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Reversal of an immunity associated plant cell death program by the growth regulator auxin.

Gopalan S - BMC Res Notes (2008)

Bottom Line: Early inhibition or late reversal of this cell death program does not affect marker genes correlated with local and systemic resistance.These data indicate that the cell death program initiated by harpin can be reversed till late in the process without effect on markers strongly correlated with local and systemic immunity.The constitutive modulation of endogenous auxin does not affect equivalent signaling processes affecting cell death or buffers these signals.

View Article: PubMed Central - HTML - PubMed

Affiliation: Present address : Department of Molecular Biology, Massachusetts General Hospital & Department of Genetics, Harvard University, Boston, MA 02114, USA. gopalan@molbio.mgh.harvard.edu.

ABSTRACT

Background: One form of plant immunity against pathogens involves a rapid host programmed cell death at the site of infection accompanied by the activation of local and systemic resistance to pathogens, termed the hypersensitive response (HR). In this work it was tested (i) if the plant growth regulator auxin can inhibit the cell death elicited by a purified proteinaceous HR elicitor, (ii) how far down the process this inhibition can be achieved, and (iii) if the inhibition affects reporters of immune response. The effect of constitutive modulation of endogenous auxin levels in transgenic plants on this cell death program was also evaluated.

Results: The HR programmed cell death initiated by a bacterial type III secretion system dependent proteinaceous elicitor harpin (from Erwinia amylovora) can be reversed till very late in the process by the plant growth regulator auxin. Early inhibition or late reversal of this cell death program does not affect marker genes correlated with local and systemic resistance. Transgenic plants constitutively modulated in endogenous levels of auxin are not affected in ability or timing of cell death initiated by harpin.

Conclusion: These data indicate that the cell death program initiated by harpin can be reversed till late in the process without effect on markers strongly correlated with local and systemic immunity. The constitutive modulation of endogenous auxin does not affect equivalent signaling processes affecting cell death or buffers these signals. The concept and its further study has utility in choosing better strategies for treating mammalian and agricultural diseases.

No MeSH data available.


Related in: MedlinePlus

Induction of defense genes are not affected by effect of auxin on harpin initiated cell death. (A) Expression of HIN1 mRNA. Northern blot using RNA from leaves infiltrated with lane 1: Buffer 4.5 h; lane 2: 50 μM 2,4-D 4.5 h; lane 3: Harpin 4.5 h; lane 4: Harpin + 50 μM 2,4-D 4.5 h; lane 5: Harpin + 50 μM 2,4-D 24 h; lane 6: harpin – necrotic (9 h); lane 7: 50 μM 2,4-D 24 h. (B) Expression of PR1 mRNA. Lane 1: Buffer 24 h; lane 2: 2,4-D 24 h; lane 3: harpin 24 h; lane 4: Harpin + 2,4-D 24 h. 10 μg total RNA per lane from infiltrated area (A) or 1 cm region surrounding the infiltrated region (B) were used for the analysis. For panel B, leaf tissue was collected from region surrounding the infiltrated region because PR1 was not induced in the infiltrated area at these time points. RNA extraction, sequence and preparation of probes and subsequent procedures used have been described earlier [10]. rRNA bands of the RNA gel used for the Northern blot, visualized by staining with ethidium bromide, is shown in the lower frame of each panel.
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Figure 2: Induction of defense genes are not affected by effect of auxin on harpin initiated cell death. (A) Expression of HIN1 mRNA. Northern blot using RNA from leaves infiltrated with lane 1: Buffer 4.5 h; lane 2: 50 μM 2,4-D 4.5 h; lane 3: Harpin 4.5 h; lane 4: Harpin + 50 μM 2,4-D 4.5 h; lane 5: Harpin + 50 μM 2,4-D 24 h; lane 6: harpin – necrotic (9 h); lane 7: 50 μM 2,4-D 24 h. (B) Expression of PR1 mRNA. Lane 1: Buffer 24 h; lane 2: 2,4-D 24 h; lane 3: harpin 24 h; lane 4: Harpin + 2,4-D 24 h. 10 μg total RNA per lane from infiltrated area (A) or 1 cm region surrounding the infiltrated region (B) were used for the analysis. For panel B, leaf tissue was collected from region surrounding the infiltrated region because PR1 was not induced in the infiltrated area at these time points. RNA extraction, sequence and preparation of probes and subsequent procedures used have been described earlier [10]. rRNA bands of the RNA gel used for the Northern blot, visualized by staining with ethidium bromide, is shown in the lower frame of each panel.

Mentions: As mentioned above the HR cell death is associated with local and systemic resistance in plants. The induction of marker genes strongly correlated with both these processes were tested. Induction of both the genes tested, HIN1 – a gene induced locally at the site of HR cell death [10], and PR1 – an established marker gene whose induction is tightly correlated with SAR, were not affected by inhibition of HR cell death by auxin – Fig. 2. While the precise contribution of HR cell death to resistance is not known, there are examples of cell death elicitation (spontaneous and induced) that can lead to resistance [15,16]. In contrast, there are also examples of or constitutive resistance without cell death [17,18]. An example of separate of HR cell death and resistance programs is the R gene (Rx) mediated recognition of potato virus X (PVX) [19]. Collectively, these data indicate that resistance phenomena while tightly associated with certain cell death processes, is triggered through a divergent signaling process that is strongly modulated by signals from cell death programs.


