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RETINOBLASTOMA-RELATED Protein Stimulates Cell Differentiation in theArabidopsisRoot Meristem by Interacting with Cytokinin Signaling
Author(s) -
Serena Perilli,
José Manuel PérezPérez,
Riccardo Di Mambro,
Cristina Llavata Peris,
Sara Diaz Trivino,
Marta Del Bianco,
Emanuela Pierdonati,
Laila Moubayidin,
Alfredo CruzRamírez,
Paolo Costantino,
Ben Scheres,
Sabrina Sabatini
Publication year - 2013
Publication title -
the plant cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.324
H-Index - 341
eISSN - 1532-298X
pISSN - 1040-4651
DOI - 10.1105/tpc.113.116632
Subject(s) - meristem , biology , arabidopsis , transcription factor , microbiology and biotechnology , cellular differentiation , cell division , cytokinin , auxin , retinoblastoma protein , cell fate determination , cell growth , arabidopsis thaliana , retinoblastoma , mitosis , cell , cell cycle , genetics , gene , mutant
Maintenance of mitotic cell clusters such as meristematic cells depends on their capacity to maintain the balance between cell division and cell differentiation necessary to control organ growth. In the Arabidopsis thaliana root meristem, the antagonistic interaction of two hormones, auxin and cytokinin, regulates this balance by positioning the transition zone, where mitotically active cells lose their capacity to divide and initiate their differentiation programs. In animals, a major regulator of both cell division and cell differentiation is the tumor suppressor protein RETINOBLASTOMA. Here, we show that similarly to its homolog in animal systems, the plant RETINOBLASTOMA-RELATED (RBR) protein regulates the differentiation of meristematic cells at the transition zone by allowing mRNA accumulation of AUXIN RESPONSE FACTOR19 (ARF19), a transcription factor involved in cell differentiation. We show that both RBR and the cytokinin-dependent transcription factor ARABIDOPSIS RESPONSE REGULATOR12 are required to activate the transcription of ARF19, which is involved in promoting cell differentiation and thus root growth.

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