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Living organisms have evolved the ability to perceive and respond to light of different wavelengths within the visible spectrum by the generation of photoreceptor proteins. Recent studies revealed the participation of these proteins in the virulence of plant pathogenic bacteria. Pseudomonas syringae pv. tomato DC3000 (Pto) is responsible for the bacterial speck, which affects tomato crops. Pto genome contains two genes encoding red/far-red light photoreceptors (BphP1: PSPTO_1902 and BphP2: PSPTO_2652). This work demonstrates the participation of Pto phytochromes and light in the bacterial physiology and during the interaction with tomato plants. We found that Pto phytochromes are implicated in the control of some features related with the bacteria capability to enter into the plant apoplast and cause bacterial speck disease, such as motility, biofilm formation, adhesion and emulsification capability. Red light and bacteriophytochromes are important during the early colonization stage of tomato phyllosphere, affecting Pto virulence. In addition, the development of disease symptoms in infiltrated leaflets is affected by light, which may be the consequence of type-two secretion system regulation.

Bacterial wilt disease caused by Ralstonia solanacearum affects a wide variety of crops, including tomatoes. Novel natural products and organisms offer opportunities for innovation in agroindustry as an alternative way to pest and pathogen controls. Gluconacetobacter diazotrophicus Pal5 (Gd) belongs to PGPBEs (Plant-Growth-Promoting Bacterial Endophytes), which facilitate plant growth via phytostimulation, biofertilization and biocontrol. In this study Rio Grande tomato seedlings were inoculated with Gd to test its ability to colonize them and its protective potential against the phytopathogen Ralstonia solanacearum A21 (Rso). Gd root and stem colonization of tomato seedlings were determined. Stem height was markedly affected by the inoculation with Gd after 80 dpi and a set of biochemical and anatomical structural changes in root, stem and leaves were triggered. The resistance mechanisms elicited in the plant after inoculation with the endophytic bacteria involved reinforcement of the cell walls in the root vascular cylinder and stem vascular bundles, with the presence of an augmented number of contact cells with dense cellular content, probably pectins, lignin and tannins. Roots and stems presented thicker and more lignified xylem vessel walls. These plants showed statistically significant differences with mock inoculated plants in several quantitative variables, such as area of the xylem vessels in root and stem. Biocontrol assays without Gd showed wilting at 9 dpi with Rso. Histological analysis showed bacteria cells filled xylem vessels and dispersal through tissue degradation. In contrast, plants with Gd remained asymptomatic and phytopathogen colonization was observed to a lesser extent in the stem and root. Anatomical changes primed by Gd were enhanced upon Rso infection and the tyloses process appeared. Therefore, Gd primes the resistance mechanism in Rio Grande tomato plants significantly reducing bacterial wilt caused by Rso.

Light modulates almost every aspect of plant physiology, including plant-pathogen interactions. Among these, the hypersensitive response (HR) of plants to pathogens is characterized by a rapid and localized programmed cell death (PCD), which is critical to restrict the spread of pathogens from the infection site. The aim of this work was to study the role of light in the interaction between Pseudomonas syringae pv. tomato DC3000 (Pto DC3000) and non-host tobacco plants. To this end, we examined the HR under different light treatments (white and red light) by using a range of well-established markers of PCD. The alterations found at the cellular level included: i) loss of membrane integrity and nuclei, ii) RuBisCo and DNA degradation, and iii) changes in nuclease profiles and accumulation of cysteine proteinases. Our results suggest that red light plays a role during the HR of tobacco plants to Pto DC3000 infection, delaying the PCD process.