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First published online September 30, 2009; 10.1105/tpc.109.069104

The Plant Cell 21:2963-2979 (2009)
© 2009 American Society of Plant Biologists

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Actin-Depolymerizing Factor2-Mediated Actin Dynamics Are Essential for Root-Knot Nematode Infection of Arabidopsis[C],[W]

Mathilde Clémenta,1,2, Tijs Ketelaarb,c,2, Natalia Rodiuca,2, Mohamed Youssef Banoraa, Andrei Smertenkoc, Gilbert Englera, Pierre Abada, Patrick J. Husseyc and Janice de Almeida Englera,3

a Unité Mixte de Recherches Interactions Biotiques et Santé Végétale, Institut National de la Recherche Agronomique, Centre National de la Recherche Scientifique, Université de Nice-Sophia Antipolis, F-06903 Sophia Antipolis, France
b Laboratory of Plant Cell Biology, Wageningen University, 6703 BD Wageningen, The Netherlands
c School of Biological and Biomedical Sciences, University of Durham, Durham DH1 3LE, United Kingdom

3 Address correspondence to janice.almeida-engler{at}sophia.inra.fr.

Reorganization of the actin and microtubule networks is known to occur in targeted vascular parenchymal root cells upon infection with the nematode Meloidogyne incognita. Here, we show that actin-depolymerizing factor (ADF) is upregulated in the giant feeding cells of Arabidopsis thaliana that develop upon nematode infection and that knockdown of a specific ADF isotype inhibits nematode proliferation. Analysis of the levels of transcript and the localization of seven ADF genes shows that five are upregulated in galls that result from the infection and that ADF2 expression is particularly increased between 14 and 21 d after nematode inoculation. Further analysis of ADF2 function in inducible RNA interference lines designed to knock down ADF2 expression reveals that this protein is required for normal cell growth and plant development. The net effect of decreased levels of ADF2 is F-actin stabilization in cells, resulting from decreased F-actin turnover. In nematode-infected plants with reduced levels of ADF2, the galls containing the giant feeding cells and growing nematodes do not develop due to the arrest in growth of the giant multinucleate feeding cells, which in turn is due to an aberrant actin network.







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