Cell Biology - Organelle Function, Cell Cycle & Signaling Flashcards

Question 1

Nucleus and Nucleolus

Accepted Answer

The **nucleus** is enclosed by a double-membrane nuclear envelope with nuclear pores; it houses genomic DNA and coordinates gene expression. The **nucleolus** is a dense sub-region within the nucleus dedicated to ribosomal RNA (rRNA) transcription, processing, and ribosome subunit assembly.

Question 2

Mitochondria Structure and Function

Accepted Answer

A double-membrane organelle responsible for ATP generation via oxidative phosphorylation and the Krebs cycle. The outer membrane is permeable to small molecules, while the inner membrane forms foldings called **cristae** (housing the electron transport chain) and encloses the **matrix** (containing mitochondrial DNA and metabolic enzymes).

Question 3

Rough vs. Smooth Endoplasmic Reticulum

Accepted Answer

**Rough ER (RER)**: Studded with ribosomes; synthesizes membrane-bound, lysosomal, and secreted proteins, initiating N-linked glycosylation. **Smooth ER (SER)**: Lacks ribosomes; synthesizes lipids/steroids, metabolizes carbohydrates, detoxifies xenobiotics, and sequesters $Ca^{2+}$ ions.

Question 4

Golgi Apparatus

Accepted Answer

A series of flattened, membrane-bound sacs (cisternae) involved in post-translational modification (e.g., O-linked glycosylation, sulfation), sorting, and packaging of proteins received at the **cis-face** from the RER, and dispatching them via vesicles at the **trans-face**.

Question 5

Lysosomes vs. Peroxisomes

Accepted Answer

**Lysosomes**: Membrane-bound organelles containing acid hydrolases (active at $pH \approx 4.5-5.0$) that digest cellular waste, endocytosed extracellular debris, and damaged organelles (autophagy).
**Peroxisomes**: Contain oxidases that perform $\beta$-oxidation of very long-chain fatty acids (VLCFAs) and catalase to neutralize toxic hydrogen peroxide ($H_2O_2$).

Question 6

Cytoskeleton Components

Accepted Answer

1. **Microfilaments (Actin, ~7 nm)**: Maintain cell shape, form microvilli, drive cell motility, and form the contractile ring during cytokinesis.
2. **Intermediate Filaments (~10 nm)**: Provide tensile strength and structural support (e.g., keratins, lamins, vimentin).
3. **Microtubules (\alpha/\beta-tubulin, ~25 nm)**: Facilitate intracellular transport via motor proteins (dynein/kinesin), form cilia/flagella ($9+2$ structure), and construct the mitotic spindle.

Question 7

Cell Cycle Phases

Accepted Answer

Divided into **Interphase** and **M phase**:
- **$G_1$ Phase**: Rapid growth and metabolic activity; synthesis of organelles.
- **S Phase**: Replication of genomic DNA.
- **$G_2$ Phase**: Protein synthesis required for cell division and organelle check.
- **M Phase**: Mitosis (karyokinesis) and Cytokinesis.
- **$G_0$ Phase**: Quiescent non-dividing state.

Question 8

Major Cell Cycle Checkpoints

Accepted Answer

1. **$G_1/S$ Checkpoint (Restriction Point)**: Evaluates growth factors, cell size, nutrient availability, and DNA damage prior to committing to replication.
2. **$G_2/M$ Checkpoint**: Ensures DNA replication is complete and undamaged before entering mitosis.
3. **Spindle Assembly Checkpoint (SAC/M-Checkpoint)**: Verifies proper bi-orientation and kinetochore attachment of all chromosomes to spindle fibers before anaphase initiation.

Question 9

Cyclins and Cyclin-Dependent Kinases (CDKs)

Accepted Answer

**CDKs** are serine/threonine protein kinases whose activity relies on binding to regulatory **cyclin** proteins. While CDK concentrations remain relatively constant throughout the cell cycle, cyclin concentrations oscillate dramatically due to targeted ubiquitin-proteasome degradation, driving sequential progression through cell cycle phases.

Question 10

Tumor Suppressors: p53 and Retinoblastoma (Rb)

Accepted Answer

- **p53**: Activated by DNA damage; acts as a transcription factor for $p21$ (a CDK inhibitor) to arrest the cell cycle in $G_1/S$, allowing time for repair or triggering apoptosis if damage is unrepairable.
- **Rb**: Unphosphorylated Rb binds and inhibits transcription factor **E2F**, blocking $S$-phase entry. Phosphorylation of Rb by Cyclin D-CDK4/6 releases E2F to express genes required for DNA replication.

