Mitosis & Cell Cycle — Comprehensive Study Notes Summary & Study Notes

🔬 DNA Packaging and Chromosome Structure

DNA in the nucleus is wrapped around histone proteins to form chromatin, which condenses further during cell division to form chromosomes. A single chromosome contains thousands of genes; the position of a gene on a chromosome is called its locus. Different forms of the same gene are alleles.

🧬 Homologous Chromosomes and Sister Chromatids

Homologous chromosomes occur as pairs in diploid cells — one maternal and one paternal — with similar size, shape and gene loci but possibly different alleles. After DNA replication, each chromosome consists of two identical sister chromatids joined at a centromere.

🧾 Karyotype and Chromosome Numbers

A karyogram shows the full set of chromosomes arranged by size. Chromosome number is species-specific: human somatic cells are diploid ($2n=46$) while gametes are haploid ($n=23$). Diploid cells result from mitosis; haploid cells result from meiosis.

🔁 Overview: The Mitotic Cell Cycle

The cell cycle consists of Interphase (G1, S, G2), M phase (mitosis), and cytokinesis. Interphase prepares the cell: G1 for growth, S for DNA replication (forming sister chromatids), and G2 for growth and centriole duplication.

⚙️ Interphase Details

G1 is focused on growth and synthesis of proteins. S phase duplicates DNA, producing sister chromatids. G2 prepares for mitosis and repairs replication errors while centrioles duplicate to form centrosomes.

🧭 Mitosis: Purpose and Biological Importance

Mitosis produces two genetically identical daughter cells with the same chromosome number as the parent. Key roles: maintaining chromosome number and genomic stability, organismal growth, tissue repair and cell replacement, and asexual reproduction.

🧩 Prophase

Chromatin condenses into visible chromosomes (each with two sister chromatids). The mitotic spindle begins to form from centrosomes, which move to opposite poles. The nuclear envelope and nucleolus break down, allowing spindle attachment.

🧭 Metaphase

Chromosomes line up at the cell equator (the metaphase plate). Spindle fibers attach to the kinetochore at each centromere, ensuring proper alignment before separation.

➗ Anaphase

The centromeres split and sister chromatids separate. Spindle microtubules shorten, pulling chromatids (now individual chromosomes) toward opposite poles with centromeres leading.

🧵 Telophase

Chromosomes reach the poles and decondense back into chromatin. The nuclear envelope and nucleolus re-form, spindle fibers break down, and cytokinesis begins to partition the cytoplasm.

✂️ Cytokinesis: Animal vs Plant Cells

In animal cells, a contractile ring of actin microfilaments forms a cleavage furrow that pinches the cell into two. In plant cells, vesicles fuse at the equator to form a cell plate, which becomes the new cell wall dividing the two daughter cells.

🛑 Cell Cycle Checkpoints and Regulation

Cell cycle progression is tightly regulated by checkpoints (G1, G2, and spindle checkpoints). Checkpoints prevent damaged or incomplete DNA from being passed on and coordinate repair or apoptosis if errors are detected.

🧬 Telomeres and Telomerase

Telomeres are repetitive nucleotide sequences at chromatid ends that protect gene loss during replication. Telomeres shorten with each mitotic division, contributing to cellular aging. Telomerase can extend telomeres; it is active in stem cells and many cancer cells, but not in most normal somatic cells.

🌱 Stem Cells: Properties and Roles

Stem cells are undifferentiated, capable of continuous division, and can self-renew due to telomerase activity. They produce one stem cell and one differentiating cell, supporting growth, tissue repair and cell replacement. Potency ranges from totipotent to pluripotent to multipotent.

🚨 Cancer: Uncontrolled Cell Division

Cancer arises from loss of normal cell-cycle control leading to uncontrolled mitosis. Cancer cells often have shortened interphase, error-prone DNA replication, disabled checkpoints, and the ability to evade apoptosis and immune detection.

🧪 Causes and Risk Factors for Cancer

Cancer often requires accumulated mutations. Contributing factors include mutagens and carcinogens such as ionising radiation (X-rays, gamma rays), UV light, free radicals, chemical agents (tar, mustard gas), and certain viruses (e.g., HPV). Other risks: hereditary predisposition, tobacco smoking, and obesity.

🔬 Molecular Mechanisms: Oncogenes and Tumour Suppressors

Mutations can convert normal proto-oncogenes into oncogenes that drive division, while tumour suppressor genes may be inactivated. Accumulated mutations enable tumour progression and resistance to normal regulatory signals.

🧫 Tumour Development and Characteristics

A tumour is a mass of undifferentiated cells with abnormal shape and high nutrient demand. Tumour development: mutation → escape from cell death and immune detection → uncontrolled proliferation → tumour mass formation → displacement/compression of tissues → angiogenesis to supply nutrients.

🔁 Types of Tumours: Benign vs Malignant

Benign tumours do not spread from their origin (e.g., warts, some ovarian cysts). Malignant tumours can metastasize via blood or lymph, invading and destroying distant tissues and forming secondary growths.

⚖️ Clinical and Biological Consequences

Cancer disrupts tissue function, consumes resources, and can be fatal if critical organs are affected. Understanding checkpoints, telomeres, and stem cell behavior informs therapies such as targeted drugs, telomerase inhibitors, and stem cell treatments.

✅ Key Terms to Remember

Chromatin, chromosome, gene, locus, allele, homologous chromosomes, sister chromatids, centromere, karyogram, diploid ($2n$), haploid ($n$), interphase (G1, S, G2), mitosis (prophase, metaphase, anaphase, telophase), cytokinesis, checkpoint, telomere, telomerase, stem cell, oncogene, tumour suppressor, tumour, metastasis, angiogenesis.