. 1997 Feb 18;94(4):1194–1199. doi: 10.1073/pnas.94.4.1194

Table 1.

Summary of experimental observations concerning calcium and mitosis

The case for calcium involvement

1. [Ca²⁺]_i oscillates in sinusoidal manner in Xenopus embryos at division frequency (5–7).

2. [Ca²⁺]_i spikes at mitosis entry and mitosis exit in sea urchin embryos (2, 3, 12).

3. [Ca²⁺]_i signals persist in absence of division in both Xenopus and sea urchin embryos (3, 5, 6).

4. Elevated [Ca²⁺]_i induces nuclear envelope breakdown (mitosis start), presumably through activation of MPF (12, 13).

4′. [Ca²⁺]_i may activate MPF through Cdc25 (14).

5. A [Ca²⁺]_i signal is necessary to induce nuclear envelope breakdown, but it is effective only after sufficient protein synthesis (13).

6. Elevated [Ca²⁺]_i induces cyclin destruction (mitosis exit), presumably through deactivation of MPF (11, 15, 16, 28).

6′. [Ca²⁺]_i deactivates MPF through the ubiquitin-dependent proteolysis pathway (15).

7. BAPTA calcium buffers delay division in intact Xenopus blastomeres (8).

8. High-concentration calcium buffer injections block division cycles (8, 12, 13).

The case that MPF oscillations are independent of calcium

9. Addition of exogenous cyclin mRNA produces multiple cell cycles in Xenopus extracts (9).

10. Division cycles in clam embryo homogenates are not affected by injection of calcium buffers or CaCl₂ (11).