IB Biology - Cell Division
IB Biology - Cell Division
IB Biology - Cell Division
6 Cell Division
TERMINOLOGY
Asexual reproduction.
Growth of organism, more cell differentiation.
Embryonic development.
Tissue repair - replace cells that die naturally.
Draw typical eukaryotic cells as they would appear during the interphase and the four
phases of mitosis.
Interphase Key features Drawing
G1 Nucleus intact.
Nucleolus visible.
DNA as chromatin (1 single
strand), unreplicated.
S and G2 DNA replicates in S.
By G2, DNA is appeared to be
replicated (i.e. chromosome)
Mitosis is divided into 4 phases
Name Key features Drawing
Prophase Nuclear membrane begins to
break.
Nucleolus disappears.
DNA supercoils into replicated
chromosomes.
Centrosomes move to opposite
pole. Spindle fibre form
between them.
Metaphase Contraction of microtubule
causes replicated chromosome
to align at the cell equator.
A protein complex called
kinetochore, located at the
centromere, connected to
microtubules (a type of spindle
fibre).
Describe the structure of a replicated chromosome, include the centromere and sister
chromatids.
Chromosome condense by supercoiling to make DNA packed more tightly together so that it
can easily be moved to the poles of the cell.
U3. Cytokinesis occurs after mitosis and is different in plant and animal cells
Define cytokinesis.
Different cytokinesis.
Plant cells must create a cell wall between the daughter cell cytoplasm.
Animal cell – no need to form cell wall.
A ring of contractile protein (actin & myosin) at the cell equator constrict, pull the cell
membrane inward creating a cleavage furrow.
The cleavage furrow continues to pinch inward until two sides of cytoplasm meets to form a
new cell.
Describe the formation of the middle lamella and cell wall in plant cell cytokinesis.
In telophase, vesicles from Golgi apparatus move to the equator of cell. Fuse to form tubular
structure.
Tubular structure merge with more vesicles to form two layers of plasma membrane – cell
plate.
Cell plate continues to develop until it connects with the existing cell’s plasma membrane.
Vesicle deposit by exocytosis, pectin & other substances in the lumen between the daughter
cells to form the middle lamella. (‘gluing’ cell tg)
Both daughter cells secrete cellulose to form new adjacent cell walls.
U4. Interphase is a very active phase of the cell cycle with many processes occurring
after mitosis and is different in plant and animal cells
The majority of cell cycle is spent in interphase (G1, S & G2). Consists of parts of cell cycle
that don’t involve cell division.
G1:
o Increase the volume of cytoplasm//cell growth, nutrients are required.
o Organelles produce & increase. (in animal – mitochondria; in plant – chloroplast).
o Proteins synthesised.
S: DNA is replicated.
G2:
o Increase the volume of cytoplasm
o Organelles produce & increase.
o Synthesise proteins needed for mitosis and cytokinesis.
Explain the role of cyclin and cyclin-CDK complexes in controlling the cell cycle.
Cyclins – a family of proteins that control the progression of cells through cell cycle.
Cells cannot progress to the next stage of cell cycle unless specific cyclin reaches its
threshold concentration.
Cyclins bind to enzymes called cyclin-dependent kinases, creating cyclin-CDK complexes.
Kinases then become active and attach phosphate to other proteins in the cell.
Phosphorylation triggers proteins to become active and carry out tasks.
A cell becomes cancerous only when mutations accumulate in the gene that control cell
cycle.
Explain the relationship between oncogenes, tumor suppressor genes and cancer.
Oncogenes are normal genes that code for proteins that help the cell move through cell
cycle.
When oncogenes are mutated, they move the cell through cell cycle even when it shouldn’t
divide.
Tumor-suppressor genes function to stop a cell from dividing when it shouldn’t.
Tumor-suppressors can mutate, leading to cell moving through cell cycle when it shouldn’t.
Cancer develops when proto-oncogenes & tumor-suppressor genes are mutated and cell
divides without control.
Outline the use of mitotic index calculations in diagnosis and treatment of cancer.
Diagnosis: higher the M.I relative to a standard M.I., more likely a tissue is cancerous,
Treatment: cancer treatment work by stopping cell division, so if M.I. decreases, treatment
is working.