Cell Division

The cell cycle in numbers

A typical mammalian somatic cycle of about 24 hours splits into interphase (G₁ ~ 10 h, S ~ 8 h, G₂ ~ 4 h) and the M phase (~ 1 h). Interphase is not a resting period: G₁ is intense growth and protein synthesis, S is DNA replication so each chromosome ends as two sister chromatids, and G₂ prepares organelles and the mitotic spindle. Punjab Textbook Chapter 12 and Campbell Chapter 12 both emphasise the three checkpoints — G₁/S (the restriction point), G₂/M, and the spindle assembly checkpoint at metaphase — controlled by cyclins and cyclin-dependent kinases (Hartwell, Hunt, Nurse, Nobel 2001).

Mitosis phase by phase

Prophase: chromatin condenses, nucleolus disappears, centrosomes migrate to opposite poles, spindle begins to form. Prometaphase: nuclear envelope breaks down and microtubules attach to kinetochores. Metaphase: chromosomes line up on the equatorial plate. Anaphase: cohesin is cleaved and sister chromatids separate, pulled by shortening kinetochore microtubules. Telophase: chromosomes decondense, nuclear envelope reforms, nucleolus reappears. Cytokinesis follows: a contractile actin-myosin ring pinches the animal cell, while a cell plate of vesicle-derived material grows outward in plant cells.

Meiosis I — the reduction division

Meiosis halves the chromosome number from diploid (2n = 46 in humans) to haploid (n = 23) and creates genetic variation. Prophase I has five sub-stages — leptotene, zygotene (synapsis forms bivalents/tetrads), pachytene (crossing-over at chiasmata), diplotene, diakinesis. Metaphase I lines up homologous pairs, not individual chromosomes. Anaphase I separates homologues with sister chromatids still joined — the key event that halves chromosome number. Telophase I and cytokinesis produce two haploid cells, each with replicated chromosomes.

Meiosis II and sources of variation

Meiosis II is essentially mitosis on haploid cells: sister chromatids separate at anaphase II, giving four genetically unique haploid daughter cells. Genetic variation comes from three sources: crossing-over in pachytene (≥ one chiasma per bivalent in humans), independent assortment at metaphase I (2²³ ≈ 8.4 million combinations in humans), and random fertilisation. Non-disjunction — failure of homologues (meiosis I) or sister chromatids (meiosis II) to separate — produces aneuploid gametes. Trisomy 21 (Down's syndrome), 47,XXY (Klinefelter's), 45,X (Turner's), 47,XXX, and 47,XYY all trace to this error.

Cancer and recurring traps

Cancer is the disease of unregulated mitosis: mutations in proto-oncogenes (gain of function, e.g. RAS) or tumour-suppressor genes (loss of function, e.g. TP53, the "guardian of the genome") override checkpoints. Common MDCAT traps: DNA replication occurs in S, not in M; chromosomes are most condensed at metaphase, easiest to count there; sister chromatids separate in anaphase of mitosis and anaphase II of meiosis (NOT anaphase I); a human gamete carries 23 chromosomes after meiosis II, but a cell at the end of meiosis I still has 23 replicated chromosomes (= 46 chromatids).

Apoptosis and comparison with necrosis

Apoptosis (programmed cell death, Kerr 1972) is a tightly controlled removal of cells via caspase cascades: cells shrink, chromatin condenses, DNA fragments at internucleosomal sites (the 200-bp ladder on a gel), and the dying cell breaks into membrane-bound apoptotic bodies cleared by macrophages without inflammation. It sculpts fingers and toes from a paddle-shaped embryonic hand by removing interdigital tissue, eliminates self-reactive lymphocytes in the thymus, and removes cells with DNA damage that cannot be repaired. Necrosis is the opposite: traumatic, passive death where cells swell, lyse, and trigger inflammation. The MDCAT loves contrasting the two — apoptosis is an active, ATP-requiring process; necrosis is not. Failure of apoptosis contributes directly to cancer because damaged cells that should self-destruct instead survive and divide.