Publication | Open Access
Jasmonate signaling involves the abscisic acid receptor PYL4 to regulate metabolic reprogramming in <i>Arabidopsis</i> and tobacco
252
Citations
38
References
2011
Year
BiologyPlant Molecular BiologyBiosynthesisSignal TransductionSystems BiologyBotanyMetabolic ReprogrammingGeneticsNatural SciencesAbscisic AcidJa ResponsePlant MetabolismGene ExpressionMedicinePhytohormones JasmonatesPlant PhysiologyPlant Hormone
Jasmonates are key elicitors of plant secondary metabolism but act within complex networks that cross‑talk with other phytohormones. The study shows that a JA‑induced ABA receptor, NtPYL4, modulates alkaloid biosynthesis in tobacco and alters JA responses in Arabidopsis, linking ABA signaling to jasmonate‑mediated growth‑defense trade‑offs.
The phytohormones jasmonates (JAs) constitute an important class of elicitors for many plant secondary metabolic pathways. However, JAs do not act independently but operate in complex networks with crosstalk to several other phytohormonal signaling pathways. Here, crosstalk was detected between the JA and abscisic acid (ABA) signaling pathways in the regulation of tobacco ( Nicotiana tabacum ) alkaloid biosynthesis. A tobacco gene from the PYR/PYL/RCAR family, NtPYL4 , the expression of which is regulated by JAs, was found to encode a functional ABA receptor. NtPYL4 inhibited the type-2C protein phosphatases known to be key negative regulators of ABA signaling in an ABA-dependent manner. Overexpression of NtPYL4 in tobacco hairy roots caused a reprogramming of the cellular metabolism that resulted in a decreased alkaloid accumulation and conferred ABA sensitivity to the production of alkaloids. In contrast, the alkaloid biosynthetic pathway was not responsive to ABA in control tobacco roots. Functional analysis of the Arabidopsis ( Arabidopsis thaliana ) homologs of NtPYL4 , PYL4 and PYL5 , indicated that also in Arabidopsis altered PYL expression affected the JA response, both in terms of biomass and anthocyanin production. These findings define a connection between a component of the core ABA signaling pathway and the JA responses and contribute to the understanding of the role of JAs in balancing tradeoffs between growth and defense.
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