Abstract

Planar cell polarity (PCP) controls convergent extension and axis elongation in all vertebrates. Although asymmetric localization of PCP proteins is central to their function, we understand little about PCP protein localization during convergent extension. Here, we use quantitative live imaging to simultaneously monitor cell intercalation behaviors and PCP protein dynamics in the Xenopus laevis neural plate epithelium. We observed asymmetric enrichment of PCP proteins, but more interestingly, we observed tight correlation of PCP protein enrichment with actomyosin-driven contractile behavior of cell-cell junctions. Moreover, we found that the turnover rates of junctional PCP proteins also correlated with the contractile behavior of individual junctions. All these dynamic relationships were disrupted when PCP signaling was manipulated. Together, these results provide a dynamic and quantitative view of PCP protein localization during convergent extension and suggest a complex and intimate link between the dynamic localization of core PCP proteins, actomyosin assembly, and polarized junction shrinking during cell intercalation in the closing vertebrate neural tube.

Highlights

  • Convergent extension (CE) is the evolutionarily conserved morphogenetic engine that drives elongation of the body axis in animals ranging from insects to mammals (Tada and Heisenberg, 2012)

  • Multiple cell behaviors can contribute to CE, but by far the most well-understood process is cell intercalation, by which cells rearrange in a polarized manner (Walck-Shannon and Hardin, 2014)

  • Our studies reveal an intimate link between the dynamic localization of core Planar cell polarity (PCP) proteins, actomyosin assembly, and polarized junction shrinking during cell intercalation of the closing vertebrate neural tube

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Summary

Introduction

Convergent extension (CE) is the evolutionarily conserved morphogenetic engine that drives elongation of the body axis in animals ranging from insects to mammals (Tada and Heisenberg, 2012). The junction shrinking mechanism for cell intercalation was initially described in Drosophila (Bertet et al, 2004; Blankenship et al, 2006) and was subsequently identified in both epithelial and mesenchymal cells in vertebrates (Lienkamp et al, 2012; Nishimura et al, 2012; Shindo and Wallingford, 2014; Trichas et al, 2012; Williams et al, 2014).

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