Reversal of an immunity associated plant cell death program by the growth regulator auxin.

Gopalan S - BMC Res Notes (2008)

Induction of defense genes are not affected by effect of auxin on harpin initiated cell death. (A) Expression of HIN1 mRNA. Northern blot using RNA from leaves infiltrated with lane 1: Buffer 4.5 h; lane 2: 50 μM 2,4-D 4.5 h; lane 3: Harpin 4.5 h; lane 4: Harpin + 50 μM 2,4-D 4.5 h; lane 5: Harpin + 50 μM 2,4-D 24 h; lane 6: harpin – necrotic (9 h); lane 7: 50 μM 2,4-D 24 h. (B) Expression of PR1 mRNA. Lane 1: Buffer 24 h; lane 2: 2,4-D 24 h; lane 3: harpin 24 h; lane 4: Harpin + 2,4-D 24 h. 10 μg total RNA per lane from infiltrated area (A) or 1 cm region surrounding the infiltrated region (B) were used for the analysis. For panel B, leaf tissue was collected from region surrounding the infiltrated region because PR1 was not induced in the infiltrated area at these time points. RNA extraction, sequence and preparation of probes and subsequent procedures used have been described earlier [10]. rRNA bands of the RNA gel used for the Northern blot, visualized by staining with ethidium bromide, is shown in the lower frame of each panel.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2626598&req=5

Figure 2: Induction of defense genes are not affected by effect of auxin on harpin initiated cell death. (A) Expression of HIN1 mRNA. Northern blot using RNA from leaves infiltrated with lane 1: Buffer 4.5 h; lane 2: 50 μM 2,4-D 4.5 h; lane 3: Harpin 4.5 h; lane 4: Harpin + 50 μM 2,4-D 4.5 h; lane 5: Harpin + 50 μM 2,4-D 24 h; lane 6: harpin – necrotic (9 h); lane 7: 50 μM 2,4-D 24 h. (B) Expression of PR1 mRNA. Lane 1: Buffer 24 h; lane 2: 2,4-D 24 h; lane 3: harpin 24 h; lane 4: Harpin + 2,4-D 24 h. 10 μg total RNA per lane from infiltrated area (A) or 1 cm region surrounding the infiltrated region (B) were used for the analysis. For panel B, leaf tissue was collected from region surrounding the infiltrated region because PR1 was not induced in the infiltrated area at these time points. RNA extraction, sequence and preparation of probes and subsequent procedures used have been described earlier [10]. rRNA bands of the RNA gel used for the Northern blot, visualized by staining with ethidium bromide, is shown in the lower frame of each panel.
Mentions: As mentioned above the HR cell death is associated with local and systemic resistance in plants. The induction of marker genes strongly correlated with both these processes were tested. Induction of both the genes tested, HIN1 – a gene induced locally at the site of HR cell death [10], and PR1 – an established marker gene whose induction is tightly correlated with SAR, were not affected by inhibition of HR cell death by auxin – Fig. 2. While the precise contribution of HR cell death to resistance is not known, there are examples of cell death elicitation (spontaneous and induced) that can lead to resistance [15,16]. In contrast, there are also examples of or constitutive resistance without cell death [17,18]. An example of separate of HR cell death and resistance programs is the R gene (Rx) mediated recognition of potato virus X (PVX) [19]. Collectively, these data indicate that resistance phenomena while tightly associated with certain cell death processes, is triggered through a divergent signaling process that is strongly modulated by signals from cell death programs.

Bottom Line: Early inhibition or late reversal of this cell death program does not affect marker genes correlated with local and systemic resistance.These data indicate that the cell death program initiated by harpin can be reversed till late in the process without effect on markers strongly correlated with local and systemic immunity.The constitutive modulation of endogenous auxin does not affect equivalent signaling processes affecting cell death or buffers these signals.

View Article: PubMed Central - HTML - PubMed

Affiliation: Present address : Department of Molecular Biology, Massachusetts General Hospital & Department of Genetics, Harvard University, Boston, MA 02114, USA. gopalan@molbio.mgh.harvard.edu.

ABSTRACT

Background: One form of plant immunity against pathogens involves a rapid host programmed cell death at the site of infection accompanied by the activation of local and systemic resistance to pathogens, termed the hypersensitive response (HR). In this work it was tested (i) if the plant growth regulator auxin can inhibit the cell death elicited by a purified proteinaceous HR elicitor, (ii) how far down the process this inhibition can be achieved, and (iii) if the inhibition affects reporters of immune response. The effect of constitutive modulation of endogenous auxin levels in transgenic plants on this cell death program was also evaluated.

Results: The HR programmed cell death initiated by a bacterial type III secretion system dependent proteinaceous elicitor harpin (from Erwinia amylovora) can be reversed till very late in the process by the plant growth regulator auxin. Early inhibition or late reversal of this cell death program does not affect marker genes correlated with local and systemic resistance. Transgenic plants constitutively modulated in endogenous levels of auxin are not affected in ability or timing of cell death initiated by harpin.

Conclusion: These data indicate that the cell death program initiated by harpin can be reversed till late in the process without effect on markers strongly correlated with local and systemic immunity. The constitutive modulation of endogenous auxin does not affect equivalent signaling processes affecting cell death or buffers these signals. The concept and its further study has utility in choosing better strategies for treating mammalian and agricultural diseases.

No MeSH data available.


Related in: MedlinePlus