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Title: Control of Arabidopsis meristem development by thioredoxin-dependent regulation of intercellular transport

Author
item BENITEZ-ALFONSO, YOSELIN - Cold Spring Harbor Laboratory
item Heck, Michelle
item SAN ROMAN, ADRIANNA - Cold Spring Harbor Laboratory
item THOMAS, CAROLE - Cold Spring Harbor Laboratory
item MAULE, ANDY - John Innes Center
item HEARN, STEPHEN - Cold Spring Harbor Laboratory
item JACKSON, DAVID - Cold Spring Harbor Laboratory

Submitted to: Proceedings of the National Academy of Sciences (PNAS)
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/7/2009
Publication Date: 3/3/2009
Citation: Benitez-Alfonso, Y., Cilia, M., San Roman, A., Thomas, C., Maule, A., Hearn, S., Jackson, D. 2009. Control of Arabidopsis meristem development by thioredoxin-dependent regulation of intercellular transport. Proceedings of the National Academy of Sciences. 106(9):3615-3620.

Interpretive Summary: The identification of proteins involving protein trafficking in plants is fundamental to understand the biology of virus movement, flowering, meristem development, and senescence. These plant processes can be exploited to enhance agricultural practices that maximize crop yield under a variety of stressful field conditions. The current research was initiated to screen for mutant Arabidopsis plants that exhibited alterations in the movement of proteins. Here we describe GAT1, defective in the gene encoding thioredoxin m3. Thioredoxins function in the redox regulation of a broad spectrum of enzymes. We provide evidence linking the loss of GAT1 with the induction of callose as a possible mechanism for the loss of protein movement out of the phloem. Furthermore, loss of GAT1 induced structural modifications of plasmodesmata, small communication channels that connect plant cells to one another. GAT1 mutants were also defective in both forming and maintaining a shoot meristem. GAT1 regulates plasmodesmal trafficking that is crucial for meristem maintenance in Arabidopsis. Furthermore, the express of GAT1 protein in plant tissues where it is not normally found, such as expanded leaves, we observed that it is sufficient to enhance cell-to-cell transport via plasmodesmata may alter senescence and flowering time. These findings suggest novel lines of research by which thioredoxin-redox pathways may be altered to enhance the accumulation of nutrients in seed and floral organs of commercially important crops.

Technical Abstract: Cell-to-cell transport in plants occurs through cytoplasmic channels called “plasmodesmata” and is regulated by developmental and environmental factors. Callose deposition modulates plasmodesmal transport in vivo, but little is known about the mechanisms that regulate this process. Here we report a genetic approach to identify mutants affecting plasmodesmal transport. We isolated 5 mutants, named gfp arrested trafficking (gat), affected in GFP unloading from the phloem into the meristem. gat1 mutants were seedling lethal and carried lesions in an m-type thioredoxin that is expressed in non-green plastids of meristems and organ primordia. Callose and hydrogen peroxide accumulated in gat1 mutants, and WT plants subjected to oxidative conditions phenocopied the gat1 trafficking defects. Ectopic expression of GAT1 in mature leaves increased plasmodesmal permeability and led to a delay in senescence and flowering time. We propose a role for the GAT1 thioredoxin in the redox regulation of callose deposition and symplastic permeability that is essential for meristem maintenance in Arabidopsis.