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First published online January 15, 2004; 10.1104/pp.103.030767

Plant Physiology 134:649-663 (2004)
© 2004 American Society of Plant Biologists

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DEVELOPMENT AND HORMONE ACTION

Morphogenesis of Maize Embryos Requires ZmPRPL35-1 Encoding a Plastid Ribosomal Protein1

Jean-Louis Magnard2, Thierry Heckel3, Agnès Massonneau, Jean-Pierre Wisniewski, Sylvain Cordelier, Hervé Lassagne, Pascual Perez, Christian Dumas and Peter M. Rogowsky*

Reproduction et Développement des Plantes, Unité Mixte de Recherche 5667, Institut National de la Recherche Agronomique-Centre National de la Recherche Scientifique-Ecole Normal Supérieure de Lyon-Université Claude Bernard Lyon I, Institut Fédératif de Recherche 128 BioSciences Lyon-Gerland, Ecole Normale Supérieure-Lyon, 46 Allée d'Italie, F–69364 Lyon cedex 07, France (J.-L.M., T.H., A.M., J.-P.W., C.D., P.M.R.); and Biogemma, Laboratoire de Biologie Cellulaire et Moléculaire, Campus Universitaire des Cézeaux, 24 Avenue des Landais, F–63177 Aubière, France (S.C., H.L., P.P.)

In emb (embryo specific) mutants of maize (Zea mays), the two fertilization products have opposite fates: Although the endosperm develops normally, the embryo shows more or less severe aberrations in its development, resulting in nonviable seed. We show here that in mutant emb8516, the development of mutant embryos deviates as soon as the transition stage from that of wild-type siblings. The basic events of pattern formation take place because mutant embryos display an apical-basal polarity and differentiate a protoderm. However, morphogenesis is strongly aberrant. Young mutant embryos are characterized by protuberances at their suspensor-like extremity, leading eventually to structures of irregular shape and variable size. The lack of a scutellum or coleoptile attest to the virtual absence of morphogenesis at the embryo proper-like extremity. Molecular cloning of the mutation was achieved based on cosegregation between the mutant phenotype and the insertion of a MuDR element. The Mu insertion is located in gene ZmPRPL35-1, likely coding for protein L35 of the large subunit of plastid ribosomes. The isolation of a second allele g2422 and the complementation of mutant emb8516 with a genomic clone of ZmPRPL35-1 confirm that a lesion in ZmPRPL35-1 causes the emb phenotype. ZmPRPL35-1 is a low-copy gene present at two loci on chromosome arms 6L and 9L. The gene is constitutively expressed in all major tissues of wild-type maize plants. Lack of expression in emb/emb endosperm shows that endosperm development does not require a functional copy of ZmPRPL35-1 and suggests a link between plastids and embryo-specific signaling events.


Article, publication date, and citation information can be found at http://www.plantphysiol.org/cgi/doi/10.1104/pp.103.030767.

1 This work was supported in part by the European Commission (contract no. BIO4–CT96–0210) and by Biogemma SA (to T.H. and J.L.M.).

2 Present address: Biotechnologies Végétales, Université Jean Monnet, 23 Rue du Docteur Paul Michelon, F-42023 Saint-Etienne cedex 02, France.

3 Present address: 125 Rue du canal, F–57820 Lutzelbourg, France.

* Corresponding author; e-mail Peter.Rogowsky{at}ens-lyon.fr; fax 334–7272–8607.

Received July 24, 2003; returned for revision October 10, 2003; accepted November 10, 2003.




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