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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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In vivo analysis of the helix-turn-helix motif of the fushi tarazu homeo domain of Drosophila melanogaster.

We report a systematic mutational analysis of the helix-turn-helix motif (HTH) of the fushi tarazu (ftz) homeo domain (HD) of Drosophila. We started out by testing the function of chimeric ftz proteins containing either a part of the Sex combs reduced (Scr) or the muscle segment homeobox ( msh) HDs. By complementation tests in transgenic flies, cotransfection assays in cultured Drosophila cells and in vitro DNA-binding assays, we have found that the ftz activity is retained in the ftz-Scr chimera but is lost in the ftz- msh chimera, which is defective in binding to an Antennapedia (Antp)-class target site. Further studies with a series of back-mutants of the ftz- msh chimera have revealed that a set of class-specific DNA backbone-contacting residues in the HTH, particularly Arg-28 and Arg-43, are required for efficient target site recognition and, hence, full ftz activity both in vitro and in vivo.[1]

References

  1. In vivo analysis of the helix-turn-helix motif of the fushi tarazu homeo domain of Drosophila melanogaster. Furukubo-Tokunaga, K., Müller, M., Affolter, M., Pick, L., Kloter, U., Gehring, W.J. Genes Dev. (1992) [Pubmed]
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