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Plants and microbial pathogens often engage in a fierce war that determines their survival. Host plants have evolved sophisticated regulatory mechanisms to fine-tune defense responses to counter attacks from pathogens, while pathogens often hijack the lipid-derived phytohormone jasmonate to cause hormonal signaling imbalances for efficient infection. This review focuses on the jasmonate-based warfare between host plants and pathogenic intruders, and further discusses approaches to uncouple plant growth and defense tradeoffs in crop breeding. [ABSTRACT FROM AUTHOR]

Jasmonate (JA) is one of the key phytohormones essential for plant development and defense processes. The core JA biosynthetic and signaling pathways have been well-characterized. Notably, post-translational modifications (PTMs), which affect the protein structures and functions, have emerged as critical mechanisms to modulate JA output at different spatiotemporal levels. Disruption of PTMs in JA biosynthesis and signaling would cause the dysfunction of vital biological processes. Here, we give an overview of the PTMs that have been identified in JA biosynthetic and signaling pathways, and provide insights into the mechanisms by which PTMs define JA responses. [ABSTRACT FROM AUTHOR]

Arabidopsis heterotrimeric G proteins regulate diverse plant growth and defense processes by coupling to 7TM AtRGS1 proteins. Although G protein mutants display alterations in response to multiple plant hormones, the underlying mechanism by which G proteins participate in the regulation of hormone responses remains elusive. Here, we show that genetic disruption of Gα and Gβ subunits results in reduced sensitivity to JA treatment. Furthermore, using confocal microscopy, VA-TIRFM, and FRET-FLIM, we provide evidence that stimulation by JA induces phosphorylation- and C-terminus-dependent endocytosis of AtRGS1, which then promotes dissociation of AtRGS1 from AtGPA1. In addition, SPT analysis reveals that JA treatment affects the diffusion dynamics of AtRGS1 and AtRGS1-ΔCt. Taken together, these findings suggest that the JA signal activates heterotrimeric G proteins through the endocytosis of AtRGS1 and dissociation of AtRGS1 from AtGPA1, thus providing valuable insight into the mechanisms of how the G protein system perceives and transduces phytohormone signals. [ABSTRACT FROM AUTHOR]