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Cell reproduction - Coggle Diagram

- - - - the alteration of the DNA sequence will result in a less functional (or non-functional) protein.
        
        The result is detrimental to the cell and will likely prevent the cell from completing the cell cycle; however, the organism is not harmed because the mutation will not be carried forward
      - Occasionally, however, a gene mutation causes a change that increases the activity of a positive regulator.
        
        example, a mutation that allows Cdk to be activated without being partnered with cyclin could push the cell cycle past a checkpoint before all of the required conditions are met.
        
        If the resulting daughter cells are too damaged to undergo further cell divisions, the mutation would not be propagated and no harm would come to the organism.
        
        However, if the atypical daughter cells are able to undergo further cell divisions, subsequent generations of cells will probably accumulate even more mutations, some possibly in additional genes that regulate the cell cycle.
      - In addition to the cell cycle regulatory proteins, any protein that influences the cycle can be altered in such a way as to override cell cycle checkpoints.
      - An oncogene is any gene that, when altered, leads to an increase in the rate of cell cycle progression.
  - - - A cell with a faulty p53 may fail to detect errors present in the genomic DNA .
      - Even if a partially functional p53 does identify the mutations, it may no longer be able to signal the necessary DNA repair enzymes.
        
        Either way, damaged DNA will remain uncorrected.
        
        At this point, a functional p53 will deem the cell unsalvageable and trigger programmed cell death (apoptosis).
        
        The damaged version of p53 found in cancer cells, however, cannot trigger apoptosis.
      - Mutated p53 might lose its ability to trigger p21 production.
        
        Without adequate levels of p21, there is no effective block on Cdk activation.
        
        Essentially, without a fully functional p53, the G1 checkpoint is severely compromised and the cell proceeds directly from G1 to S regardless of internal and external conditions.
        
        At the completion of this shortened cell cycle, two daughter cells are produced that have inherited the mutated p53 gene.
        
        Given the non-optimal conditions under which the parent cell reproduced, it is likely that the daughter cells will have acquired other mutations in addition to the faulty tumor suppressor gene. Cells such as these daughter cells quickly accumulate both oncogenes and non-functional tumor suppressor genes. Again, the result is tumor growth.
- - - - In prokaryotes, the genome is composed of a single, double-stranded DNA molecule in the form of a loop or circle
        
        Bacteria can exchange these plasmids with other bacteria, sometimes receiving beneficial new genes that the recipient can add to their chromosomal DNA. Antibiotic resistance is one trait that often spreads through a bacterial colony through plasmid exchange.)
        
        Some prokaryotes also have smaller loops of DNA called plasmids that are not essential for normal growth
      - In eukaryotes, the genome consists of several double-stranded linear DNA molecules, -
        
        Each species of eukaryotes has a characteristic number of chromosomes in the nuclei of its cells
        
        A typical body cell, or somatic cell, contains two matched sets of chromosomes, a configuration known as diploid.
        
        The letter n is used to represent a single set of chromosomes; therefore, a diploid organism is designated 2 n
        
        Human cells that contain one set of chromosomes are called gametes, or sex cells; these are eggs and sperm, and are designated 1n, or haploid.
        
        Matched pairs of chromosomes in a diploid organism are called homologous (“same knowledge”) chromosomes
        
        Homologous chromosomes are the same length and have specific nucleotide segments called genes in exactly the same location, or locus
        
        Each copy of a homologous pair of chromosomes originates from a different parent; therefore, the genes themselves are not identical
        
        variation of individuals within a species is due to the specific combination of the genes inherited from both parents
        
        However, if the entire DNA sequence from any pair of human homologous chromosomes is compared, the difference is less than one percent
        
        The sex chromosomes, X and Y, are the single exception to the rule of homologous chromosome uniformity: Other than a small amount of homology that is necessary to accurately produce gametes, the genes found on the X and Y chromosomes are different.
  - - - The DNA-histone complex is part of the chromatin. Each beadlike histone-DNA complex is called a nucleosome, and DNA connecting the nucleosomes is called linker DNA
      - A DNA molecule in this form is about seven times shorter than the double helix without the histones
    - - This coiling further shortens the chromosome so that it is now about 50 times shorter than the extended form
    - - These fibrous proteins also ensure that each chromosome in a non-dividing cell occupies a particular area of the nucleus that does not overlap with that of any other chromosome
    - - After replication, the chromosomes are composed of two linked sister chromatids
      - When fully compact, the pairs of identically packed chromosomes are bound to each other by cohesin proteins
      - The connection between the sister chromatids is closest in a region called the centromere.
- - - - An event may be as simple as the death of a nearby cell or as sweeping as the release of growth-promoting hormones
        
