Reversal of an Immunity Associated Plant Cell Death Program by the Growth Regulator Auxin

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Reversal of an Immunity Associated Plant Cell Death Program by the Growth Regulator Auxin

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Title: Reversal of an Immunity Associated Plant Cell Death Program by the Growth Regulator Auxin
Author: Gopalan, Suresh
Citation: Gopalan, Suresh. 2008. Reversal of an immunity associated plant cell death program by the growth regulator auxin. BMC Research Notes 1: 126.
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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.
Published Version: doi://10.1186/1756-0500-1-126
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626598/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:4724759

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