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#calcium

8 public questions tagged with this topic.

Sea urchin -lll

Ca²⁺ ions during fertilization are sourced from:

Fertilization calcium transient releases calcium principally from intracellular stores rather than influx from seawater, despite high external concentration. Experiments in calcium-free seawater confirm wave persists. Storage organelle is endoplasmic reticulum, particularly cortical ER clustered beneath plasma membrane studded with IP3 receptors and ryanodine receptors. IP3 generated at sperm entry diffuses to ER opening channels via calcium-induced calcium release amplifying wave globally. Mitochondria and nucleus contain calcium but not primary sources. ER sequestration via SERCA pumps reloads stores after activation, preparing embryo for subsequent mitotic calcium transients regulating cell cycle resumption and activation.

Ref: NCBI Bookshelf, Fertilization, Chapter: Calcium released from ER during sea urchin fertilization wave.

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Fertilization in mammals-iv

Essential ions for compaction:

Compaction transforms loosely adherent eight-cell mammalian morula into tightly apposed epithelium-like structure, prerequisite for blastocyst formation. Process depends critically on extracellular calcium enabling homophilic interaction of E-cadherin (uvomorulin) between blastomeres. Calcium stabilizes cadherin extracellular domains, allowing adherens junction formation and recruitment of catenins and actin cytoskeleton. This strengthens intercellular adhesion, induces cell polarization, peripheral microvilli loss and basolateral sealing. Chelation of calcium with EGTA reverses compaction, demonstrating calcium-cadherin-catenin axis indispensability for morula polarization and subsequent lineage specification via Hippo pathway.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Morula compaction - E-cadherin, calcium dependence and Hippo signaling polarization.

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Cytoskeleton

The interaction between myosin and actin filaments is regulated by:

Coordinated muscle contraction depends on interplay between chemical fuel and regulatory ion signals ensuring contraction only when needed. ATP provides both detach signal and energy currency: ATP binding to myosin head after power stroke dissociates rigor cross bridge, while its hydrolysis to ADP Pi stores elastic energy in lever arm for next stroke, and Pi plus ADP release execute mechanical work. Without ATP muscle enters rigor state as observed in cadaveric stiffness. Calcium provides temporal switch: at rest sarcoplasmic reticulum SERCA maintains cytosolic calcium about 100 nM insufficient for troponin C binding keeping tropomyosin blocked and myosin light chain kinase inactive. In striated excitation opens ryanodine receptors raising calcium tenfold unlocking thin filament. In smooth calcium calmodulin activates myosin light chain kinase phosphorylating regulatory light chains increasing actin activated ATPase. Dynein is microtubule minus end motor unrelated to actin myosin regulation. Hence availability of ATP determines whether cycles can turn while calcium determines whether they are permitted to start linking excitation to contraction.

Ref: Gordon et al., Physiol Rev 2000; Alberts Chapter 16 – Regulation of actin-myosin by ATP and Ca2+ availability.

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