Transcriptome Analysis Reveals New Insights into the Bacterial Wilt Resistance Mechanism Mediated by Silicon in Tomato

Abstract

Bacterial wilt is a devastating disease of tomato caused by soilborne pathogenic bacterium Ralstonia solanacearum. Previous studies found that silicon (Si) can increase tomato resistance against R. solanacearum, but the exact molecular mechanism remains unclear. RNA sequencing (RNA-Seq) technology was used to investigate the dynamic changes of root transcriptome profiles between Si-treated (+Si) and untreated (−Si) tomato plants at 1, 3, and 7 days post-inoculation with R. solanacearum. The contents of salicylic acid (SA), ethylene (ET), and jasmonic acid (JA) and the activity of defense-related enzymes in roots of tomato in different treatments were also determined. The burst of ET production in roots was delayed, and SA and JA contents were altered in Si treatment. The transcriptional response to R. solanacearum infection of the +Si plants was quicker than that of the untreated plants. The expression levels of differentially-expressed genes involved in pathogen-associated molecular pattern-triggered immunity (PTI), oxidation resistance, and water-deficit stress tolerance were upregulated in the Si-treated plants. Multiple hormone-related genes were differentially expressed in the Si-treated plants. Si-mediated resistance involves mechanisms other than SA- and JA/ET-mediated stress responses. We propose that Si-mediated tomato resistance to R. solanacearum is associated with activated PTI-related responses and enhanced disease resistance and tolerance via several signaling pathways. Such pathways are mediated by multiple hormones (e.g., SA, JA, ET, and auxin), leading to diminished adverse effects (e.g., senescence, water-deficit, salinity and oxidative stress) normally caused by R. solanacearum infection. This finding will provide an important basis to further characterize the role of Si in enhancing plant resistance against biotic stress.

Role of Silicon in Mitigation of Heavy Metal Stresses in Crop Plants

“…However, many plant species particularly belonging to family brassicaceae [69], solanaceae [70], and Linaceae [71] does not carry any Si-transporter (NIP-III Aquaporin) and are known as poor Si accumulators. However, several reports suggesting Si derived benefits in such species make it more difficult to understand the molecular consequences [72,73]. So far, the Si-mediated mechanisms for the reduction of metal toxicity are less understood at the genetic and molecular levels.…”

Silicification of Root Tissues

“…These biotic stressors cause retardation of growth, yield production, and shortening of lifespan in hosts. According to the experimental studies, Si in plant roots can alleviate the stress after bacterial [140][141][142], fungal [143][144][145], insect [146,147], nematode [148,149], and plant [150,151] attack, but also stress from auto-toxicity of the same plant [152]. The level of its beneficial effect is Si concentration dependent.…”

“…They improved the soil urease and soil acid phosphatase activity and caused a decrease in the numbers of wilt causing bacteria in both the soil [162] and the plants [156]. It has been shown that Si-mediated enhanced resistance and tolerance in tomato to R. solanacearum is associated also with differential expression of genes involved in pathogen-associated molecular pattern-triggered immunity via modification of signaling pathways and energy metabolism [141,142]. Coconut palms (Cocos nucifera) infected by phytoplasma that causes root wilt were able to influence the rhizosphere via secretion of compounds that promote beneficial microorganisms, such as N 2 -fixers, silicate solubilizers, and actinomycetes.…”

Effects of Jasmonic Acid in ER Stress and Unfolded Protein Response in Tomato Plants

“…Rapid changes in JA levels in the infected or damaged organs could be crucial for the plants to survive [35,38,39]. Several authors proved that JA accumulation and JA-mediated gene expression occur within several hours after the pathogen infection [65][66][67][68]. The results of Pozo et al [69] showed the transcript levels of the JA marker Lipoxygenase2 (LOX2) started to rise at 1 h after exogenous 50 mM MeJA treatment and reached the maximum at 6 h, but it significantly decreased after 12 h. Based on these observations, the effects of JA at the 6 th hour were selected to investigate the physiological role of JA under ER stress in more detail.…”