Abstract

The delayed leaf senescence process has been engineered in transgenic Petunia x hybrida plants containing the homeobox knotted-1 gene (kn1), a mutant maize gene that is thought to be involved in cytokinin metabolism. Petunia plants were transformed with the kn1 gene fused to a senescence-associated promoter (SAG 12 ) using Agrobacterium. Putative P SAG12 -kn1 lines were subjected to drought stress treatments, and leaf senescence was evaluated in the To and T 1 generations. A wide range of delayed senescence phenotypes was observed, indicating that the promoter SAG 12 did not always present complete regulation. Although expression of the kn1 transgene delayed leaf senescence, it also caused some morphological and physiological alterations, which ranged from mild to severe in their intensity. Most of the plants with a non-senescent phenotype showed only mild phenotypic alterations, which were not considered detrimental to plant performance. Along with the trait of delayed leaf senescence, plants with mild phenotypes had a more compact architecture, whereas plants with a severe phenotype were stunted in growth. Our data support the concept that the P SAG12 -kn1 genetic construct can be used to delay leaf senescence, but the mechanism(s) by which kn1 gene affects the senescence process remains to be elucidated.

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