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Two molecular models of initial left-right asymmetry generation
1Cell Biology Department, Harvard Medical School, Boston, MA 02115, USA. mlevin@husc.harvard.edu
Medical Hypotheses
|January 9, 1998
Summary
Two models propose how left-right asymmetry arises in embryos. Motor protein dynein may localize cellular determinants, while connexin-43 (Cx43) gap junctions could establish electrical potentials for large-scale patterning.
Area of Science:
- Developmental Biology
- Cell Biology
- Biophysics
Background:
- Left-right (LR) asymmetry is crucial for vertebrate embryonic development.
- The molecular mechanisms establishing initial LR asymmetry remain largely unknown.
- Genes involved in LR patterning have been identified, but their upstream regulation is unclear.
Purpose of the Study:
- To propose novel molecular models for the origin of LR asymmetry.
- To investigate the potential roles of dynein and connexin-43 (Cx43) in establishing LR patterning.
- To provide a framework for future experimental validation.
Main Methods:
- Theoretical modeling based on existing biological findings.
- Hypothesizing the function of motor protein dynein in intracellular LR determinant localization.
- Proposing the role of connexin-43 (Cx43) gap junctions in generating intercellular electrical potentials.
Main Results:
- Model (a) suggests dynein-mediated asymmetric localization of LR determinants within cells, creating cell-autonomous bias.
- Model (b) posits that asymmetric Cx43 gap junction activity generates electrical fields in multicellular tissues, driving large-scale LR asymmetry.
- Both models are supported by previous experimental observations.
Conclusions:
- Dynein and Cx43 are presented as key molecular players in initiating LR asymmetry.
- Asymmetric intracellular localization and asymmetric intercellular signaling via electrical potentials are proposed as fundamental mechanisms.
- These models offer testable hypotheses for understanding the origins of LR asymmetry in development.
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