Biology Chapter 8 - The Cell Cycle

The life cycle of a prokaryotic cell, involving replication (R-phase), division (D-phase), and interval (I-phase).

The process of cell division in prokaryotes, where a single cell divides into two.

The stage of binary fission where the bacterial chromosome is replicated.

The stage of binary fission where the cell divides into two daughter cells.

The stage of binary fission between division and replication.

The life cycle of a eukaryotic cell, including interphase (G1, S, and G2 phases) and the M phase (mitosis).

The part of the eukaryotic cell cycle where the cell grows and prepares for division, consisting of G1, S, and G2 phases.

A resting phase where some eukaryotic cells exit the cell cycle to specialize.

A type of cancer caused by defects in DNA repair mechanisms, particularly those involved in double-strand breaks (DSBs).

A rare genetic disorder characterized by DNA repair deficiencies, leading to increased cancer risk and neurological symptoms.

A gene responsible for producing a protein that helps repair damaged DNA, especially double-strand breaks.

The irreversible arrest of cell proliferation, preventing damaged or aging cells from continuing to divide.

Programmed cell death, a normal process in multicellular organisms that eliminates damaged or unneeded cells.

A family of proteases involved in apoptosis that activate each other in a cascade, leading to cell death.

Apoptosis initiated by external signals, like binding of Fas ligand to Fas receptor on the cell surface.

Apoptosis triggered by internal cellular damage, involving the release of pro-apoptotic proteins from mitochondria.

Processes that correct errors or damage in DNA, ensuring genome integrity.

A set of mechanisms that control the cell cycle progression, ensuring DNA is repaired before proceeding to the next phase.

The eukaryotic cell cycle is divided into two main stages: Interphase (G1, S, and G2) and Mitosis (M phase). During interphase, the cell grows and duplicates its DNA. In the M phase, the cell divides into two daughter cells.

The G0 phase is a resting phase where some eukaryotic cells exit the cell cycle to specialize. These cells either become quiescent or senescent. While quiescent cells can re-enter the cell cycle, senescent cells cannot.

Cyclin-dependent kinases (CDKs) are key regulatory proteins that control the cell cycle. They require association with cyclins to become active. The activity of CDKs is essential for progression through different cell cycle phases.

Cyclins are proteins whose concentration fluctuates throughout the cell cycle. They bind to CDKs, activating their kinase activity. Different cyclins activate specific CDKs at different stages of the cycle.

Checkpoints are surveillance mechanisms within the cell cycle. They monitor the order, integrity, and fidelity of crucial events in the cell cycle, ensuring accurate completion.

The G1/restriction checkpoint monitors cell size, nutrient availability, growth factors, and DNA damage. It's a primary decision point for the cell to proceed into the S phase.

The S-phase checkpoint safeguards DNA replication. It ensures the integrity of DNA replication forks, preventing errors that can lead to instability.

The G2-phase checkpoint protects the cell from entering mitosis with damaged DNA. It senses DNA damage and halts cell division until the damage is repaired.

The M-phase checkpoint ensures proper attachment of chromosomes to the mitotic spindle. This prevents premature separation of chromosomes, leading to accurate chromosome segregation.

The p53 protein is a tumor suppressor. It's a transcription factor that can bind to specific DNA sequences. When activated by DNA damage, it triggers cell cycle arrest or apoptosis.

pRB is a key regulator of cell division. This tumor suppressor protein promotes the G0-G1 transition when phosphorylated by CDK3/cyclin-C. It's like a 'brake pedal' that keeps cells in a non-dividing state.

DNA damage can occur from both endogenous (spontaneous mutations) and exogenous (induced mutations) sources. These agents can cause damage to DNA, potentially harming the cell.

DNA repair mechanisms exist to correct damage to DNA, preventing replication errors and maintaining genetic integrity. These processes are essential for cell survival and genome stability.

Mismatch repair (MMR) corrects replication errors, such as base mismatches and small insertion/deletion loops. It aims to maintain fidelity during the DNA replication process.

Nucleotide excision repair (NER) removes damage caused by environmental factors, such as radiation or chemical mutagens. It's especially important for repairing UV-induced damage.