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Background  Through  in vivo  loss-of-function studies, vertebrate members of the Male abnormal 21 (mab-21) gene family have been implicated in gastrulation, neural tube formation and eye morphogenesis. Despite mounting evidence of their considerable importance in development, the biochemical properties and nature of MAB-21 proteins have remained strikingly elusive. In addition, genetic studies conducted in  C. elegans  have established that in double mutants  mab-21  is epistatic to genes encoding various members of a Transforming Growth Factor beta (TGF-beta) signaling pathway involved in the formation of male-specific sensory organs.    Results  Through a gain-of-function approach, we analyze the interaction of  Mab21l2  with a TGF-beta signaling pathway in early vertebrate development. We show that the vertebrate  mab-21  homolog  Mab21l2  antagonizes the effects of  Bone Morphogenetic Protein 4  ( BMP4 ) overexpression  in vivo , rescuing the dorsal axis and restoring wild-type distribution of  Chordin  and  Xvent2  transcripts in  Xenopus  gastrulae. We show that MAB21L2 immunoprecipitates  in vivo  with the BMP4 effector SMAD1, whilst  in vitro  it binds SMAD1 and the SMAD1-SMAD4 complex. Finally, when targeted to an heterologous promoter, MAB21L2 acts as a transcriptional repressor.    Conclusions  Our results provide the first biochemical and cellular foundation for future functional studies of mab-21 genes in normal neural development and its pathological disturbances.

MAB21L2, a vertebrate member of the Male-abnormal 21 family, modulates BMP signaling and interacts with SMAD1.