אסיף מאגר המחקר החקלאי

Interplay of MYB factors in differential cell expansion, and consequences for tomato fruit development

Year:

2011

Source of publication :

Authors :

Volume :

68

Co-Authors:

MacHemer, K., Plant Biotechnology Center, Department of Molecular Genetics, Ohio State University, Columbus, OH 43210, United States
Shaiman, O., Institute of Plant Sciences, Agricultural Research Organization, Volcani Center, PO Box 6, Bet-Dagan 50250, Israel
Salts, Y., Institute of Plant Sciences, Agricultural Research Organization, Volcani Center, PO Box 6, Bet-Dagan 50250, Israel
Shabtai, S., Institute of Plant Sciences, Agricultural Research Organization, Volcani Center, PO Box 6, Bet-Dagan 50250, Israel
Sobolev, I., Institute of Plant Sciences, Agricultural Research Organization, Volcani Center, PO Box 6, Bet-Dagan 50250, Israel
Belausov, E., Institute of Plant Sciences, Agricultural Research Organization, Volcani Center, PO Box 6, Bet-Dagan 50250, Israel
Grotewold, E., Plant Biotechnology Center, Department of Molecular Genetics, Ohio State University, Columbus, OH 43210, United States
Barg, R., Institute of Plant Sciences, Agricultural Research Organization, Volcani Center, PO Box 6, Bet-Dagan 50250, Israel

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Abstract:

We previously identified SlFSM1 as an early fruit-specific gene encoding a short protein harboring a non-canonical SANT/MYB-like domain. Here, we investigated the role of FSM1 during fruit development in tomato and its mode of action. By analyzing tomato plants ectopically expressing FSM1, we established that it negatively affects cell expansion, particularly of those cells with the highest potential to expand, such as those residing inner to the vascular bundles in the fruit pericarp. This function of FSM1 differs from that of the snapdragon FSM1-like gene, RAD, which through an antagonistic activity with DIV participates in establishing floral asymmetry. Revealing an additional component of the FSM1/RAD regulatory complex, we show here that FSM1 physically interacts with FSB1, a previously uncharacterized factor harboring an atypical MYB repeat. We also demonstrate that FSB1 physically interacts with the transcription factor MYBI, a homolog of DIV. Our results show that the formation of the FSB1-MYBI complex is competed by FSM1, which recognizes in FSB1 the same region as MYBI does. Taken together, these studies expose a function for the FSM1/FSB1/MYBI complex in controlling tomato cell expansion, while revealing a mechanism by which competing MYB-MYB interactions could participate in the control of gene expression. © 2011 Blackwell Publishing Ltd.

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