AP Biology 细胞周期 — AP 生物学

1. 细胞周期的核心定义和阶段 ★★☆☆☆ ⏱ 4 min

细胞周期是真核体细胞经历的有序、受调控的生长、DNA复制和分裂序列，用于产生基因相同的子细胞。它约占AP生物学第4单元内容的三分之一，占AP考试总分的10-15%，经常出现在选择题和自由作答题部分。

1. **G1（第一间隙期）**：细胞生长，合成复制机制，通过G1检查点；若未接收到分裂信号则退出进入G0期。G0可以是暂时的（肝细胞），也可以是永久的（神经元、骨骼肌细胞）。
2. **S（合成期）**：所有核DNA完成复制；每条染色体现在有两个连接在同一个着丝粒上的相同姐妹染色单体。
3. **G2（第二间隙期）**：细胞继续生长，合成有丝分裂所需机制，通过G2检查点，确认DNA复制无错误。
4. **有丝分裂（M）期**：包括有丝分裂（核分离）和胞质分裂（细胞质分裂），产生两个子细胞。

Exam tip: 如果考试问题要求染色体数而非DNA含量，请记住着丝粒的数量（不是染色单体）决定染色体数，因此S期后染色体数不会改变。

2. 细胞周期检查点和调控 ★★★☆☆ ⏱ 5 min

细胞周期检查点是调控控制点，细胞在此处暂停进程，直到条件有利于继续进行。三个主要检查点控制细胞周期进程：

• **G1（限制点）检查点**：G1末期，在进入S期前检查细胞大小足够、营养充足、有生长信号、DNA未受损。
• **G2检查点**：G2末期，在进入M期前确认所有DNA已完全准确复制。
• **纺锤体（M）检查点**：中期末期，在进入后期前检查所有染色体动粒都正确连接到纺锤体微管。

Regulation of checkpoints relies on two key protein groups: *cyclins* (regulatory proteins whose concentration oscillates throughout the cell cycle) and *cyclin-dependent kinases (CDKs)* (protein kinases that are always present in the cell in an inactive form). CDKs only become active when bound to a specific cyclin, and active cyclin-CDK complexes phosphorylate target proteins to push the cell through the checkpoint.

Exam tip: AP自由作答题几乎总是要求你解释细胞周期蛋白浓度与MPF活性的关系图——一定要明确说明CDK浓度是恒定的，只有细胞周期蛋白浓度周期性变化，因此活性依赖于细胞周期蛋白结合。

3. 细胞周期调控异常与癌症 ★★★☆☆ ⏱ 4 min

Cancer is defined as uncontrolled cell division caused by mutations that disrupt cell cycle regulation. For cancer to develop, mutations typically disrupt two classes of cell cycle regulatory genes:

• **Proto-oncogenes**: Normal genes that code for proteins that stimulate cell division (e.g., growth factor receptors, cyclins). A gain-of-function mutation converts a proto-oncogene to an oncogene, causing constant, excessive stimulation of cell division even without growth signals. Only one mutated copy is needed for this effect.
• **Tumor suppressor genes**: Normal genes that code for proteins that inhibit cell division, repair DNA errors, or trigger apoptosis (programmed cell death) for damaged cells (e.g., p53, Rb, BRCA1). Loss-of-function mutations that inactivate both copies of the gene remove the "brake" on cell division, allowing damaged cells to continue dividing and accumulate more mutations.

Normal cells follow density-dependent inhibition (stop dividing when they form a single layer) and anchorage dependence (must attach to a substrate to divide), while cancer cells ignore both rules.

Exam tip: Always remember the difference between mutation types: gain-of-function for proto-oncogenes/oncogenes (one mutation is enough) vs loss-of-function for tumor suppressors (two hits required). AP exam writers love to test this distinction.

4. AP-Style Practice Problem: Flow Cytometry Calculation ★★★★☆ ⏱ 5 min