Sine oculis, a member of the SIX family of transcription factors, directs eye formation.
The initiation of eye formation in all seeing animals is controlled by a group of selector genes that together forms the retinal determination cascade. In Drosophila, mice and humans, loss-of-function mutations lead to defects in eye and/or head development. While ectopic expression of these genes is sufficient to direct non-retinal tissues towards an eye fate, the ability of each gene to initiate eye formation is neither unlimited nor equal. A particularly enigmatic observation has been that one member of the cascade, sine oculis (so), which is a member of the SIX family of homeobox transcription factors, is unable to initiate eye development in non-retinal tissues. It is in contrast to every other retinal determination gene including optix, another Six family member, which can induce eye formation when expressed on its own. Here we demonstrate that, in contrast to published reports, expression of so on its own is sufficient to induce eye development within non-retinal tissues. We have extended results from prior reports on binding partner selectivity and DNA binding sites by conducting a structure/function analysis of the SO and OPTIX proteins. Here we demonstrate that the SIX domains and C-terminal portions of the SO and OPTIX proteins are required for functional specificity of SIX class transcription factors while the homeodomain of these proteins are interchangeable. Taken together, these results shed new light on the role that so plays in eye specification.
Weasner
Brandon
B
Department of Biology, Indiana University, 1001 E. 3rd Street, Bloomington, IN 47405, USA.
Salzer
Claire
C
Kumar
Justin P
JP
D000595:Amino Acid Sequence; D000818:Animals; D030801:Animals, Genetically Modified; D004330:Drosophila / Q000235:genetics / Q000254:growth & development* / Q000378:metabolism*; D029721:Drosophila Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D005123:Eye / Q000254:growth & development* / Q000378:metabolism*; D005124:Eye Abnormalities / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D005136:Eye Proteins / Q000235:genetics / Q000378:metabolism*; D017353:Gene Deletion; D018507:Gene Expression Regulation, Developmental; D017344:Genes, Insect; D018398:Homeodomain Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D008855:Microscopy, Electron, Scanning; D008954:Models, Biological; D008969:Molecular Sequence Data; D050506:Mutant Chimeric Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D009154:Mutation; D010641:Phenotype; D012160:Retina / Q000254:growth & development / Q000378:metabolism; D017386:Sequence Homology, Amino Acid; D014157:Transcription Factors / Q000737:chemistry / Q000235:genetics / Q000378:metabolism
D029721:Drosophila Proteins; D005136:Eye Proteins; D018398:Homeodomain Proteins; D050506:Mutant Chimeric Proteins; C409102:Optix protein, Drosophila; C087345:So protein, Drosophila; D014157:Transcription Factors