Text of P P.s. tabaci Null P.s. syringae Hrp - (TTSS) mutant HR P.s. syringae >50 pathovars based on host...
Tobacco Bean Tomato hosts tomato and Arabidopsis Hrp type III secretion system (TTSS) This is a slide depicting the different macro and microscopic reactions that Pseudomonas has in plants. Sepcifically, the tobacco plant. On the left most panel, macroscopically, we see disease, and this is Pathovar tabaci infecting its natural host tobacco. Microscopically the bacteria thriving,as you see in this coinfocal image taken by Wen-Ling Deng. – The bacteria are labelled with GFP, and the red is autofluorescent. AS you can see the bacteria are extracellular – they thrive in the intercellular space of plant cells known as the apoplast. In the middle, we have infiltration of P. syringae, a bean pathogen on a nonhost, tobacco. Macroscopically we see the hypersensitive response, a localized programmed cell death that restricts the pathogen from infecting the whole plant. The orange in this panel are phenolic compounds which make up part of a chemical burst the plant induces when it recognizes a pathogen. this HR occurs because the bacteria is delivering proteins into the plant cell that the plant recognizes through its defense system Finally we have a bean pathogen mutant that does not cause HR on tobacco, and this is because the mechanism by which it delivers proteins into the plant cell is not functional dues to a mutation, hrcC, in the delivery apparatus. The plant does not recognize this bacteria, and the bacteria cannot thrive in this environment becaseu it cannot put viruelnce proteins into the plant. The system that delivers proteins is encoded by genes in the hrp/hrc cluster. -starting from the left: tabaci causes disease on tobacc; the plant does not recognize the pathogen until it is too late. -Pseduomonas syrngae can cause two types of reactions on plants: a hypersensitive response (HR) or disease -in the HR, the plant immediately recognizes the pathogen, and induces a. --secretion mutant cannot cause HR -Red is autofluorescnence of chlorplasts -P the bacteria is huge!! ROBIN BUELL - TIGR ALAN COLLMER Cornell JIM ALFANO - Nebraska XIAOYAN TANG - Kansas ARUN CHATTERJEE - Missouri GREG MARTIN - BTI SANDY LAZAROWITZ - Cornell TERRY DELANEY - Cornell Experimental biology Computational biology Functional Genomics of the Interactions of Tomato and Pseudomonas syringae pv tomato DC3000 http://pseudomonas-syringae.org http://monod.cornell.edu Molecular/cellular determinants of plant- bacterium interactions complementary approaches to total biology use red and blue arrows 2e Virulence-related ORFs newly found by Hidden Markov Model search of P.s. tomato DC3000 genome Fouts, Abramovitch, Alfano, Baldo, Buell, Cartinhour, Chatterjee, D'Ascenzo, Gwinn, Lazarowitz, Lin, Martin, Rehm, Schneider, van Dijk, Tang, and Collmer. 2002. Proc. Natl. Acad. Sci. USA 99:2275-2280. ORF BLAST found effectors but note: 6.5 Mb 5,763 ORFs 7% of genome mobile genetic elements 298 ORFs implicated in virulence, including 38 confirmed TTSS substrates pDC3000A carries at least 4 avr/hop genes The problem of genomewide identification of Hrp effector genes in P. syringae HR avr hrp hrp HR hrp R avr R R HR hrp R hrp Disease -35 -10 All known avr genes preceded by "Hrp box" promoters Secretion/injection "Hops" testable, but slow classic method that keen and staskawicz pioneered in 1984 but not useful for genomewide, systematic effector mining explain hop and effector (copy animal workers) so that is where our effector mining began EEL CEL tRNAleu orf4 orf3 orf2 tnpA orf1 orf8 orf1 avrE avrF orf3 orf4 hrpW orf5 orf6 orf7 avrPto avrPtoB mini-Tn5gus tagging of genes activated by HrpL alternative sigma factor hrp hrpL tRNAleu Fouts, Abramovitch, Alfano, Baldo, Buell, Cartinhour, Chatterjee, D'Ascenzo, Gwinn, Lazarowitz, Lin, Martin, Rehm, Schneider, van Dijk, Tang, and Collmer. 2002. Proc. Natl. Acad. Sci. USA 99:2275-2280. EEL CEL here is hrp pai a c e d b Violations: Violations: none ORF1-'AvrRpt2 ORF2-'AvrRpt2 The rules successfully predict which unknown ORFs encode effectors Petnicki-Ocwieja, Schneider, Tam, Chancey, Shan, Jamir, Schechter, Buell, Tang, Collmer, and Alfano. 2002. Proc. Natl. Acad. Sci. USA 99:7652-7657. ORF1-avrPphF M K N A F D L L V E G L A K D Y N M P P L P D K K H I D E V Y C F E F Q S G M N ORF2-avrPphF M G N I C G T S G S R H V Y S P S H T Q R I T S A P S T S T H V G G D T L T S I a. Position 3 or 4 is I, V, or L, and between this residue and the starting M is a polar, positively charged or P residue b. No MIVLFYW residues appear in position 5. c. No D or E in first 12 residues. d. The first 50 residues are amphipathic, rich in polar amino acids, and never have more than 3 of the MIVLFYW group in a row. e. No C between positions 5 and 50
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