4.8 Article

Genetic induction and mechanochemical propagation of a morphogenetic wave

期刊

NATURE
卷 572, 期 7770, 页码 467-+

出版社

NATURE PORTFOLIO
DOI: 10.1038/s41586-019-1492-9

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资金

  1. ERC [323027, 788308]
  2. Human Frontier Science Program Long-Term Fellowship [LT000733/2011-L]
  3. CNRS
  4. LabEx INFORM [ANR-11-LABX-0054]
  5. A*MIDEX project [ANR-11-IDEX-0001-02]
  6. Investissements d'Avenir French government program
  7. NIGMS [1RO1 GM098441-06]
  8. French National Research Agency [ANR-10-INBS-04-01]
  9. European Research Council (ERC) [323027, 788308] Funding Source: European Research Council (ERC)

向作者/读者索取更多资源

Tissue morphogenesis arises from coordinated changes in cell shape driven by actomyosin contractions. Patterns of gene expression regionalize cell behaviours by controlling actomyosin contractility. Here we report two modes of control over Rho1 and myosin II (MyoII) activation in the Drosophila endoderm. First, Rho1-MyoII are induced in a spatially restricted primordium via localized transcription of the G-protein-coupled receptor ligand Fog. Second, a tissue-scale wave of Rho1-MyoII activation and cell invagination progresses anteriorly away from the primordium. The wave does not require sustained gene transcription, and is not governed by regulated Fog delivery. Instead, MyoII inhibition blocks Rho1 activation and propagation, revealing a mechanical feedback driven by MyoII. We find that MyoII activation and invagination in each row of cells drives adhesion to the vitelline membrane mediated by integrins, apical spreading, MyoII activation and invagination in the next row. Endoderm morphogenesis thus emerges from local transcriptional initiation and a mechanically driven cycle of cell deformation.

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