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Imposed glutathione-mediated redox switch modulates the tobacco wound-induced protein kinase and salicylic acid-induced protein kinase activation state and impacts on defence against Pseudomonas syringae.

Matern S, Peskan-Berghoefer T, Gromes R, Kiesel RV, Rausch T - J. Exp. Bot. (2015)

Bottom Line: Similarly, rapid activation of MAPKs could be induced in WT tobacco by exposure to either reduced or oxidized glutathione.When HGL plants were challenged with adapted or non-adapted Pseudomonas syringae pathovars, the cytosolic redox shift was further amplified and the defence response was markedly increased, showing a priming effect for SA and callose; however, the initial and transient hyperactivation of MAPK signalling was attenuated in HGLs.The results suggest that, in tobacco, MAPK and SA signalling may operate independently, both possibly being modulated by the glutathione redox potential.

View Article: PubMed Central - PubMed

Affiliation: Centre for Organismal Studies Heidelberg, Department of Plant Molecular Physiology, Heidelberg University, 69120 Heidelberg, Germany The Hartmut Hoffmann-Berling International Graduate School of Molecular and Cellular Biology (HBIGS), Heidelberg University, 69120 Heidelberg, Germany.

No MeSH data available.


Related in: MedlinePlus

In tobacco HGLs, steady-state transcript levels for PR protein genes and immunity marker genes are upregulated without an increase in free SA. (A) Transcript levels for PR protein genes and NPR1. (B) Transcript levels for immunity marker genes PTI5 and CYP71D20. (C) Transcript levels for ICS1 and contents of free SA and total SA in WT and HGLs. For gene expression analysis, numbers indicate fold induction in comparison with normalized expression in WT. Ribosomal protein L25 was used as a reference gene. Results represent mean values of three biological replicates±standard error. For SA measurements, results represent mean values of five biological replicates±standard deviation. Student’s t-test was employed to calculate significant differences (*P<0.05, **P<0.01) between WT and HGLs. Experiments were repeated three to five times with similar results.
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Figure 4: In tobacco HGLs, steady-state transcript levels for PR protein genes and immunity marker genes are upregulated without an increase in free SA. (A) Transcript levels for PR protein genes and NPR1. (B) Transcript levels for immunity marker genes PTI5 and CYP71D20. (C) Transcript levels for ICS1 and contents of free SA and total SA in WT and HGLs. For gene expression analysis, numbers indicate fold induction in comparison with normalized expression in WT. Ribosomal protein L25 was used as a reference gene. Results represent mean values of three biological replicates±standard error. For SA measurements, results represent mean values of five biological replicates±standard deviation. Student’s t-test was employed to calculate significant differences (*P<0.05, **P<0.01) between WT and HGLs. Experiments were repeated three to five times with similar results.

Mentions: To assess the potential impact of MAPK signalling in HGLs as caused by the changed glutathione redox state on downstream defence signalling in the absence of pathogen challenge, an expression analysis was performed for selected genes considered to be specific for various defence-signalling pathways (van Loon, 1985). Expression of several PR protein genes was strongly (and constitutively) upregulated in HGLs when compared with WT (Fig. 4A). Upregulated genes included PR1, PR2, PR4, and PR5, known to be activated by SA in NPR1-dependent and -independent modes (Cao et al., 1994; Rao et al., 2002; Thibaud et al., 2004). Two established PTI marker genes for Nicotiana, namely CYP71D20 (Lacombe et al., 2010) and PTI5 (Nguyen et al., 2010), were also significantly induced in HGLs (Fig. 4B), whereas transcripts for PR10 and NPR1 remained unchanged (Fig. 4A). Since SA-mediated signalling is thought to be required for induction of PR genes in response to biotrophic or hemi-biotrophic pathogens such as P. syringae (Katagiri et al., 2002), the contents of free SA and total SA, including its glucoside form (SAG), were also determined. Interestingly, SA did not differ between HGLs and WT, consistent with unchanged (or even lowered) transcript amounts for isochorismate synthase (ICS1), an enzyme involved in SA biosynthesis. However, all HGLs had a significantly increased content of total SA, due to the presence of low amounts of the SA conjugate SAG, which was almost absent in WT (Fig. 4C).


