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First published online July 10, 2003; 10.1104/pp.103.021717

Plant Physiology 132:2116-2125 (2003)
© 2003 American Society of Plant Biologists

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ENVIRONMENTAL STRESS AND ADAPTATION

Thylakoid-Bound Ascorbate Peroxidase Mutant Exhibits Impaired Electron Transport and Photosynthetic Activity1

Cristian H. Danna2, Carlos G. Bartoli, Francisco Sacco, Lorena R. Ingala, Guillermo E. Santa-María, Juan J. Guiamet and Rodolfo A. Ugalde*

Instituto de Investigaciones Biotecnológicas, Universidad Nacional de General San Martín, Avenida General Paz entre Albarellos y Constituyentes, Instituto Nacional de Tecnología Industrial (Edificio 24), CP 1650, San Martín, Provincia de Buenos Aires, Argentina (C.H.D., G.E.S.-M., R.A.U.); Instituto de Fisiología Vegetal, Facultad de Ciencias Agrarias y Forestales, Universidad Nacional de La Plata, La Plata, Provincia de Buenos Aires, Argentina (C.G.B., J.J.G.); and Instituto de Genética "Ewald A. Favret", Centro Nacional de Investigaciones Agropecuarias-Instituto Nacional de Tecnología Agropecuana, Castelar, Provincia de Buenos Aires, Argentina (F.S., L.R.I.)

In chloroplasts, stromal and thylakoid-bound ascorbate peroxidases (tAPX) play a major role in the removal of H2O2 produced during photosynthesis. Here, we report that hexaploid wheat (Triticum aestivum) expresses three homeologous tAPX genes (TaAPX-6A, TaAPX-6B, and TaAPX-6D) mapping on group-6 chromosomes. The tAPX activity of a mutant line lacking TaAPX-6B was 40% lower than that of the wild type. When grown at high-light intensity photosystem II electron transfer, photosynthetic activity and biomass accumulation were significantly reduced in this mutant, suggesting that tAPX activity is essential for photosynthesis. Despite the reduced tAPX activity, mutant plants did not exhibit oxidative damage probably due to the reduced photochemical activity. This might be the result of a compensating mechanism to prevent oxidative damage having as a consequence a decrease in growth of the tAPX mutant plants.


1 This work was supported by the National Research Council of Argentina (CONICET; to R.A.U.) and by the Agencia Nacional de Promoción Científica y Tecnológica of Argentina (ANPCIT; grant no. PICT 01–06565 to R.A.U.). C.H.D. is recipient of a fellowship from CONICET. C.G.B., G.E.S.-M., and R.A.U. are career researchers of CONICET. J.J.G. is a researcher of the Comisión de Investigaciones Científicas-Provincia de Buenos Aires. L.R.I. is a recipient of a fellowship from ANPCIT. F.S. is a researcher of Centro Nacional de Investigaciones Agropecuarias-Instituto Nacional de Tecnología Agropecuana, Castelar.

2 Present address: Department of Genetics, Harvard Medical School and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114.

* Corresponding author; e-mail rugalde{at}iib.unsam.edu.ar; fax 54–11–4752–9639.

Received February 6, 2003; returned for revision March 14, 2003; accepted April 28, 2003.




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