The nodal signaling pathway has been shown to play crucial roles in inducing and 
patterning the mesoderm and endoderm, as well as in regulating neurogenesis and 
left-right axis asymmetry. Here, we present the first complete cDNA and genomic 
sequences as well as the promoter predication of the Dnah9 gene in the Japanese 
flounder. The 15,558-bp-long cDNA is divided into 96 exons and spread over 138 
kb of genomic DNA. Protein sequence comparison showed that it shares higher 
identity with other vertebrate orthologs, with an ATP binding dynein motor, AAA 
domain and microtubule binding stalk of dynein motor. Dnah9 exhibited maternal 
and ubiquitous expression in all cells of the early development stages, but 
became concentrated in the head at 1 DAH, as identified by qRT-PCR and in situ 
hybridization methods. Furthermore, after nodal signaling was inhibited, the 
level of Southpaw did not change significantly at early development stage (50 % 
epiboly) but increased significantly at late stages (27-somite stages and 1 
DAH), as well as the expression of Lefty, an inhibitor of nodal signaling, 
increased continuously. On the other hand, the expression level of Dnah9 
decreased. The transcription factor binding site of FAST-1 (SMAD interacting 
protein) was identified in the transcription region of Dnah9 by the promoter 
analysis, which might format the complexes of SMADs, FAST-1 and the 
transcription region of Dnah9 served as a bridge of Dnah9 and nodal signaling. 
All evidences indicated that Dnah9 might be downstream of nodal during the early 
development stages, and an indirect function through SMADs for nodal signaling 
pathway.