英国伦敦大学学院Roberto Mayor团队发现，神经嵴诱导能力受静水压力控制。该项研究成果于2024年3月18日在线发表在《自然—细胞生物学》杂志上。

研究人员揭示了静水压在控制神经嵴细胞（一种胚胎细胞群）能力中的作用。研究人员发现，神经嵴的能力会随着胚泡静水压的增加而降低，胚泡静水压是与未来神经嵴接触的胚胎腔。通过在体内操纵静水压，研究人员发现静水压的增加会抑制Yap信号的传递，并影响反应组织中Wnt的激活，而这正是神经嵴诱导所需的。研究人员进一步表明，静水压控制着两栖动物和小鼠胚胎以及人类细胞中的神经嵴诱导，这表明在脊椎动物中存在一种保守的机制。这项研究揭示了组织力学如何与信号通路相互作用来调节胚胎能力。

研究人员表示，胚胎诱导是发育过程中的一种关键机制，相当于信号与反应组织之间的相互作用，导致反应组织的分化方向发生改变。在识别诱导信号方面已经取得了相当大的进展，但人们对组织如何控制其对这些信号的反应能力（即能力）仍然知之甚少。虽然分子信号在能力中的作用已得到研究，但组织力学如何影响能力仍未得到探讨。

附：英文原文

Title: Competence for neural crest induction is controlled by hydrostatic pressure through Yap

Author: Alasaadi, Delan N., Alvizi, Lucas, Hartmann, Jonas, Stillman, Namid, Moghe, Prachiti, Hiiragi, Takashi, Mayor, Roberto

Issue&Volume: 2024-03-18

Abstract: Embryonic induction is a key mechanism in development that corresponds to an interaction between a signalling and a responding tissue, causing a change in the direction of differentiation by the responding tissue. Considerable progress has been achieved in identifying inductive signals, yet how tissues control their responsiveness to these signals, known as competence, remains poorly understood. While the role of molecular signals in competence has been studied, how tissue mechanics influence competence remains unexplored. Here we investigate the role of hydrostatic pressure in controlling competence in neural crest cells, an embryonic cell population. We show that neural crest competence decreases concomitantly with an increase in the hydrostatic pressure of the blastocoel, an embryonic cavity in contact with the prospective neural crest. By manipulating hydrostatic pressure in vivo, we show that this increase leads to the inhibition of Yap signalling and impairs Wnt activation in the responding tissue, which would be required for neural crest induction. We further show that hydrostatic pressure controls neural crest induction in amphibian and mouse embryos and in human cells, suggesting a conserved mechanism across vertebrates. Our work sets out how tissue mechanics can interplay with signalling pathways to regulate embryonic competence.

DOI: 10.1038/s41556-024-01378-y

Source: https://www.nature.com/articles/s41556-024-01378-y