“…Mediolateral cell intercalation is, in turn, driven by bipolar, mediolaterally directed protrusive activity and cell‐on‐cell traction (Domingo & Keller, 1995; Keller et al., 2000; Keller & Sutherland, 2020; Shih & Keller, 1992a, 1992b). This cell polarity is affected by many factors, including molecules in the noncanonical Wnt/planar cell polarity (PCP) pathway, the small GTPases and related molecules (Choi & Han, 2002; Goto et al., 2005; Goto & Keller, 2002; Kim & Han, 2005; Popov et al., 2018), molecular signaling and structural effects of fibrils of extracellular matrices (Davidson et al., 2008; Goto et al., 2005; Skoglund & Keller, 2007), the dependence of PCP signaling on fibronectin–integrin signaling (Davidson et al., 2006), chemokine molecules (Goto & Asashima, 2011; Goto et al., 2013, 2018), and cytoskeletal molecules (Bonacci et al., 2012; Pfister et al., 2016; Rolo et al., 2009; Skoglund et al., 2008). When CE movements were inhibited by loss of cell polarity, embryos had very short axes and widely opened neural folds (Goto & Asashima, 2011; Goto & Keller, 2002).…”