Open Access

ARTICLE

Apparent cross-talk of two signaling pathways that regulate Zea mays coleoptile growth

by Buentello Volante¹, B, F Díaz de León-Sánchez¹, F Rivera-Cabrera¹, R Aguilar Caballero², M Ponce-Valadez¹, E Sánchez de Jiménez², LJ Pérez-F lores¹

1 Departamento de Ciencias de la Salud Universidad Autónoma Metropolitana-Iztapalapa, Av. San Rafael Atlixco No. 186 Col. Vicentina Iztapalapa 09270 México, D.F.
2 Departamento de Bioquímica, Facultad de Química, Universidad Nacional Autónoma de México. Circuito Institutos, Ciudad Universitaria 04510 México, D.F.
Address Correspondence to: Dra. Laura Josefina Pérez-F lores, email: ljpf@xanum.uam.mx; fax 052-55-58044727, phone 052-55-58046481 and E. Sánchez de Jiménez, email: estelas@servidor.unam.mx; Fax 052-55-56225329, phone 052-55-56225278.

Phyton-International Journal of Experimental Botany 2010, 79(all), 101-108. https://doi.org/10.32604/phyton.2010.79.101

Abstract

Auxin and insulin promote Zea mays embryo growth, induce S6 ribosomal protein (S6rp) phosphorylation, and promote specific protein synthesis. The objective of this research was to test a possible cross-talk between insulin and auxin transduction pathways in Z. mays coleoptiles, typical auxin target tissues. Auxin and insulin produced differential quantitative and qualitative stimulation of cytoplasmic and ribosomal protein phosphorylation, and specific patterns of de novo synthesized cytoplasmic proteins. In addition, insulin induced S6rp phosphorylation was strongly inhibited by rapamycin, indicating target of rapamycin (TOR) kinase participation; auxin-induced S6rp phosphorylation was insensitive to this inhibitor. Phosphatidic acid (PA), a second messenger of TOR in metazoan, was also tested. It produced similar results to insulin and rapamycin sensitiveness, supporting the existence of TOR pathway in plants and the participation of PA as an intermediate of insulin action. These results seem to imply that auxin and insulin induce Z. mays coleoptile growth through two independent signal transduction pathways.

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