Yuhang Guo

Contemporary scholars often separate the instrumental rationality embodied in biosemiotic systems from practical rationality, adopting deontological and virtue-ethical frameworks as the normative basis for biosemiotic ethics. However, strong accountability models fail to recognize the ethical dimensions of non-human semiotic processes, while weak accountability models struggle to address genuine ecological responsibility and meaning generation. Without confronting the inherited techno-linguistic hegemonies embedded in human history, it is difficult to envision a shared good life oriented toward living beings. This article contends that a utilitarian semiotics—defined by the genuine circulation of meaning and grounded in the material and institutional substrates of semiotic regulation—ought to serve as a central framework for moral evaluation. Its framework does not presuppose consciousness or intention, but is manifested in the historical adaptability of semiotic behavior, the physiological basis of perceptual conflicts, and the multi-level response-feedback mechanisms among living systems.

© 2015 Macmillan Publishers Limited. Matrix stiffness potently regulates cellular behaviour in various biological contexts. In breast tumours, the presence of dense clusters of collagen fibrils indicates increased matrix stiffness and correlates with poor survival. It is unclear how mechanical inputs are transduced into transcriptional outputs to drive tumour progression. Here we report that TWIST1 is an essential mechanomediator that promotes epithelial-mesenchymal transition in response to increasing matrix stiffness. High matrix stiffness promotes nuclear translocation of TWIST1 by releasing TWIST1 from its cytoplasmic binding partner G3BP2. Loss of G3BP2 leads to constitutive TWIST1 nuclear localization and synergizes with increasing matrix stiffness to induce EMT and promote tumour invasion and metastasis. In human breast tumours, collagen fibre alignment, a marker of increasing matrix stiffness, and reduced expression of G3BP2 together predict poor survival. Our findings reveal a TWIST1-G3BP2 mechanotransduction pathway that responds to biomechanical signals from the tumour microenvironment to drive EMT, invasion and metastasis.