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Caenorhabditis elegans Embryo: Establishment of Asymmetry

  1. Eugenel B Espiritu,
  2. Lesilee S Rose

Published Online: 15 APR 2013

DOI: 10.1002/9780470015902.a0001506.pub3

eLS

eLS

How to Cite

Espiritu, E. B. and Rose, L. S. 2013. Caenorhabditis elegans Embryo: Establishment of Asymmetry. eLS.

Author Information

  1. University of California, Davis, California, USA

Publication History

  1. Published Online: 15 APR 2013

Abstract

In Caenorhabditis elegans, asymmetry is established in the one-cell embryo in response to the position of the sperm provided centrosome. Asymmetric contraction of actin and myosin at the cortex leads to the localisation of the conserved PAR (partitioning defective) polarity proteins into anterior and posterior cortical domains. The PAR proteins and associated protein kinases generate cytoplasmic gradients of polarity mediators, which in turn regulate the anterior/posterior cytoplasmic localisation of downstream cell fate regulators. The PAR proteins also regulate a conserved G protein pathway that coordinates the division plane with the anterior/posterior axis. Thus, the first division is asymmetric and the daughter cells have different developmental fates. During the next few divisions, anterior/posterior asymmetries and cell–cell signalling events establish the dorsal/ventral and left–right axes of the embryo and further refine cell fates.

Key Concepts:

  • The C. elegans embryo exhibits an invariant pattern of asymmetric cell divisions that generates diverse cell types.

  • Asymmetric divisions are regulated by the conserved PAR proteins, which become localised in anterior and posterior cortical domains during polarity establishment after fertilisation.

  • Polarity establishment occurs in response to an unknown cue associated with the sperm centrosome, which causes an actomyosin cortical flow that localises the anterior PAR proteins.

  • PAR polarity cues create a cytoplasmic gradient of the polarity mediators MEX-5 and MEX-6, which act together with other polarity mediators to generate the asymmetric localisation of cell fate determinants.

  • Asymmetric localisation of cell fate determinants is accomplished mainly through protein degradation and translational regulation.

  • The localisation of cell fate determinants combined with cell–cell signalling events leads to specification of different developmental programmes in cells of the early embryo.

  • A conserved G protein pathway functions with the microtubule motor dynein to position the mitotic spindle on the polarity axis during asymmetric divisions.

Keywords:

  • asymmetric division;
  • polarity;
  • PAR;
  • actomyosin;
  • spindle position;
  • protein degradation;
  • translational control