What are the main phases of the eukaryotic cell cycle?
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Explore the molecular mechanisms controlling cell division and how cells repair DNA damage to maintain genomic integrity.
Mastering this deck will enhance your understanding of how cells regulate division and maintain genome stability, which is essential for advancing in fields like cancer biology, genetics, and molecular medicine. You'll be able to explain key pathways and identify molecular targets for therapies related to cell cycle dysregulation and DNA repair defects.
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| # | Front | Back | Hint |
|---|---|---|---|
| 1 | What are the main phases of the eukaryotic cell cycle? | The main phases are G1 (gap 1), S (DNA synthesis), G2 (gap 2), and M (mitosis). Some models also include G0, a resting state outside the cycle. | Think of the cycle as a sequence of growth, copying, preparing, and dividing. |
| 2 | Which cyclin-dependent kinase (CDK) complexes are active during the G1 to S phase transition? | The CDK4/6-cyclin D complex initiates the G1 phase, and the CDK2-cyclin E complex promotes the G1 to S transition. | Cyclins bind CDKs to activate them at specific cell cycle stages. |
| 3 | What is the role of the retinoblastoma protein (Rb) in cell cycle regulation? | Rb inhibits E2F transcription factors, preventing progression from G1 to S phase. Phosphorylation of Rb releases E2F, allowing DNA replication genes to be expressed. | Rb acts as a brake that is released by phosphorylation. |
| 4 | Which kinase activity is responsible for driving the cell into mitosis? | Cyclin B-CDK1 (also known as maturation-promoting factor, MPF) activity drives the cell into mitosis. | Think of Cyclin B-CDK1 as the 'mitosis switch.' |
| 5 | What is the function of the anaphase-promoting complex/cyclosome (APC/C)? | APC/C is an E3 ubiquitin ligase that targets securin and cyclins for degradation, triggering progression from metaphase to anaphase and exit from mitosis. | APC/C acts as a molecular 'cleanup crew' to move the cell cycle forward. |
| 6 | Name one key tumor suppressor gene involved in cell cycle regulation. | TP53 (p53) is a critical tumor suppressor that regulates cell cycle arrest, apoptosis, and DNA repair in response to DNA damage. | p53 is often called the 'guardian of the genome.' |
| 7 | What is the primary function of DNA repair mechanisms? | DNA repair mechanisms identify and correct DNA damage to maintain genomic integrity and prevent mutations that could lead to diseases like cancer. | Think of DNA repair as the cell's 'quality control' system. |
| 8 | Name the main pathways involved in repairing double-strand DNA breaks. | Homologous recombination (HR) and non-homologous end joining (NHEJ). | HR uses a sister chromatid as a template; NHEJ directly joins broken ends. |
| 9 | Which protein complex detects DNA double-strand breaks and initiates repair signaling? | The MRN complex (MRE11-RAD50-NBS1) detects DSBs and activates ATM kinase. | This complex acts as the cell's 'damage sensor.' |
| 10 | What is the role of ATM kinase in DNA damage response? | ATM phosphorylates several key proteins, including p53 and H2AX, to activate cell cycle arrest and DNA repair pathways following double-strand breaks. | ATM is the 'first responder' to DSBs. |
| 11 | How does the tumor suppressor protein p53 facilitate DNA repair? | p53 induces cell cycle arrest, allowing time for DNA repair, and can initiate apoptosis if the damage is irreparable. | Think of p53 as the cell's 'quality inspector.' |
| 12 | What is the function of the G2/M checkpoint? | It prevents cells with damaged or unreplicated DNA from entering mitosis, ensuring genomic integrity before cell division. | Think of it as a 'security gate' before mitosis. |
| 13 | Which protein kinase is activated at the G2/M checkpoint to promote mitotic entry? | Cyclin B-CDK1 (MPF) is activated when inhibitory phosphorylations are removed in response to checkpoint signals. | Activation of this complex is the 'green light' for mitosis. |
| 14 | What is the role of BRCA1 and BRCA2 in DNA repair? | Both are involved in homologous recombination repair of double-strand breaks; BRCA1 also functions in DNA damage signaling. | Mutations in these genes are linked to breast and ovarian cancers. |
| 15 | What is the consequence of defects in DNA mismatch repair (MMR)? | Defects lead to microsatellite instability and increased mutation rates, contributing to cancers such as Lynch syndrome. | Think of MMR as the 'proofreading' system for DNA replication. |
| 16 | Which enzyme initiates base excision repair (BER)? | DNA glycosylases recognize and remove damaged bases, creating an abasic site. | This is the first step in repairing small, non-helix-distorting base lesions. |
| 17 | What is nucleotide excision repair (NER) primarily responsible for repairing? | It repairs bulky DNA lesions such as thymine dimers caused by UV light. | NER acts as a 'damage removal crew' for bulky lesions. |
| 18 | How does non-homologous end joining (NHEJ) differ from homologous recombination (HR)? | NHEJ directly joins DNA ends without a homologous template, often leading to mutations; HR uses a sister chromatid for error-free repair. | NHEJ is quicker but less accurate than HR. |
| 19 | What role does the protein p21 play in cell cycle regulation after DNA damage? | p21 inhibits cyclin-CDK complexes, causing cell cycle arrest to allow DNA repair. | p21 is a downstream effector of p53. |
| 20 | Name a key difference between apoptosis and necrosis. | Apoptosis is a programmed, orderly cell death involving specific signaling pathways, whereas necrosis is uncontrolled cell death often due to injury, resulting in inflammation. | Think of apoptosis as 'cell suicide' with a plan. |
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