IB Biology HL D2.1 Cell and nuclear division Notes

All cells arise from pre-existing parent cells by cell division. The point of the process is not just making more cells: daughter cells are needed for growth, replacement, repair, or reproduction.

Cell division supplies new daughter cells.

Cytokinesis is the division of cytoplasm after nuclear division. Animal cells use a contractile ring to pinch the cell membrane inward, while plant cells form a vesicle-derived cell plate that becomes the new partition between cells.

Same goal, different mechanism.

Cytokinesis can be equal or unequal. Equal cytokinesis gives daughter cells similar amounts of cytoplasm, while unequal cytokinesis gives one cell more cytoplasm than the other, as in oogenesis and yeast budding.

Cytoplasm can be shared equally or unequally.

Mitosis and meiosis solve different problems. Mitosis maintains chromosome number for growth, repair, and asexual reproduction, while meiosis halves chromosome number for gametes and generates genetic diversity.

Choose division type by purpose and chromosome number.

DNA must be replicated in interphase before chromosomes can be separated. Replication produces chromosomes made of sister chromatids, and the sister chromatids remain joined at centromeres until they separate during nuclear division.

Replication prepares chromosomes for separation.

Mitosis and meiosis share machinery for moving DNA safely. Chromatin condenses into movable chromosomes using histones and nucleosomes, while spindle microtubules and motor proteins organize chromosome movement.

Packaging and movement machinery work together.

Mitosis is easiest to learn as a movement sequence. In prophase chromosomes condense, in metaphase they align at the equator, in anaphase sister chromatids separate, and in telophase nuclei reform around identical chromosome sets.

Use chromosome position to read mitosis.

To identify mitosis phases in diagrams, micrographs, or root-tip squashes, look at chromosome cues. Condensed but not aligned suggests prophase, alignment at the equator suggests metaphase, separated chromatids suggest anaphase, and reforming nuclear membranes suggest telophase.

Phase ID comes from visual evidence.

Meiosis is reduction division because it halves chromosome number. After one round of DNA replication, there are two nuclear divisions; homologous chromosomes separate in meiosis I, producing haploid nuclei.

Meiosis reduces chromosome number through homologue separation.

Non-disjunction means chromosomes fail to separate properly in meiosis. If homologues or sister chromatids fail to separate, a gamete can receive an abnormal chromosome number; after fertilization, trisomy 21 usually results in Down syndrome.

Failed separation can change chromosome number.

Meiosis generates variation by reshuffling allele combinations. Crossing over at chiasmata exchanges DNA between non-sister chromatids, random orientation of bivalents shuffles maternal and paternal homologues, and fertilization combines gametes to create new allele combinations.

Meiosis reshuffles alleles before fertilization combines gametes.

Cell proliferation means increasing cell number by repeated mitosis. It is expected in plant meristems, early embryos, skin replacement, and wound healing, where many genetically similar cells are needed.

Proliferation increases cell number through mitosis.

The cell cycle is the repeating sequence of interphase, mitosis, and cytokinesis. Interphase contains G1 growth, S-phase DNA replication, and G2 preparation before the cell enters mitosis and divides cytoplasm.

Interphase prepares the cell before division.

Interphase is not a resting state. It is metabolically active: cells synthesize proteins, replicate DNA, grow cytoplasm, and increase organelles so the cell is ready for division.

Interphase is active preparation for division.

Cell-cycle control depends on cyclin levels changing over time. Cyclin concentrations rise and fall, cyclins activate cyclin-dependent kinases, and CDK-cyclin complexes such as MPF control checkpoints and entry into mitosis.

Cyclin-CDK complexes control cell-cycle transitions.

Cancer is linked to loss of cell-cycle control. Proto-oncogene activation can push division signals too strongly, while tumour suppressor loss removes brakes at checkpoints; accumulated mutations can lead to uncontrolled proliferation and cancer.

Cancer can result from lost cell-cycle control.

Tumours differ by invasion and spread. Benign tumours grow locally, malignant tumours invade neighbouring tissues, and metastasis occurs when cancer cells spread to form secondary tumours.

Tumour severity depends on invasion and spread.

All cells arise from pre-existing parent cells by cell division, producing daughter cells for growth, replacement, repair, or reproduction. Cytokinesis splits cytoplasm after nuclear division; animal cells use a contractile ring and plant cells form a vesicle-derived cell plate. Equal cytokinesis gives daughter cells similar amounts of cytoplasm, while unequal cytokinesis occurs in oogenesis and yeast budding. Mitosis maintains chromosome number for growth, repair, and asexual reproduction; meiosis halves chromosome number for gametes and generates genetic diversity. DNA replication in interphase produces chromosomes with sister chromatids joined at centromeres until separation. Mitosis and meiosis both condense chromatin into movable chromosomes; histones, nucleosomes, spindle microtubules, and motor proteins organize movement. In mitosis, prophase condenses chromosomes, metaphase aligns them at the equator, anaphase separates chromatids, and telophase reforms nuclei, producing identical nuclei. Mitosis phases are identified in diagrams, micrographs, and root-tip squashes using chromosome condensation, equator alignment, separation, and nuclear membrane cues. Meiosis has two nuclear divisions after one round of DNA replication; homologous chromosomes separate in meiosis I, producing haploid nuclei. Non-disjunction is failed separation of homologues or sister chromatids in meiosis; Down syndrome usually results from trisomy 21 after non-disjunction. Crossing over at chiasmata exchanges DNA between non-sister chromatids; random orientation of bivalents and fertilization create new allele combinations.

Use this for SL/core questions about cell origin, cytokinesis, mitosis versus meiosis, replicated chromosomes, mitosis phase identification, meiosis reduction division, non-disjunction/Down syndrome, and variation.

Cell proliferation increases cell number by repeated mitosis, as in plant meristems, early embryos, skin replacement, and wound healing. The cell cycle includes interphase, mitosis, and cytokinesis; interphase has G1 growth, S-phase DNA replication, and G2 preparation. Interphase is metabolically active, not resting; cells synthesize proteins, replicate DNA, grow cytoplasm, and increase organelles. Cyclin concentrations rise and fall to activate cyclin-dependent kinases; CDK-cyclin complexes such as MPF control checkpoints and mitosis entry. Proto-oncogene activation and tumour suppressor loss disrupt checkpoints; accumulated mutations can cause uncontrolled proliferation and cancer. Benign tumours grow locally, malignant tumours invade neighbouring tissues, and metastasis spreads cancer cells to form secondary tumours.

Use this for HL questions about cell proliferation, cell-cycle phases, active interphase, cyclin-CDK control, checkpoint disruption, cancer, and tumour spread.