Fig. 6. The proposed interactions among different signaling molecules involved in the lateralization of the left LPM in the chick. Unilateral Shh induces left-sided expression domains of Nodal and Car adjacent to Hensen’s node (Levin et al., 1995; Rodriguez-Esteban et al., 2001). Car probably allows the spread of Nodal to the lateral plate. BMP2, which is present in mesendoderm at stage 4 and in pharyngeal endoderm beginning at HH stage 5 (Andrée et al., 1998) maintains the expression of Cfc and ActrIIa. Both genes provide competence to respond to the incoming Nodal signal. Nodal upregulates Pitx2 and Nkx3.2 (Liu et al., 2001; Logan et al., 1998; Schneider et al., 1999). Expression of Pitx2 at least in mice is maintained by the homeobox gene Nkx2.5 (Shiratori et al., 2001). Expression of Nkx2.5 in the mesoderm is dependent on BMP2 signals and thus, BMP2 ochestrates competence for long-range Nodal signals and maintenance of Pitx2 expression. Expression of Lefty in the midline is dependent on CFC (Schlange et al., 2001) and Shh (Tsukui et al., 1999). Ectopic BMP interferes with Lefty expression probably by downregulating Shh expression. The main function of Lefty is probably to prevent Nodal signals from spreading to the right side. On the right side, FGF8 controls the expression of Snr (Boettger et al., 1999). The proposed function of Snr is to prevent expression of Nodal and Pitx2 on the right side (Patel et al., 1999).