Actin-myosin contraction has been shown to play a major role in early morphogenetic movements in Drosophila (fly) and Xenopus (frog) [1,2]. However, the specific role of actomyosin contractility in amniote embryos (reptiles, birds, and mammals) during primitive streak (PS) formation, the "organizing center" for gastrulation (formation of three primary germ layers), is not known. Current theories regarding primitive streak formation in higher order amniotes center around cell-cell intercalation or chemotactic cell movement [3, 4]. We hypothesize that contraction via actin-myosin (AM) filaments is conserved from anamniotes and drives formation of the PS and the associated morphogenetic cell movements. To test this hypothesis, we use particle image velocimetry (PIV) analysis of fluorescently-labeled epiblast cells in conjunction with time-lapse microscopy and cell tracking to observe the real-time motions of cells forming the PS. To study the role of actomyosin contractile forces on PS formation, we used drugs that specifically inhibit phosphorylation of nonmuscle myosin regulatory light chain (MRLC) or actin-myosin interaction.
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