Wars between microbes on roots and fruits

Abstract

Microbes in nature often live in unfavorable conditions. To survive, they have to occupy niches close to food sources and efficiently utilize nutrients that are often present in very low concentrations. Moreover, they have to possess an arsenal of attack and defense mechanisms against competing bacteria. In this review, we will discuss strategies used by microbes to compete with each other in the rhizosphere and on fruits, with a focus on mechanisms of inter- and intra-species antagonism. Special attention will be paid to the recently discovered roles of volatile organic compounds. Several microbes with proven capabilities in the art of warfare are being applied in products used for the biological control of plant diseases, including post-harvest control of fruits and vegetables.

Keywords: antibiotic resistance; biocontrol; competitive colonization; fusaric acid; postharvest control; rhizosphere; volatile organic compounds.

Figure 1.. Scanning electron microscopy of colonization of Fusarium oxysporum f. sp. radicis-lycopersici (Forl) hyphae by cells of Pseudomonas fluorescens WCS365 after incubation for 72 hours in tomato root exudate.

The right photo is a detail from the left photo but with a higher magnification (the arrow indicates a bacterial microcolony). Reproduced from Kamilova et al. by permission of the publisher.

Figure 2.. Major mechanisms used by microbes to defend themselves against antibiotic attack by other microbes.

Microbe A (top) produces antibiotic molecules (red squares), which enter the antibiotic-sensitive Microbe B (bottom) and fit snugly in their molecular target, thereby inactivating Microbe B (see left part of figure). A variety of mechanisms can be used by Microbe B to defend itself. The numbers in brackets refer here, and in the figure, to the various defense mechanisms. {1} Microbe B can secrete a secondary metabolite (SM), which represses the expression of the antibiotic biosynthetic genes at the level of their promoter. In many cases, acyl homoserine lactones (AHLs) are required for activating antibiotic synthesis (see top right). In such a case, Microbe B can develop one of two different mechanisms. Firstly, it can secrete an SM which inhibits the synthesis of the AHL {2}. Secondly, Microbe B can secrete an enzyme which inactivates the AHL {3}. Also, after the antibiotic has entered Microbe B, B can develop various defense mechanisms. Firstly, it can produce an enzyme which inactivates the antibiotic {4}. Secondly, the antibiotic can be recognized by an efflux pump, by which it is secreted from the cell before it can do much harm {5}. Finally, the receiving microbe can alter its target in such a way that the antibiotic is not recognized any longer {6}. For further explanation, see the section titled “Defense strategies of pathogens”.