Skip to main content
. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: Curr Opin Genet Dev. 2018 Nov 1;51:111–119. doi: 10.1016/j.gde.2018.09.002

Table 1:

Biological control of physical quantities across scales

Physical Quantity
Scale Volumetric Growth Active Forces Material Properties
Global tissue • Spatial inhomogeneities in cell proliferation controlled by gradients in signaling molecules (BMP4, RA, FGF, etc.; see e.g.[5])
• Global tissue mechanical forces affect both orientation (anisotropy) and rate of cell proliferation (see e.g.[58,62]).
• Spatial inhomogeneities in active forces controlled by transcription factors spatial localization (see e.g., {Heer:2017hm, Leptin:1990ub})
• Force anisotropy controlled by planar cell polarity (see e.g., {Zallen:2004wg, Rauzi:2008gz, Wallingford:2000c})
• Unknown signaling control.
Supracellular • Cell proliferation/apopt osis. Cell shape and local forces affect both orientation and rate of cell division (see e.g., [60,61]).
• Extracellular matrix deposition (see e.g.{Kalson:2015ez,Rozario:2010fz}).
• Supracellular actomyosin networks(see e.g. [21,40,41])
• Supracellular forces depend on cell adhesion and the connection of cell cortex and adhesion complexes (e.g. α-catenin) (see e.g. {Mongera:2018wv,Vasquez:2016dy,Lecuit:2015hd,Lecuit:2011ec })
• Collective cell migration[74]
• Supracellular mechanical properties depend on cortical tensions (seee.g.{Heisenberg:2013tla, Lecuit:2007cw, Zhou:2009hz}), cell-cell or cell-matrix adhesion{Mongera:2018 wv, Serwane:2017ht}, extracellular matrix properties and remodeling (via matrix metalloproteinases{Bon nans:2014kn}), cell-cell rearrangements and extracellular spaces{Mongera:2018wv}, etc.{Khalilgharibi:2016c z, Campas:2016gd}.
Cell/subcellular •Molecularregulators of cell growth, shrinkage, proliferation and apoptosis control cell and local tissue growth (see e.g., [43,75,76]). • Acto-myosincontractility (e.g. cortical tension[40,41])
• Osmotic pressure changes (through ion channels[43])
• Actin polymerization, especially during collective migration (e.g. formation of filopodia and lamellipodia[74]).
• Intracellular cytoskeletal structures{Khalilgharibi :2016cz}, especially the cell cortex. Adhesion molecules. Connection of actin cortex to adhesion molecules {Vasquez:2016dy, Lecuit:2015hd}.
• Force generating molecules, especially non-muscle myosin II force generation at the cell cortex[40,41].
• Secretion of extracellular matrix components and matrix metalloproteinases[17,77].