomes, chromosome segments, or entire sets of chromosomes. In some cases, deviations from traditional cell cycle patterns that lead to abnormal chromosome content are inherent to normal development. It is often associated with polyploidy, while aneuploidy is mostly the result of errors in chromosome segregation. In most normal tissue cells, a surveillance system strongly dependent on the tumor suppressor p53 is activated in response to the presence of abnormal chromosomal material and leads to cell cycle arrest, cell death or senescence (Figure 1) [ May affect 2, 3, 4, 5. ]
Cells that lose or gain less than a complete set of chromosomes during cell division are called aneuploids. Cells exhibit chromosomal instability with a tendency to rapidly lose or gain chromosomes (see Table 1 for definition). Some genotypes may be inherently prone to persistent chromosomal instability, leading to a diverse generation of aneuploid offspring. Alternatively, cells may be aneuploid but relatively stable in terms of chromosome content. Cells can also undergo growth of an entire set of chromosomes, a condition known as polyploidy. Polyploid cells often contain more than two centrosomes. During subsequent cell divisions, centrosomes sometimes produce multipolar spindles in which chromosomes segregate into three or more daughter cells, resulting in aneuploid cells with variable numbers of chromosomes. The cumulative consequences of chromosome segregation errors are wide-ranging, as they affect cell physiology, tissue homeostasis, and the adaptation of cells and organisms in many ways.
Chromosome segregation requires the coordination of two important pathways: chromosome movement in M phase and cell cycle regulation, a key element of which is the mitotic spindle checkpoint. As detailed elsewhere in this series, defects in mitotic spindle assembly and chromosome alignment activate the spindle checkpoint, delaying cells in M phase. Optimally, this delay allows the spindle to re-establish normal and balanced chromosome segregation. However, delay can have many consequences. Mammalian cells remaining in M phase eventually show markers of DNA damage [ 6 , 7 ]. Cells in which the spindle checkpoint is deliberately activated using microtubule drugs often undergo apoptotic cell death, either directly in mitosis or in the M to G1 phase (Figure 1) [1, 8]. After exiting the One of the key pathways regulating cell death during M phase arrest is Cdk1-dependent phosphorylation, followed by degradation of the antiapoptotic member of the Bcl-2 family, Mcl-1 [9, 10, 11, 12]. Is. Some aspects of apoptotic signaling are suppressed in M phase, but partial activation of these pathways can lead to cell death in the later G1 phase [ 13 ]. In cells with normal p53 function, even a relatively short delay in M phase can lead to cell cycle arrest after entry into G1 [ 14 ]. Cells with chromosomal segregation defects that escape apoptosis produce offspring with altered chromosomal content. These cells can continue to cycle, especially if p53 is inactive. Chromosome segregation errors lead to aneuploid or polyploid cells and are generally harmful to both the cell and the organism. However, in some cases, changes in ploidy are programmed into normal development and physiology. Sometimes accidental deviations from euploidy can also result in favorable evolutionary adaptations, especially in unicellular organisms. In this review, we describe the consequences of aneuploidy and polyploidy due to segregation errors in mitosis and meiosis, focusing on recent ideas and topics relevant to human health.
Chapter 13. The Cell Cycle & Mitosis
In diploid organisms, except in special cases such as animal sex chromosomes, genes are present in two duplicated copies. Gaining or losing a copy changes the amount of gene product produced, a property known as gene dosage. Unlike whole-genome doubling in polyploidy, where the increase in gene dosage is equal to each chromosome, the loss or gain of a single chromosome or chromosome fragment causes unbalanced changes in the cellular proteome. Studies in fungal and mammalian systems have shown that changes in mRNA and protein levels from genes on aneuploid chromosomes are roughly proportional to changes in chromosome copy number [ 15 , 16 , 17 , 18 , 19 ]. Aneuploidy of large, gene-rich chromosomes can alter the expression of thousands of genes. In addition, transcription factors encoded on aneuploid chromosomes alter the expression of genes on other chromosomes [ 19 ]. Consequently, aneuploidy can induce a different spectrum of changes in a cell’s proteome, depending on whether specific chromosomes are lost or gained. Finally, aneuploidy itself can cause additional chromosomal instability, a topic discussed in more detail below.
The euploid karyotype is the result of natural selection for optimal genetic fit.