2025/03/16

Molecular key-lock mechanisms behind Biblical kinds

Different Kinds are based on differences between molecular key-lock mechanisms

Extracellular vesicles (EVs) are membrane-bound structures secreted by cells, playing a crucial role in intercellular communication by transferring proteins, lipids, and nucleic acids between cells. The specificity of EV interactions with target cells is largely determined by "key-lock" mechanisms involving surface molecules on both EVs and recipient cells. These mechanisms ensure that EVs deliver their cargo to appropriate cells, maintaining the integrity of species and preventing unintended cross-species interactions.​

1. Compatibility of EV Key-Lock Mechanisms Within a Species Group (a Kind = e.g., Canidae):

Within a species group, or "kind," EVs exhibit compatible key-lock mechanisms that facilitate effective intercellular communication and, in some cases, hybridization. This compatibility is primarily mediated by conserved surface proteins and lipids that enable EVs to recognize and bind to target cells within the same group. Key molecules involved in this process include:​

  • Tetraspanins: These are four-transmembrane proteins abundantly present on EV surfaces. Tetraspanins, such as CD9, CD63, CD81, and CD82, interact with integrins and adhesion receptors, facilitating EV docking and uptake by target cells. The presence of tetraspanin-enriched microdomains (TEMs) on EVs allows for selective binding interactions, contributing to target cell selection within the same species group. ​

  • Integrins: These heterodimeric membrane proteins regulate various biological processes, including cell proliferation, differentiation, and migration. Integrins on EVs interact with corresponding receptors on target cells, mediating cell-EV interactions that are crucial for maintaining species-specific communication. ​

  • Lectins: These are the real key-lock elements. These proteins recognize and bind specific glycan moieties, facilitating cell-to-cell communication. Lectins on EVs can interact with glycan structures on target cells, promoting selective uptake and ensuring compatibility within the species group. ​The conservation and compatibility of these surface molecules within a species group enable EVs to effectively communicate and transfer genetic material, supporting processes like hybridization and intraspecies variation.


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2. Incompatibility of EV Key-Lock Mechanisms Between Different Species Groups:

Between different species groups, EV key-lock mechanisms are incompatible, preventing unintended interspecies communication and maintaining species boundaries. This incompatibility arises from variations in surface molecules that hinder the recognition and binding of EVs to target cells of different species. Factors contributing to this incompatibility include:​

  • Species-Specific Tetraspanins and Integrins: Differences in the expression patterns and structures of tetraspanins and integrins between species can lead to ineffective EV docking and uptake by target cells of another species. This specificity ensures that EV-mediated communication occurs primarily within the same species group. ​

  • Lectin-Glycan Specificity: Lectins exhibit binding specificity to particular glycan structures, which can vary significantly between species. Such specificity restricts EV interactions to target cells within the same species group, as the necessary glycan structures for lectin binding may not be present on cells of different species. ​

These molecular incompatibilities in EV surface molecules act as barriers to interspecies hybridization, preserving the genetic integrity of distinct species groups.​

Conclusion:

The specificity of EV key-lock mechanisms, dictated by surface molecules like tetraspanins, integrins, and lectins, plays a vital role in regulating intercellular communication. Within a species group, the compatibility of these mechanisms facilitates effective communication and hybridization, supporting intraspecies variation. Conversely, incompatibility between different species groups prevents unintended interspecies interactions, thereby maintaining species boundaries and genetic integrity.

In summary, the incompatibility of cellular key-lock mechanisms between different taxa is primarily due to species-specific variations in the molecular structures of tetraspanins, integrins, and lectins. These variations prevent the proper formation of protein complexes and signaling pathways necessary for cellular functions, thereby maintaining species barriers.

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