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Arabidopsis responds to Alternaria alternata volatiles by triggering plastid phosphoglucose isomerase-independent mechanisms

AuthorsSánchez-López, Ángela María ; Bahaji, Abdellatif ; Diego, Nuria de; Muñoz Pérez, Francisco José ; Almagro, Goizeder ; Ricarte-Bermejo, A. ; Ciordia, Sergio; Mena Valverde, Mª Carmen; Navajas, Rosana; Baroja-Fernández, Edurne ; Pozueta Romero, Javier
Issue DateNov-2016
PublisherAmerican Society of Plant Biologists
CitationPlant Physiology 172(3): 1989-2001 (2016)
AbstractVolatile compounds (VCs) emitted by phylogenetically diverse microorganisms (including plant pathogens and microbes that do not normally interact mutualistically with plants) promote photosynthesis, growth, and the accumulation of high levels of starch in leaves through cytokinin (CK)-regulated processes. In Arabidopsis (Arabidopsis thaliana) plants not exposed to VCs, plastidic phosphoglucose isomerase (pPGI) acts as an important determinant of photosynthesis and growth, likely as a consequence of its involvement in the synthesis of plastidic CKs in roots. Moreover, this enzyme plays an important role in connecting the Calvin-Benson cycle with the starch biosynthetic pathway in leaves. To elucidate the mechanisms involved in the responses of plants to microbial VCs and to investigate the extent of pPGI involvement, we characterized pPGI-null pgi1-2 Arabidopsis plants cultured in the presence or absence of VCs emitted by Alternaria alternata. We found that volatile emissions from this fungal phytopathogen promote growth, photosynthesis, and the accumulation of plastidic CKs in pgi1-2 leaves. Notably, the mesophyll cells of pgi1-2 leaves accumulated exceptionally high levels of starch following VC exposure. Proteomic analyses revealed that VCs promote global changes in the expression of proteins involved in photosynthesis, starch metabolism, and growth that can account for the observed responses in pgi1-2 plants. The overall data show that Arabidopsis plants can respond to VCs emitted by phytopathogenic microorganisms by triggering pPGI-independent mechanisms.
DescriptionSánchez-López, Ángela María et al.
Publisher version (URL)http://doi.org/10.1104/pp.16.00945
Identifierse-issn: 1532-2548
issn: 0032-0889
Appears in Collections:(IDAB) Artículos
(CNB) Artículos
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