AI Article Synopsis

  • Researchers used a whole-genome microarray to analyze gene expression in the biocontrol strain Pseudomonas protegens Pf-5 on pea seed surfaces, identifying the influence of two global regulators (GacA and RpoS) on various genes.
  • The study found that 897 genes were affected by these regulators, with many linked to functions like biofilm formation, iron management, and secondary metabolism, highlighting their activity in the seed environment.
  • Mutants of the GacA and RpoS genes were used to measure secondary metabolite production, which aligned with gene expression patterns, suggesting that understanding these genes could enhance strategies for disease suppression in seedlings.

Article Abstract

Gene expression profiles of the biological control strain Pseudomonas protegens Pf-5 inhabiting pea seed surfaces were revealed using a whole-genome oligonucleotide microarray. We identified genes expressed by Pf-5 under the control of two global regulators (GacA and RpoS) known to influence biological control and secondary metabolism. Transcript levels of 897 genes, including many with unknown functions as well as those for biofilm formation, cyclic diguanylate (c-di-GMP) signalling, iron homeostasis and secondary metabolism, were influenced by one or both regulators, providing evidence for expression of these genes by Pf-5 on seed surfaces. Comparison of the GacA and RpoS transcriptomes defined for Pf-5 grown on seed versus in broth culture overlapped, but most genes were regulated by GacA or RpoS under only one condition, likely due to differing levels of expression in the two conditions. We quantified secondary metabolites produced by Pf-5 and gacA and rpoS mutants on seed and in culture, and found that production profiles corresponded generally with biosynthetic gene expression profiles. Future studies evaluating biological control mechanisms can now focus on genes expressed by Pf-5 on seed surfaces, the habitat where the bacterium interacts with seed-infecting pathogens to suppress seedling diseases.

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Source
http://dx.doi.org/10.1111/1462-2920.12066DOI Listing

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