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<p>Shaping embryonic tissues requires spatiotemporal changes in genetic and signaling activity as well as in tissue mechanics. Studies linking specific molecular perturbations to changes in the tissue physical state remain sparse. Here we study how specific genetic perturbations affecting different posterior tissues during zebrafish body axis elongation change their physical state, the resulting large-scale tissue flows, and posterior elongation. Using a custom analysis software to reveal spatiotemporal variations in tissue fluidity, we show that dorsal tissues are most fluid at the posterior end, rigidify anterior of this region, and become more fluid again yet further anteriorly. In the absence of notochord (<i>noto</i> mutants) or when the presomitic mesoderm is substantially reduced (<i>tbx16</i> mutants), dorsal tissues elongate normally. Perturbations of posterior-directed morphogenetic flows in dorsal tissues (<i>vangl2</i> mutants) strongly affect the speed of elongation, highlighting the essential role of dorsal cell flows in delivering the necessary material to elongate the axis.</p>

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The physical roles of different posterior tissues in zebrafish axis elongation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月21日

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  • Georgina A. Stooke-Vaughan,
  • Sangwoo Kim,
  • Shuo-Ting Yen,
  • Kevin Son,
  • Samhita P. Banavar,
  • James Giammona,
  • David Kimelman,
  • Otger Campàs

摘要

Shaping embryonic tissues requires spatiotemporal changes in genetic and signaling activity as well as in tissue mechanics. Studies linking specific molecular perturbations to changes in the tissue physical state remain sparse. Here we study how specific genetic perturbations affecting different posterior tissues during zebrafish body axis elongation change their physical state, the resulting large-scale tissue flows, and posterior elongation. Using a custom analysis software to reveal spatiotemporal variations in tissue fluidity, we show that dorsal tissues are most fluid at the posterior end, rigidify anterior of this region, and become more fluid again yet further anteriorly. In the absence of notochord (noto mutants) or when the presomitic mesoderm is substantially reduced (tbx16 mutants), dorsal tissues elongate normally. Perturbations of posterior-directed morphogenetic flows in dorsal tissues (vangl2 mutants) strongly affect the speed of elongation, highlighting the essential role of dorsal cell flows in delivering the necessary material to elongate the axis.