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Hendrich, C. G.

Publications and source records attributed to Hendrich, C. G..

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Lectins and polysaccharide EPS I have flow-responsive roles in the attachment and biofilm mechanics of plant pathogenic Ralstonia

Bacterial biofilm formation and attachment to hosts are mediated by carbohydrate- binding lectins, exopolysaccharides, and their interactions in the extracellular matrix (ECM). During tomato infection Ralstonia pseudosolanacearum (Rps) GMI1000 highly expresses three lectins: LecM, LecF, and LecX. The latter two are uncharacterized. We evaluated the roles in bacterial wilt disease of LecF, a fucose-binding lectin, LecX, a xylose-binding lectin, and the Rps exopolysaccharide EPS I. Interestingly, single and double lectin mutants attached to tomato roots better and formed more biofilm under static conditions in vitro. Consistent with this finding, static bacterial aggregation was suppressed by heterologous expression of lecFGMI1000 and lecXGMI1000 in other Ralstonia strains that naturally lack these lectins. Crude ECM from a {Delta}lecF/X double mutant was more adhesive than the wild-type ECM, and LecF and LecX increased Rps attachment to ECM. The enhanced adhesiveness of the {Delta}lecF/X ECM could explain the double mutants hyper-attachment in static conditions. Unexpectedly, mutating lectins decreased Rps attachment and biofilm viscosity under shear stress, which this pathogen experiences in plant xylem. LecF, LecX, and EPS I were all essential for biofilm development in xylem fluid flowing through cellulose-coated microfluidic channels. These results suggest that under shear stress, LecF and LecX increase Rps attachment by interacting with the ECM and plant cell wall components like cellulose. In static conditions such as on root surfaces and in clogged xylem vessels, the same lectins suppress attachment to facilitate pathogen dispersal. Thus, Rps lectins have a dual biological function that depends on the physical environment. Author SummaryBacterial wilt diseases caused by Ralstonia species inflict significant losses on diverse, globally important agricultural plants. The pathogen first colonizes roots and ultimately the water-transporting xylem. There it attaches to host cell walls and other bacterial cells to form biofilms that eventually block xylem vessels and disrupt sap flow. It is not well known how Ralstonia spp. modulate attachment, but precise control of both attachment and dispersal is critical for successful host colonization over the disease cycle. Excessive adhesion could trap bacteria in a toxic or nutrient-depleted environment. Conversely, insufficient adhesion in a flowing environment could displace bacteria from an optimal niche. We provide evidence of dual, environment-specific roles of carbohydrate-binding lectins and exopolysaccharide EPS I in Ralstonia pseudosolanacearum (Rps) attachment. In static conditions, which Rps experiences on a host root, two lectins suppress bacterial aggregation and adhesion to roots. However, in flowing conditions, which Rps experiences in healthy xylem vessels, the same two lectins and EPS I are essential for biofilm development. The lectins increase the biofilm viscosity and support colony structural integrity, likely by interacting with polysaccharides in the biofilm matrix. This novel multifunctionality of bacterial lectins reveals how pathogens adapt to a physically dynamic host environment.

microbiology↗

NorA, HmpX, and NorB cooperate to reduce NO toxicity during denitrification and plant pathogenesis in Ralstonia solanacearum

