“ALL CELLS COME FROM PRE- EXISTING CELLS”

Cell Division What are two different types of reproduction? WHAT MUST TAKE PLACE FOR A CELL OR ORGANISM TO REPRODUCE?

Bacterial cell division (binary fission)

Eukaryotic Cell Division (Mitosis) is much more complex What are some of the roles of mitosis in eukaryotes?

The functions of Mitotic cell division: 1.) Reproduction Asexual reproduction of a unicellular, eukaryotic organism

2.) Development

3.) Tissue renewal in adults

Figure 12.2 Eukaryotic chomosomes

Figure 12.3 Chromosome duplication and distribution during mitosis

Figure 12.0 Mitosis

Figure 12.4 The cell cycle

Figure 12.5 The stages of mitotic cell division in an animal cell: G 2 phase; prophase; prometaphase

Figure 12.5 The stages of mitotic cell division in an animal cell: metaphase; anaphase; telophase and cytokinesis. Pig cell mitosis

Figure 12.8 Cytokinesis in animal and plant cells

“To divide or not to divide, that is the question”

Anchorage Dependence and Density-dependent inhibition of cell division

External Signaling: G 1 checkpoint, Growth factors Ex. PDGF receptor cell cycle control

BIOLOGY OF CANCER Cancer is the loss of normal cell cycle regulation (a cell starts dividing out of control) What can cause this? Genes that play a role in normal cell cycle control are altered in some way. 1. Genes that stimulate cell division Normal version of gene: Proto-oncogene Mutated version: Oncogene

Mechanical analogy for the cell cycle control system

2. Tumor Suppressor Genes: Two Classes - Genes involved in blocking cell division (checkpoints) - DNA Repair Genes (fix mutations in DNA) Most common examples: Rb, retinoblastoma. Involved in childhood cancer (two defective copies are required for disease ), but also in adult tumors such as bladder, breast and lung carcinoma. The Rb protein is a key target for the oncogene products of many tumor viruses, including SV40, adenoviruses, and papillomaviruses. They all bind to Rb and inhibit its activity. P53 is mutated in 50% of all cancers. It’s a target of the same tumor viruses That target Rb. P53 is required for apoptosis induced by DNA damage APC: is mutated in hereditary colon cancer BRCA1 and 2: responsible for hereditary breast cancer

To develop cancer it takes multiple mutations in the same cell. At least two mutations: One oncogene, one tumor suppressor gene. Some people are predisposed to getting a particular type of cancer. (Genetic Pre-dispositions)

The growth and metastasis of a malignant breast tumor Terminology: Tumor (benign and malignant) Metastasis

So what causes these mutations that can result in the development of Cancer??? Environmental Exposure: -Radiation -Viruses -Air (indoor and outdoor) and water pollution -Consumer products -Food -Cosmetics -Medicines -TIME!

How do we cure cancer? Prevention Treatment old and new drugs Examples: endostatin and angiostatin retinoic acid to induce differentiation inhibitors of farnesylation (Ras oncogene) Herceptin (antibodies against erbB-2 gene) Inhibitor of specific protein tyrosine-kinases (Gleevec)

“ASEXUAL OR SEXUAL, THAT IS THE QUESTION” REPRODUCTION

Figure 13.1 The asexual reproduction of a hydra

Figure 13.2 Two families

The human life cycle

Three sexual life cycles differing in the timing of meiosis and fertilization (syngamy) Alternation of generations

Human female chromosomes shown by bright field G-banding

Homologous pair Haploid chromosome # = n (humans: n =23) Diploid # =2n (humans: 2n = 46) Eggs & sperm All other cells (somatic)

The human life cycle

Overview of meiosis: how meiosis reduces chromosome number

The stages of meiotic cell division: Meiosis I

The stages of meiotic cell division: Meiosis II

A comparison of mitosis and meiosis

Figure 13.9 The results of alternative arrangements of two homologous chromosome pairs on the metaphase plate in meiosis I (Independent Assortment)

For 2 homologous chromosomes: 4 possible gametes (2 2 ) For 23 homologous chromosomes: 2 23 = 8 million possible gametes! So, upon formation of a zygote, 8 mil. X 8 mil. = 64 trillion!

Figure The results of crossing over during meiosis

Sources of genetic variability: 1.Independent assortment 2.Crossing over (recombination) 3.Random fertilization of ovum by sperm. 4.MUTATION - ultimate source of genetic variability

ERRORS IN MEIOSIS

Testing a fetus for genetic disorders

The risk of nondisjunction increases dramatically with age. 30 yr. old mother: 1/1000, 40 yr. old mother: 1/100

GAMETOGENESIS Spermatogenesis- 48 days

Oogenesis years