D2.1 Cell and nuclear division

Every one of the roughly thirty trillion cells in your body traces back to a single fertilised egg, copied again and again with astonishing fidelity. That copying is the job of cell division, and the rule the IB wants you to remember is simple: before a cell splits, it must first make a complete and accurate copy of its DNA, then share that DNA equally between the two daughter cells. Nuclear division by mitosis keeps the chromosome number constant and produces genetically identical cells — the basis of growth, tissue repair and asexual reproduction. When the controls on this process fail, the same machinery drives the unchecked growth we call cancer.

The cell cycle: interphase and the M phase

The cell cycle is the ordered sequence of events from the formation of a cell to its own division. Most of the cycle is spent in interphase, a period of intense activity (not, as the name might suggest, a resting stage). Interphase is divided into three sub-phases:

• G₁ phase: the cell grows, makes proteins and increases its number of organelles.
• S phase: DNA is replicated, so each chromosome now consists of two identical sister chromatids joined at a centromere.
• G₂ phase: further growth and preparation for division, including checking that DNA was copied correctly.

Division itself happens in the M phase, which is nuclear division (mitosis) followed by division of the cytoplasm (cytokinesis). A key syllabus understanding is that DNA replication is semi-conservative and depends on complementary base pairing — each new molecule keeps one original (parental) strand and one newly built strand, which is what allows the copy to be so accurate.

Mitosis: keeping the chromosome number constant

Mitosis divides the nucleus so that each daughter nucleus receives an identical set of chromosomes. It is conventionally split into four continuous stages — remember PMAT:

• Prophase: chromosomes condense and become visible, each as two sister chromatids; the spindle of microtubules begins to form and the nuclear membrane breaks down.
• Metaphase: chromosomes line up on the equator (the metaphase plate), attached to spindle fibres at their centromeres.
• Anaphase: the centromeres split and the spindle fibres pull the sister chromatids to opposite poles of the cell.
• Telophase: chromosomes decondense, a nuclear membrane re-forms around each set, and two genetically identical nuclei now exist.

Because the sister chromatids made in S phase are separated and shared equally, the two daughter cells are genetically identical to each other and to the parent cell, with the chromosome number unchanged. This is why mitosis is used for growth, repair of tissues, replacement of dead cells and asexual reproduction. Contrast this with meiosis, which halves the chromosome number and generates variation — do not confuse the two.

Cytokinesis in animal and plant cells

Cytokinesis is the division of the cytoplasm to produce two separate cells, and it differs between the two cell types — a reliable comparison question:

• In animal cells the plasma membrane is pulled inwards by a ring of contractile protein filaments, forming a cleavage furrow that pinches the cell in two.
• In plant cells the rigid cell wall prevents pinching, so vesicles gather at the centre and fuse to build a new cell plate outwards until it joins the existing wall, separating the two cells.

Cytokinesis is usually accompanied by a roughly equal sharing of organelles between the daughter cells. In most cases this division is symmetrical, but unequal cytokinesis also occurs — for example in the budding of yeast and in oogenesis, where one large egg cell and small polar bodies are produced. The IB highlights this to show that cell division does not always create two cells of equal size.

Control of the cycle: cyclins and cancer

The cell cycle is tightly regulated so that cells divide only when needed. Control depends on a family of signalling proteins called cyclins. Cyclins bind to and activate enzymes (cyclin-dependent kinases), and these only push the cell into the next stage of the cycle once cyclin concentrations rise above a threshold. This ensures that, for example, a cell does not enter mitosis before DNA replication is complete.

When the genes controlling the cycle mutate, this control can be lost. Mutations in proto-oncogenes and tumour-suppressor genes can cause cells to divide repeatedly and uncontrollably, forming a tumour. Agents that increase the chance of such mutations are mutagens; those that specifically cause cancer are carcinogens (for example the chemicals in tobacco smoke). A tumour that stays in one place is benign; one whose cells break away and spread to form secondary tumours elsewhere is malignant, and this spreading is called metastasis. The link the syllabus wants is clear: the very machinery that makes controlled division possible becomes dangerous when its regulation fails.