Imposed glutathione-mediated redox switch modulates the tobacco wound-induced protein kinase and salicylic acid-induced protein kinase activation state and impacts on defence against Pseudomonas syringae.

Matern S, Peskan-Berghoefer T, Gromes R, Kiesel RV, Rausch T - J. Exp. Bot. (2015)

In tobacco HGLs, steady-state transcript levels for PR protein genes and immunity marker genes are upregulated without an increase in free SA. (A) Transcript levels for PR protein genes and NPR1. (B) Transcript levels for immunity marker genes PTI5 and CYP71D20. (C) Transcript levels for ICS1 and contents of free SA and total SA in WT and HGLs. For gene expression analysis, numbers indicate fold induction in comparison with normalized expression in WT. Ribosomal protein L25 was used as a reference gene. Results represent mean values of three biological replicates±standard error. For SA measurements, results represent mean values of five biological replicates±standard deviation. Student’s t-test was employed to calculate significant differences (*P<0.05, **P<0.01) between WT and HGLs. Experiments were repeated three to five times with similar results.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4378631&req=5

Figure 4: In tobacco HGLs, steady-state transcript levels for PR protein genes and immunity marker genes are upregulated without an increase in free SA. (A) Transcript levels for PR protein genes and NPR1. (B) Transcript levels for immunity marker genes PTI5 and CYP71D20. (C) Transcript levels for ICS1 and contents of free SA and total SA in WT and HGLs. For gene expression analysis, numbers indicate fold induction in comparison with normalized expression in WT. Ribosomal protein L25 was used as a reference gene. Results represent mean values of three biological replicates±standard error. For SA measurements, results represent mean values of five biological replicates±standard deviation. Student’s t-test was employed to calculate significant differences (*P<0.05, **P<0.01) between WT and HGLs. Experiments were repeated three to five times with similar results.
Mentions: To assess the potential impact of MAPK signalling in HGLs as caused by the changed glutathione redox state on downstream defence signalling in the absence of pathogen challenge, an expression analysis was performed for selected genes considered to be specific for various defence-signalling pathways (van Loon, 1985). Expression of several PR protein genes was strongly (and constitutively) upregulated in HGLs when compared with WT (Fig. 4A). Upregulated genes included PR1, PR2, PR4, and PR5, known to be activated by SA in NPR1-dependent and -independent modes (Cao et al., 1994; Rao et al., 2002; Thibaud et al., 2004). Two established PTI marker genes for Nicotiana, namely CYP71D20 (Lacombe et al., 2010) and PTI5 (Nguyen et al., 2010), were also significantly induced in HGLs (Fig. 4B), whereas transcripts for PR10 and NPR1 remained unchanged (Fig. 4A). Since SA-mediated signalling is thought to be required for induction of PR genes in response to biotrophic or hemi-biotrophic pathogens such as P. syringae (Katagiri et al., 2002), the contents of free SA and total SA, including its glucoside form (SAG), were also determined. Interestingly, SA did not differ between HGLs and WT, consistent with unchanged (or even lowered) transcript amounts for isochorismate synthase (ICS1), an enzyme involved in SA biosynthesis. However, all HGLs had a significantly increased content of total SA, due to the presence of low amounts of the SA conjugate SAG, which was almost absent in WT (Fig. 4C).

Bottom Line: Similarly, rapid activation of MAPKs could be induced in WT tobacco by exposure to either reduced or oxidized glutathione.When HGL plants were challenged with adapted or non-adapted Pseudomonas syringae pathovars, the cytosolic redox shift was further amplified and the defence response was markedly increased, showing a priming effect for SA and callose; however, the initial and transient hyperactivation of MAPK signalling was attenuated in HGLs.The results suggest that, in tobacco, MAPK and SA signalling may operate independently, both possibly being modulated by the glutathione redox potential.

View Article: PubMed Central - PubMed

Affiliation: Centre for Organismal Studies Heidelberg, Department of Plant Molecular Physiology, Heidelberg University, 69120 Heidelberg, Germany The Hartmut Hoffmann-Berling International Graduate School of Molecular and Cellular Biology (HBIGS), Heidelberg University, 69120 Heidelberg, Germany.

No MeSH data available.


Related in: MedlinePlus