2-Furanacetyl ACP as an Alternate Substrate to Study the Activity of EsaI in Pantoea stewartii

Presentation Date

7-2015

Abstract

Bacteria release signal molecules called autoinducers to detect their population density through a Quorum Sensing (QS) mechanism. The plant pathogen, Pantoea stewartii, uses QS to form Stewart’s Wilt and leaf-blight disease in corn. P. stewartii uses the enzyme EsaI to produce 3-oxohexanoyl homoserine lactone, an autoinducer. The autoinducer is formed in a reaction between S-adenosyl-L-methionine and 3-oxohexanoyl ACP. Inhibition of EsaI could, in principle, reduce virulence and prevent Stewart’s Wilt in corn. However, 3-oxohexanoyl ACP is unstable and difficult to synthesize, thus making it challenging to study EsaI and its activity. To address this issue, we have synthesized and evaluated alternate substrates, such as 2-furanacetyl ACP, for characterizing EsaI. We propose that the use of alternate substrates should speed up mechanistic studies on wild-type EsaI enzyme. This approach should help us design inhibitors that prevent virulence and increase corn crop yield.

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2-Furanacetyl ACP as an Alternate Substrate to Study the Activity of EsaI in Pantoea stewartii

Bacteria release signal molecules called autoinducers to detect their population density through a Quorum Sensing (QS) mechanism. The plant pathogen, Pantoea stewartii, uses QS to form Stewart’s Wilt and leaf-blight disease in corn. P. stewartii uses the enzyme EsaI to produce 3-oxohexanoyl homoserine lactone, an autoinducer. The autoinducer is formed in a reaction between S-adenosyl-L-methionine and 3-oxohexanoyl ACP. Inhibition of EsaI could, in principle, reduce virulence and prevent Stewart’s Wilt in corn. However, 3-oxohexanoyl ACP is unstable and difficult to synthesize, thus making it challenging to study EsaI and its activity. To address this issue, we have synthesized and evaluated alternate substrates, such as 2-furanacetyl ACP, for characterizing EsaI. We propose that the use of alternate substrates should speed up mechanistic studies on wild-type EsaI enzyme. This approach should help us design inhibitors that prevent virulence and increase corn crop yield.