Xanthomonas vesicatoria virulence factors involved in early stages of bacterial spot development in tomato

2018 ◽  
Vol 67 (9) ◽  
pp. 1936-1943 ◽  
Author(s):  
V. Felipe ◽  
A. M. Romero ◽  
M. S. Montecchia ◽  
A. A. Vojnov ◽  
M. I. Bianco ◽  
...  
1966 ◽  
Vol 46 (5) ◽  
pp. 525-530 ◽  
Author(s):  
P. K. Basu

Bacterial canker, spot, and speck of tomatoes (Lycopersicon esculentum Mill.) caused by Corynebacterium michiganense (E.F.S.) Jensen, Xanthomonas vesicatoria (Doidge) Dows., and Pseudomonas tomato (Okabe) Burk., respectively, were symptomatologically differentiated on 2- to 3-week-old spray-inoculated seedlings only under conditions of 87–97% relative humidity and 23–28 °C temperature. The numerical threshold of infection of both C. michiganense and P. tomato was 1 × 106 cells/ml and that of X. vesicatoria was 1 × 103 cells/ml. Preinoculation host injury and an inoculum concentration of 1 × 108 cells/ml were most favorable for high incidence of the diseases.Characteristic symptoms incited by the canker organism were (1) small whitish pimple-like spots developing into raised blister-like lesions on the lamina, (2) elongated swellings on veins, and (3) cankers on the hypocotyl. The distinctive symptoms of the bacterial spot disease were (1) small greenish-yellow to brown leaf spots, (2) large yellow blotches becoming necrotic and producing a severe blight effect on leaves, and (3) light-brown streaks on the hypocotyl. The distinguishing symptoms of the speck disease were discrete dark-brown spots and occasional marginal necrotic areas on leaves and cotyledons. On cotyledons, both C. michiganense and X. vesicatoria produced identical minute whitish flaky spots often with greenish centers. Sometimes these spots coalesced and resulted in wrinkling of the surface of the cotyledon.


2020 ◽  
Vol 9 (16) ◽  
Author(s):  
Marcela Ríos-Sandoval ◽  
Evangelina Esmeralda Quiñones-Aguilar ◽  
Guillermo Alejandro Solís-Sánchez ◽  
Jhony Navat Enríquez-Vara ◽  
Gabriel Rincón-Enríquez

Bacteriophage ΦXaF18 infects Xanthomonas vesicatoria, which is the causal agent of bacterial spot in tomato (Solanum lycopersicum L.) and pepper (Capsicum annuum L.). In this announcement, we present the complete genome of X. vesicatoria bacteriophage ΦXaF18, a 47,407-bp genome with 67 protein-coding genes.


2018 ◽  
Author(s):  
Liting Wan ◽  
Jian Lin ◽  
Hongwen Du ◽  
Alejandra Bravo ◽  
Mario Soberón ◽  
...  

ABSTRACTPathogenic bacteria use different strategies to infect their hosts including the simultaneous production of pore forming toxins and several virulence factors that help to synergize their pathogenic effects. However, how the pathogenic bacteria are able to complete their life cycle and break out the host intestinal barrier is poorly understood. The infectious cycle ofBacillus thuringiensis(Bt) bacterium inCaenorhabditis elegansis a powerful model system to study the early stages of the infection process. Bt produces Cry pore-forming toxins during the sporulation phase that are key virulence factors involved in Bt pathogenesis. Here we show that during the early stages of infection, the Cry toxins disrupt the midgut epithelial tissue allowing the germination of spores. The vegetative Bt cells then trigger a quorum sensing response that is activated by PlcR regulator resulting in production of different virulence factors, such as the metalloproteinases ColB and Bmp1, that besides Cry toxins are necessary to disrupt the nematode epithelial junctions causing efficient bacterial host infection and dead of the nematode. Overall our work describes a novel mechanism for Bt infection, targeting the epithelial junctions of its host midgut cells.Author summaryThe entomopathogenic bacteriaBacillus thuringiensis(Bt) are used worldwide as biopesticides due to their insecticidal properties. Crystal proteins (Cry) produced by Bt during the sporulation phase of growth are mainly responsible for their insecticidal properties. The infection process of Bt includes three successive steps, virulence, necrotrophic, and sporulation processes. During the virulence process, after ingestion by the susceptible hosts, the Cry toxins form pores in the apical membrane of intestinal cells, inducing favorable conditions for bacterial spore germination. Vegetative bacteria multiply in the host and coordinate their behavior by using the quorum sensor regulator PlcR, which leads to the production of virulence factors allowing the bacteria to kill the host. However, how the bacteria are able to disrupt the host intestinal barrier during the early stages of infection remains unknown. Here we show that Bt employs the nematicidal Cry toxins and additional virulence factors controlled by the PlcR regulon to disrupt the intestinal epithelial junctions ofC. elegansat the early stages of infection allowing that Bt bacteria complete its life cycle in the worms. Our work provides new insights into the pathogenesis of Bt, and highlights the importance of breaking down host epithelial junctions for a successful infection, a similar mechanism could be used by other pathogens-host interactions since epithelial junctions are conserved structures from insects to mammals.


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