Past studies have shown that the mechanical environment plays a critical role in regulating tissue development and function. For example, in the embryonic heart abnormal internal pressures cause morphological adaptation leading to aberrant morphogenesis [1]. Similarly, increasing luminal pressure in the early brain results in hyper-proliferation of the neuroepithelium [2]. Less is known, however, about how embryonic precursor cells quantitatively adapt to changes in loading, especially in vivo and across tissue types. These data would be valuable in determining the role of altered mechanical loads in congenital defects.

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