Ralstonia solanacearum, which causes bacterial wilt disease of many crops, needs denitrifying respiration to succeed inside its plant host. In the hypoxic environment of plant xylem vessels this pathogen confronts toxic oxidative radicals like nitric oxide (NO), which is generated by both bacterial denitrification and host defenses. R. solanacearum has multiple distinct mechanisms that could mitigate this stress, including Repair of Iron Cluster (RIC) homolog NorA, nitric oxide reductase NorB, and flavohaemoglobin HmpX. During denitrification and tomato pathogenesis and in response to exogenous NO, R. solanacearum upregulated norA, norB, and hmpX. Single mutants lacking{Delta} norB, {Delta}norA, or{Delta} hmpX increased expression of many iron and sulfur metabolism genes, suggesting that losing even one NO detoxification system demands metabolic compensation. Single mutants suffered only moderate fitness reductions in host plants, possibly because they upregulated their remaining detoxification genes. However,{Delta} norA/norB, {Delta}norB/hmpX, and{Delta} norA/hmpX double mutants grew poorly in denitrifying culture and in planta. Loss of norA, norB, and hmpX may be lethal, since the methods used to construct the double mutants did not generate a triple mutant. Aconitase activity assays showed that NorA, HmpX and especially NorB are important for maintaining iron-sulfur cluster proteins. Additionally, plant defense genes were upregulated in tomatoes infected with the NO-overproducing{Delta} norB mutant, suggesting that bacterial detoxification of NO reduces pathogen visibility. Thus, R. solanacearums three NO detoxification systems each contribute to and are collectively essential for overcoming metabolic oxidative stress during denitrification, for virulence and growth in tomato, and for evading host plant defenses. ImportanceThe soilborne plant pathogen Ralstonia solanacearum (Rs) causes bacterial wilt, a serious and widespread threat to global food security. Rs is metabolically adapted to low oxygen conditions, using denitrifying respiration to survive in the host and cause disease. However, bacterial denitrification and host defenses generate nitric oxide (NO), which is toxic and also alters signaling pathways in both plants and the pathogen. Rs mitigates NO with a trio of mechanistically distinct proteins: NO-reductase NorB, Repair of Iron Centers NorA, and oxidoreductase HmpX. This redundancy, together with analysis of mutants and in-planta dual transcriptomes, indicates that maintaining low NO levels is integral to Rs fitness in tomatoes (because NO damages iron-cluster proteins) and to evading host recognition (because bacterially produced NO can trigger plant defenses).

microbiology↗

Nitric Oxide Regulates the Ralstonia solanacearum Type 3 Secretion System

Ralstonia solancearum causes bacterial wilt disease on diverse plant hosts. R. solanacearum cells enter a host from soil or infested water through the roots, then multiply and spread in the water-transporting xylem vessels. Despite the low nutrient content of xylem sap, R. solanacearum grows very well inside the host, using denitrification to respire in this hypoxic environment. R. solanacearum growth in planta also depends on the successful deployment of protein effectors into host cells via a Type III Secretion System (T3SS). The T3SS is absolutely required for R. solanacearum virulence, but it is metabolically costly and can trigger host defenses. Thus, the pathogens success depends on optimized regulation of the T3SS. We found that a byproduct of denitrification, the toxic free-radical nitric oxide (NO), positively regulates the R. solanacearum T3SS both in vitro and in planta. Using chemical treatments and R. solanacearum mutants with altered NO levels, we show that the expression of a key T3SS regulator is induced by NO in culture. Analyzing the transcriptome of R. solanacearum responding to varying levels of NO both in culture and in planta revealed that the T3SS and effectors were broadly upregulated with increasing levels of NO. This regulation was specific to the T3SS and was not shared by other stressors. Our results suggest that R. solanacearum experiences an NO-rich environment in the plant host and may use this NO as a signal to activate T3SS during infection.

microbiology↗

Roq1 confers resistance to Xanthomonas, Pseudomonas syringae and Ralstonia solanacearum in tomato

Xanthomonas species, Pseudomonas syringae and Ralstonia solanacearum are bacterial plant pathogens that cause significant yield loss in many crop species. Current control methods for these pathogens are insufficient but there is significant potential for generating new disease-resistant crop varieties. Plant immune receptors encoded by nucleotide-binding, leucine-rich repeat (NLR) genes typically confer resistance to pathogens that produce a cognate elicitor, often an effector protein secreted by the pathogen to promote virulence. The diverse sequence and presence / absence variation of pathogen effector proteins within and between pathogen species usually limits the utility of a single NLR gene to protecting a plant from a single pathogen species or particular strains. The NLR protein Recognition of XopQ 1 (Roq1) was recently identified from the plant Nicotiana benthamiana and mediates perception of the effector proteins XopQ and HopQ1 from Xanthomonas and P. syringae respectively. Unlike most recognized effectors, alleles of XopQ/HopQ1 are highly conserved and present in most plant pathogenic strains of Xanthomonas and P. syringae. A homolog of XopQ/HopQ1, named RipB, is present in many R. solanacearum strains. We found that Roq1 also mediates perception of RipB and confers immunity to Xanthomonas, P. syringae, and R. solanacearum when expressed in tomato. Strong resistance to Xanthomonas perforans was observed in three seasons of field trials with both natural and artificial inoculation. The Roq1 gene can therefore be used to provide safe, economical and effective control of these pathogens in tomato and other crop species and reduce or eliminate the need for traditional chemical controls. SummaryA single immune receptor expressed in tomato confers strong resistance to three different bacterial diseases.

plant biology↗