        such as human growth hormone (HGH). A lack of HGH can inhibit cell division, resulting in dwarfism, whereas too much HGH can result in gigantism.
      - Crowding of cells can also inhibit cell division.
      - The size of the cell: as a cell grows, it becomes inefficient due to its decreasing surface-to-volume ratio. The solution to this problem is to divide.
    - - A checkpoint is one of several points in the eukaryotic cell cycle at which the progression of a cell to the next stage in the cycle can be halted until conditions are favorable. These checkpoints occur near the end of G1, at the G2/M transition, and during metaphase
  - - - Therefore, the failure of a single regulator may have almost no effect on the cell cycle, especially if more than one mechanism controls the same event.
      - Conversely, the effect of a deficient or non-functioning regulator can be wide-ranging and possibly fatal to the cell if multiple processes are affected.
    - - cyclins and cyclin-dependent kinases (Cdks), are responsible for the progress of the cell through the various checkpoints
      - Increases in the concentration of cyclin proteins are triggered by both external and internal signals. After the cell moves to the next stage of the cell cycle, the cyclins that were active in the previous stage are degraded.
      - Cyclins bound to Cdks to fully active and this complex must be phosphorylated in specific locations
        
        Cdks are enzymes (kinases) that phosphorylate other proteins. The proteins phosphorylated by Cdks are involved in advancing the cell to the next phase. (Figure 10.12).
        
        The levels of Cdk proteins are relatively stable throughout the cell cycle; however, the concentrations of cyclin fluctuate and determine when Cdk/cyclin complexes form.
        
        regulation of the cell cycle usually occurs by either the Cdk molecules alone or the Cdk/cyclin complexes
        
        Without a specific concentration of fully activated cyclin/Cdk complexes, the cell cycle cannot proceed through the checkpoints.
        
        The different cyclins and Cdks bind at specific points in the cell cycle and thus regulate different checkpoints.
        
        Molecules that prevent the full activation of Cdks are called Cdk inhibitors. The block placed on Cdks by inhibitor molecules will not be removed until the specific event that the inhibitor monitors is completed.
    - - retinoblastoma protein (Rb)
        
        Retinoblastoma proteins are a group of tumor-suppressor proteins common in many cells
        
        Rb exerts its regulatory influence on other positive regulator proteins and chiefly Rb monitors cell size.
        
        In the active, dephosphorylated state, Rb binds to proteins called transcription factors, most commonly, E2F
        
        Transcription factors “turn on” specific genes, allowing the production of proteins encoded by that gene.
        
        When Rb is bound to E2F, production of proteins necessary for the G1/S transition is blocked.
        
        As the cell increases in size, Rb is slowly phosphorylated until it becomes inactivated.
        
        Rb releases E2F, which can now turn on the gene that produces the transition protein, and this particular block is removed.
        
        For the cell to move past each of the checkpoints, all positive regulators must be “turned on,” and all negative regulators must be “turned off.”
      - p53
        
        functional molecular masses of the proteins (p) in kilodaltons
        
        has a major impact on the commitment of a cell to division because it acts when there is damaged DNA in cells that are undergoing the preparatory processes during G1.
        
        If damaged DNA is detected, p53 halts the cell cycle and recruits enzymes to repair the DNA. If the DNA cannot be repaired, p53 can trigger apoptosis, or cell suicide, to prevent the duplication of damaged chromosomes.
        
        As p53 levels rise, the production of p21 is triggered
      - p21
        
        p21 enforces the halt in the cycle dictated by p53 by binding to and inhibiting the activity of the Cdk/cyclin complexes.
        
        As a cell is exposed to more stress, higher levels of p53 and p21 accumulate, making it less likely that the cell will move into the S phase.
      - In damaged or non-functional in cells that had begun to replicate uncontrollably (became cancerous).
      - In each case, the main cause of the unchecked progress through the cell cycle was a faulty copy of the regulatory protein.
      - These three act primarily on G1 checkpoint