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Role of TRIPTYCHON in trichome patterning in Arabidopsis
BACKGROUND: Trichome patterning in Arabidopsis thaliana is governed by three types of activators, R2R3MYB, bHLH and WD40 proteins, and six R3MYB inhibitors. Among the inhibitors TRIPTYCHON (TRY) seems to fulfill a special function. Its corresponding mutants produce trichome clusters whereas all othe...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3196707/ https://www.ncbi.nlm.nih.gov/pubmed/21951724 http://dx.doi.org/10.1186/1471-2229-11-130 |
Sumario: | BACKGROUND: Trichome patterning in Arabidopsis thaliana is governed by three types of activators, R2R3MYB, bHLH and WD40 proteins, and six R3MYB inhibitors. Among the inhibitors TRIPTYCHON (TRY) seems to fulfill a special function. Its corresponding mutants produce trichome clusters whereas all other inhibitors are involved in trichome density regulation. RESULTS: To better understand the role of TRY in trichome patterning we analyzed its transcriptional regulation. A promoter analysis identified the relevant regulatory region for trichome patterning. This essential region contains a fragment required for a double negative feedback loop such that it mediates the repression of TRY/CPC auto-repression. By transforming single cells of pTRY:GUS lines with p35S:GL1, p35S:GL3 and p35S:TTG1 in the presence or absence of p35S:TRY or p35S:CPC we demonstrate that TRY and CPC can suppress the TRY expression without the transcriptional down regulation of the activators. We further show by promoter/CDS swapping experiments for the R3MYB inhibitors TRY and CPC that the TRY protein has specific properties relevant in the context of both, cluster formation and trichome density. CONCLUSIONS: Our identification of a TRY promoter fragment mediating a double negative feedback loop reveals new insight in the regulatory network of the trichome patterning machinery. In addition we show that the auto-repression by TRY can occur without a transcriptional down regulation of the activators, suggesting that the differential complex formation model has a biological significance. Finally we show that the unique role of TRY among the inhibitors is a property of the TRY protein. |
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