Question 11

Stages of Mitosis

Accepted Answer

1. **Prophase**: Chromatin condenses into visible chromosomes; mitotic spindle forms.
2. **Prometaphase**: Nuclear envelope breaks down; kinetochores attach to spindle fibers.
3. **Metaphase**: Chromosomes align along the metaphase plate.
4. **Anaphase**: Sister chromatids are pulled apart to opposite poles by microtubule shortening.
5. **Telophase**: Nuclear envelopes reassemble around separated genomes; chromosomes decondense.

Question 12

G Protein-Coupled Receptor (GPCR) Mechanism

Accepted Answer

GPCRs are 7-transmembrane domain receptors. Ligand binding causes a conformational change in the receptor, inducing the bound heterotrimeric G protein to exchange $GDP$ for $GTP$ on its $G_\alpha$ subunit. The active $G_\alpha-GTP$ dissociates from $G_{\beta\gamma}$ to modulate downstream target enzymes.

Question 13

$G_s$ and $G_i$ Signaling Pathway ($cAMP$ Cascade)

Accepted Answer

- **$G_{\alpha s}$**: Stimulates **Adenylyl Cyclase**, increasing cytosolic $[cAMP]$, which activates **Protein Kinase A (PKA)** to phosphorylate downstream targets.
- **$G_{\alpha i}$**: Inhibits Adenylyl Cyclase, reducing $[cAMP]$.
- Signal termination occurs when **Phosphodiesterase (PDE)** degrades $cAMP$ into $5'-AMP$.

Question 14

$G_q$ Signaling Pathway ($IP_3$ / $DAG$ Cascade)

Accepted Answer

$G_{\alpha q}$ activates **Phospholipase C (PLC)**, which hydrolyzes $PIP_2$ into two second messengers:
1. **$IP_3$**: Binds to receptors on the Smooth ER, triggering the release of intracellular $Ca^{2+}$.
2. **$DAG$**: Remains in the plasma membrane and, along with free $Ca^{2+}$, activates **Protein Kinase C (PKC)**.

Question 15

Receptor Tyrosine Kinases (RTKs)

Accepted Answer

Cell-surface receptors for growth factors (e.g., EGF, Insulin). Signaling involves:
1. Ligand binding inducing receptor **dimerization**.
2. Trans-autophosphorylation of tyrosine residues on the intracellular domains.
3. Recruitment of downstream signaling proteins containing **SH2** or **PTB** domains.

Question 16

Ras-MAPK Signaling Cascade

Accepted Answer

Activated RTKs recruit Grb2/SOS, which acts as a GEF to swap $GDP$ for $GTP$ on monomeric **Ras**. Active **Ras-GTP** triggers a sequential phosphorylation cascade:
$$	ext{Ras-GTP} ightarrow 	ext{Raf (MAPKKK)} ightarrow 	ext{MEK (MAPKK)} ightarrow 	ext{ERK (MAPK)}$$
Phosphorylated ERK translocates to the nucleus to induce transcription of genes driving cellular proliferation.

Question 17

Modes of Intercellular Communication

Accepted Answer

1. **Endocrine**: Hormones travel through the circulatory system to distant target cells.
2. **Paracrine**: Signals diffuse locally through extracellular fluid to nearby target cells.
3. **Autocrine**: Signals bind to receptors on the same cell that secreted them.
4. **Juxtacrine**: Direct contact-dependent signaling via membrane-bound ligands/receptors or gap junctions.

Question 18

Apoptosis vs. Necrosis

Accepted Answer

- **Apoptosis**: Active, ATP-dependent programmed cell death. Features cell shrinkage, chromatin condensation, membrane blebbing, and formation of apoptotic bodies without inducing an inflammatory response.
- **Necrosis**: Passive, unprogrammed cell death resulting from acute injury. Features ATP depletion, cell swelling, loss of membrane integrity, organelle lysis, and release of cytosolic contents that trigger an **inflammatory response**.

Question 19

Intrinsic (Mitochondrial) Apoptotic Pathway

Accepted Answer

Triggered by internal cellular stress or DNA damage. Pro-apoptotic proteins (**Bax/Bak**) permeabilize the outer mitochondrial membrane, releasing **Cytochrome c** into the cytosol. Cytochrome c binds **Apaf-1** and procaspase-9 to form the **apoptosome**, which cleaves and activates initiator **Caspase-9**, activating executioner caspases (Caspase-3/6/7).

Question 20

Extrinsic Apoptotic Pathway

Accepted Answer

Triggered by extracellular death ligands (e.g., FasL, $TNF-\alpha$) binding to transmembrane death receptors (e.g., Fas, TNFR1). Receptor trimerization recruits adapter proteins (such as FADD) to form the **Death-Inducing Signaling Complex (DISC)**, which cleaves and activates initiator **Caspase-8** or **Caspase-10**, leading to executioner caspase activation.

Cell Biology - Organelle Function, Cell Cycle & Signaling

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