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• W2068163901 startingPage "e972806" @default.
• W2068163901 abstract "Salicylic acid (SA) has a central role in activating plant resistance to pathogens. SA levels increase in plant tissue following pathogen infection and exogenous SA enhances resistance to a broad range of pathogens. To study the relevance of the SA signaling in the flg22 response, we investigated the responses of SA-related mutants to flg22, a 22-amino acid peptide of the flagellin bacterial protein. We identified SA as an important component of the flg22-triggered oxidative burst, a very early event after flg22 detection, and gene induction, an early event. SA acted partially by enhancing accumulation of FLS2 mRNA. We also provide new evidence that NPR1 play a role in SA-induced priming event that enhances the flg22-triggered oxidative burst, which is correlated with enhancement of the flg22-induced callose deposition. Based on these observations, we conclude that SA signaling is required for early as well as late flg22 responses." @default.
• W2068163901 created "2016-06-24" @default.
• W2068163901 creator A5015295682 @default.
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• W2068163901 date "2014-10-31" @default.
• W2068163901 modified "2023-09-26" @default.
• W2068163901 title "How does SA signaling link the Flg22 responses?" @default.
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• W2068163901 doi "https://doi.org/10.4161/15592316.2014.972806" @default.
• W2068163901 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4622841" @default.
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