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. 2013 Oct 1;140(19):4102–4109. doi: 10.1242/dev.096933

Fig. 1.

Fig. 1.

Knockdown of Sdc2 in zebrafish KV causes laterality defects. (A,B) Heart looping is visualized by labeling the heart with an RNA in situ hybridization probe for cardiac myosin light chain 2 (cmlc2) at 40 hpf. (A) Normal heart looping. (B) Reversed heart looping. (C) Both SB and AUG sdc2 morphants had a statistically significant increase in reversed heart looping (SB1 MO: 32%, n=221; AUG MO: 24%, n=369) compared with wild-type (WT) embryos (3%, n=500), *P<0.001. Error bars indicate s.e.m. (D) Examples of morphant embryos at the 18-somite stage displaying left-sided, right-sided, bilateral and absent spaw expression. Somites are labeled with myod1 which is used as a marker for staging embryo development. (E) Expression of Nodal family member spaw is mostly left-sided in wild-type embryos (n=331) but in global sdc2 morphants spaw expression is randomized (SB1 MO, n=215; SB2 MO, n=229; AUG MO, n=190; all P<0.001). Aberrant spaw expression is partially rescued with co-injection of a MO-resistant sdc2 mRNA (n=123; P<0.001 compared with morphants). Targeting MO to the DFCs (DFCsdc2MO embryos, n=147) randomized spaw expression, but targeting MO exclusively to the yolk cell did not (yolksdc2MO embryos, n=181; P<0.001 compared with global and DFC morphants). These results indicate that the role of Sdc2 in LR development is cell-autonomous within the DFCs and that extra-embryonic Sdc2 is not involved in LR development. P-values by Student’s t-test.