determine the LR asymmetry in morphogenesis. [2] For example, chirality has been found in Xenopus egg cortex before fertilization, [1] and can be passed down to more differentiated cells that establish LR body axis of animal body plan, [7] organ distribution, [8-10] and epithelial movement that leads to axial torsion and overall handedness of hindgut. [11,12] For specialized adult cells derived from somatic tissue, footprints of cell chirality can still be seen by their ability of generating cellular torque, [6,13] migration with LR bias, [14-16] or forming specific alignment in the multicellular level. [15,17,18] Through cell-cell communication, the chiral behavior causes LR-biased cell assembly of multicellular structure [15] and regulates permeability of intercellular junctions. [19] Clearly, cell chirality can be manifested in diverse forms and coordinate different morphogenic dynamics, resulting in distinct forms of tissue and organ architecture. Actin cytoskeleton plays an important role in cell chirality. When cultured on micropatterned substrate, the accumulation of actomyosin stress fibers at micropattern boundary is essential to activate the LR bias in cell migration and orientation. [15,17] Molecular studies suggest helical motion of actin filament as the underlying mechanism for the chirality at cellular level. [20,21] Functioning as a built-in machinery, actomyosin cytoskeleton allows chiral nucleus rotation of single cell [21] and generation of cellular torque with rotational bias. [13] Through a series of amplification process, the actin chirality ultimately determines the symmetry breaking in early embryonic development, [1,7,22] cardiac looping, [4,8,23] and organ laterality [9] in vivo. To give rise to such diverse forms of cell chirality, cell differentiation should play a role. [13,15,17] Cell differentiation is a process coupling with chemical [24] and physical factors. [25-27] Based on variation of key proteins in cytoskeleton, [28] cytoskeleton can be changed at early stage of cell differentiation, as shown by upregulation of cytoskeletal contractility [29] and cell morphological features, which can even forecast the cell lineage fate. [28] It suggests that cytoskeletal components, particularly actin, may early respond to the induction of cell differentiation and then actively participate the signal cascades to engage cell fate. Evidences can be found by regulation of cell differentiation via changed cell shape and cell spreading by physical cues [30-38]
