Cell division is a fundamental biological process underpinning the growth, repair, and reproduction of all living organisms. In humans, mitosis creates new body cells for development and tissue maintenance, while meiosis forms specialized reproductive cells (sperm and eggs). Errors can occasionally arise, leading to various cellular and systemic consequences.
How Cell Division Goes Astray
Cell division can deviate from its precise pathway through errors in chromosome distribution or DNA replication. One common type of chromosomal error is non-disjunction, where homologous chromosomes or sister chromatids fail to separate properly during cell division. This can occur in meiosis, leading to reproductive cells with an abnormal number of chromosomes, or in mitosis, affecting somatic cells. The result of non-disjunction is aneuploidy, an abnormal number of chromosomes in the daughter cells, such as an extra chromosome (trisomy) or a missing chromosome (monosomy).
Other chromosomal aberrations include anaphase lag, where a chromosome fails to move to either pole and is subsequently lost, or chromosome breaks. These errors can involve entire chromosomes or segments, altering the genetic content passed to new cells. Beyond chromosomal segregation, mistakes can also emerge during DNA replication. Inaccurate copying can introduce mutations, which are changes in the DNA sequence. If these replication errors are not detected and corrected, they can be passed on to daughter cells.
The Cell’s Internal Safeguards
Cells possess internal safeguards to detect and manage errors during division, preventing the propagation of faulty cells. Cell cycle checkpoints monitor the cell’s conditions at various stages, such as the G1, G2, and M phases. These checkpoints pause the cell cycle if problems like DNA damage or improperly aligned chromosomes are detected, allowing time for repairs. The G2 checkpoint ensures that all chromosomes have been replicated accurately and that the DNA is not damaged before the cell enters mitosis.
Beyond checkpoints, cells employ various DNA repair mechanisms to correct genetic damage before division proceeds. If the damage is too severe to repair, or if errors persist, cells can initiate a process called apoptosis, or programmed cell death. This self-destruction mechanism eliminates severely flawed cells, preventing them from dividing. Cells can also enter cellular senescence, a state of irreversible growth arrest, where they stop dividing but remain metabolically active. Senescence can be triggered by significant cellular stress, including DNA damage, and acts as a barrier against uncontrolled cell proliferation.
Systemic Consequences of Errors
When cell division errors bypass internal safeguards, they impact an organism. Errors occurring during meiosis, particularly non-disjunction, can lead to genetic disorders. For example, non-disjunction of chromosome 21 in a reproductive cell can result in Down syndrome, where an individual has three copies of chromosome 21 instead of two. Other conditions, such as Turner syndrome (a missing X chromosome) or Klinefelter syndrome (an extra X chromosome), also arise from meiotic errors affecting sex chromosomes. These chromosomal abnormalities are typically present from conception and can lead to developmental delays.
Uncorrected errors in mitosis, particularly those that accumulate in somatic cells, are linked to the development of cancer. Mutations in genes that regulate cell growth and division can lead to uncontrolled cell proliferation and tumor formation. Cancer often involves a series of accumulated somatic mutations, changes in DNA that occur in non-reproductive cells and are passed down to daughter cells. These mutations can affect proto-oncogenes, which promote cell division, or tumor suppressor genes, which normally inhibit it, leading to a loss of cell cycle control.
Accumulated cell division errors over a lifetime also contribute to the aging process and age-related diseases. As cells repeatedly divide, the chance of errors increases. While the body has repair mechanisms, some errors can persist, leading to cellular dysfunction or the accumulation of senescent cells. This accumulation of errors and dysfunctional cells can impair tissue function and contribute to the overall decline associated with aging.