title: Premature leaf senescence modulated by the Arabidopsis PHYTOALEXIN DEFICIENT4 gene is associated with defense against the phloem-feeding green peach aphid.
abstract: Aphids, which are phloem-feeding insects, cause extensive loss of plant productivity and are vectors of plant viruses. Aphid feeding causes changes in resource allocation in the host, resulting in an increase in flow of nutrients to the insect-infested tissue. We hypothesized that leaf senescence, which is involved in the programmed degradation of cellular components and the export of nutrients out of the senescing leaf, could be utilized by plants to limit aphid growth. Using Arabidopsis (Arabidopsis thaliana) and green peach aphid (GPA; Myzus persicae Sulzer), we found that GPA feeding induced premature chlorosis and cell death, and increased the expression of SENESCENCE ASSOCIATED GENES (SAGs), all hallmarks of leaf senescence. Hypersenescence was accompanied by enhanced resistance against GPA in the Arabidopsis constitutive expresser of PR genes5 and suppressor of SA insensitivity2 mutant plants. In contrast, resistance against GPA was compromised in the phytoalexin deficient4 (pad4) mutant plant. The PAD4 gene, which is expressed at elevated level in response to GPA feeding, modulates the GPA feeding-induced leaf senescence. In comparison to the wild-type plant, GPA feeding-induced chlorophyll loss, cell death, and SAG expression were delayed in the pad4 mutant. Although PAD4 is associated with camalexin synthesis and salicylic acid (SA) signaling, camalexin and SA signaling are not important for restricting GPA growth; growth of GPA on the camalexin-biosynthesis mutant, pad3, and the SA deficient2 and NahG plants and the SA-signaling mutant, nonexpresser of PR genes1, were comparable to that on the wild-type plant. Our results suggest that PAD4 modulates the activation of senescence in the aphid-infested leaves, which contributes to basal resistance to GPA.
authors.affiliation: Division of Biology and the Molecular Cellular and Developmental Biology Program, Kansas State University, Manhattan, Kansas 66506-4901, USA.
authors.forename: Venkatramana
authors.initials: V
authors.lastname: Pegadaraju
authors.forename: Caleb
authors.initials: C
authors.lastname: Knepper
authors.forename: John
authors.initials: J
authors.lastname: Reese
authors.forename: Jyoti
authors.initials: J
authors.lastname: Shah
mesh_terms: D000818:Animals; D001042:Aphids / Q000472:pathogenicity; D017360:Arabidopsis / Q000235:genetics* / Q000469:parasitology*; D029681:Arabidopsis Proteins / Q000235:genetics*; D001483:Base Sequence; D002265:Carboxylic Ester Hydrolases / Q000235:genetics*; D018744:DNA, Plant / Q000235:genetics; D017343:Genes, Plant; D009154:Mutation; D010935:Plant Diseases / Q000235:genetics / Q000469:parasitology; D018515:Plant Leaves / Q000469:parasitology
chemical_list: D029681:Arabidopsis Proteins; D018744:DNA, Plant; D002265:Carboxylic Ester Hydrolases; C400766:PAD4 protein, Arabidopsis