Skip to main content
ARS Home » Research » Publications at this Location » Publication #181386
Title: Biocontrol Elicited Systemic Resistance in Sugarbeet is Salicylic Acid Independent and NPR1 Dependent.

Author
item Larson, Rebecca
item JACOBSEN, BARRY - MONTANA STATE UNIVERSITY

Submitted to: Journal of Sugarbeet Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/11/2006
Publication Date: 6/1/2007
Citation: Larson, R.L., Jacobsen, B.J. Biocontrol Elicited Systemic Resistance in Sugarbeet is Salicylic Acid Independent and NPR1 Dependent. Journal of Sugarbeet Research. 44(1):17-33. 2007

Interpretive Summary: INTERPRETIVE SUMMARY: Systemic acquired resistance provides defense against a wide array of pathogens in many plant systems. Numerous triggers are capable of inducing systemic resistance following different signal transduction pathways. In the current study, two major signaling components, salicylic acid and NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1), were examined for their potential role in signaling for systemic acquired resistance induction in sugar beet using two bacterial biological control agents as elicitors of resistance, Bacillus mycoides isolate Bac J and Bacillus mojavensis isolate 203-7. Both biological control agents induce resistance independent of salicylic acid accumulation, however both were reliant upon NPR1 activation. This information, taken along with previous data acquired using this system suggest that the biological control agents induce resistance through a novel signaling pathway.

Technical Abstract: ABSTRACT: Salicylic acid (SA) and NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) are both key players in the establishment of systemic acquired resistance (SAR). Previously we demonstrated that biological control agents (BCAs) Bacillus mycoides isolate Bac J (BmJ) and Bacillus mojavensis isolate 203-7 (203-7) induce pathogenesis-related proteins and biphasic hydrogen peroxide production associated with SA- and NPR1-dependent resistance mechanisms. Here we show the BCAs elicit systemic resistance while failing to induce an increase in SA level in sugar beet leaf tissue over a 48 hour timeline following treatment with BmJ or 203-7. Additionally, the SA trend over time was similar to that observed following water and Bacillus pumulis isolate BMH5E-33 (BMH5E-33) treatment, experimental negative controls. Both BmJ and 203-7 activate NPR1, a protein associated with transcriptional activation of pathogenesis-related genes. NPR1 was activated within 3 hours post treatment with BmJ. Furthermore, 203-7, SA and acibenzolar-S-methyl all induced activation of NPR1 by 48 hours post treatment. This timing of activation corresponds to the conclusion of the secondary hydrogen peroxide burst elicited by BmJ. The information obtained in this current investigation show that the BCAs BmJ and 203-7 induce resistance in an SA-independent and NPR1-dependent manner. Further development of a working model for understanding signaling in BmJ- and 203-7-induced resistance in sugar beet is presented.