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Transcript
Stomatal Responses to Pathogens Plants must undergo photosynthesis to produce their own energy. Crucial to the photosynthetic process is gas exchange. The plant requires CO2, and gives off O2 throughout the sugar production pathway, most actively during the daytime hours when there is an abundance of sunlight. The plant will facilitate gas exchange through small pores on the undersurface of its leaves, called stomata. Two specialized cells known as guard cells, which regulate opening and closing, surround each stoma. Guard cells respond to various abiotic cues in their control of the size of the opening. For example, during the day, when photosynthesis is occurring, the stomata will be open to allow for gas exchange. However, at night, when the lack of sunlight halts photosynthesis, the guard cells will close the stomata to prevent water loss. Turgor pressure of the guard cells (regulated by osmotic uptake of water) also dictates the stomatal status. A plant that is water-deprived will close its stomata in order to prevent further water loss from the leaves. This occurs as a result of low turgor pressure in the guard cells that causes them to go flaccid and the opening to close. Relative solute concentrations also have an impact on the opening and closing due to the concept of water potential (Reece et al., 2011). Ion and solute flux therefore has a major effect on the status of the stomata. Stomatal pores open when the plasma membrane H+-ATPase of guard cells is allowed to be active. The activity of this proton pump generates a large transmembrane electrochemical gradient that drives the uptake of charged solutes and, as a consequence, water, which causes the guard cells to swell and the pore between them to open. This mechanism can be Travor 1 seen in Figure 1 below, which illustrates some of these key points. Figure 1: Depiction of stomata. A) An electron micrograph of a stoma. B) An open stoma, as a result of water moving into the guard cells due to the water potential gradient. C) A closed stoma, as a result of flaccid guard cells from a net movement of water out of the cells. Image from: http://ap-bio-chsplants.wikispaces.com/Control+of+Stomata Recent studies suggest that plant stomata also respond to biotic cues. For example, plants interact with pathogens just as animals do, but clearly in different mechanisms. Major plant pathogens include fungi, bacteria, viruses, and insect pests. Previously it was thought that pathogens infected plants passively, merely taking advantage of open stomata or wounds in the plant’s surface, and that the plants had little in the way of defenses. However, recent studies suggest a more active relationship between the pathogen and the plant. Plants are in fact better adapted for defense than scientists had thought for a long time. It turns out that plants have preformed systems in place to prevent the entrance of pathogens, and then have inducible responses that can also prevent them from spreading (Reece et al., 2011). Travor 2 Preformed defenses include chemical secretions, a Casparian strip in the roots, thick lignified cell walls, and various other generalized defenses that prevent easy access for pathogenic organisms. Other methods of defense include nonspecific-triggered immunity, in response to molecules secreted by the attacking pathogen. These molecular signals perceived by the plant cells are known as pathogen associated molecular patterns (PAMPs), and they induce a response known as PAMP triggered immunity, or PTI (Anderson et al., 2010). These PAMPs are recognized on the part of the plant by pattern recognition receptors, or PRRs, which then induce the PTI response through a signal transduction pathway (Chisholm et al., 2006). Plants with the PRR corresponding to the produced PAMP are able to detect the presence of the pathogen, even at very small concentrations. In many cases, PTI responses involve rapid closure of stomata to prevent the pathogens from entering via those openings (Melotto et al., 2006). Given that the PTI response is widespread among plant genera, the question arises, how do phytopathogens still manage to cause disease? Recent inquiries into this topic have shown that certain pathogens, bacteria in particular, have evolved methods of circumventing the PTI in order to gain access to the plant. The focus is primarily on bacteria as they lack compounds that can degrade plant cell walls, or mechanical means of gaining access that other pests such as fungi or insects may have. Bacteria have developed compounds that specifically inhibit the ability of plants to close their stomata. For example, in their review on the role of stomata in bacterial invasion, (Underwood et al., 2007) mentioned that coronatine produced by several pathovars of P. syringae functions in Travor 3 reopening the stomata of Arabidopsis. This again shows a more active back and forth relationship than researchers previously suspected. There have been various other related studies done that serve to generalize these results to many varieties of plant pathogens (Gudesblat et al., 2009). Additionally, the ability to reopen stomata is seen as an important adaptation that enables the transition from an epiphytic to an endophytic parasitism (Melotto et al., 2008). Some research has been done on the role of proteins that may act in conjunction with the plasma membrane H+-ATPase and have effects on stomatal action. Particularly, (Liu et al., 2009) showed in their study that the protein RIN4 acts in conjunction with that ATPase to regulate stomatal closing during the PTI response. The figure below is from their paper, and illustrates the aforementioned interaction. Figure 2: Model of PAMP induced stomatal closure. RIN4 acts in conjunction with other membrane components and the H+-ATPase to regulate stomatal openings in response to pathogenic attack during the PTI response. A) Virulent pathogens overcome the PTI and induce reopening of stomata. Activation of the H+-ATPase leads to an efflux of H+ ions and a subsequent influx of K+ ions, which then causes water uptake, leading to higher guard cell turgor and opening the stoma. B) RIN4 is a negative regulator of innate immunity. Removal or inactivation of RIN4 inhibits the association between RIN4 and the H+ATPase, keeping it from being activation. The lack of H+ ion efflux prevents the reaction in A, and the stoma stays closed (Liu et al., 2009). Travor 4 Despite these pathogenic adaptations to cause disease through reversal of stomatal closure, induced susceptibility and successful infection is relatively rare. As one would expect, the continued selective pressure on each side has caused a coevolution process to be maintained. This coevolution has led to the development of more specific, and more rapid targeted defense mechanisms by plants against invasion. Plant-pathogen interactions are governed by specific interactions between corresponding sets of genes in the plant (resistance or R genes) and pathogen (avirulence or avr genes). When the corresponding genes are present in both organisms, disease resistance (on the part of the plant) results. If either is absent or switched off, disease results (Dangl and Jones, 2001). This process is known as effector triggered immunity, or ETI. Stomatal closure has been shown to be a part of this response as well (Freeman and Beattie, 2009). When a host plant recognizes the pathogen, often a response known as the hypersensitive response (HR) occurs. This generally includes programmed cell death to limit the spread of the pathogen, and also precedes a systemic response in the rest of the plant, that leads to systemic acquired resistance. Other pathogens, such as fungi, infect plants as well. In their study on the fungal foliar pathogen Cercospora zeaemaydis (Kim et al., 2011) provide the first molecular confirmation that the fungus does not randomly encounter the stomatal pore, but rather exhibits a tropism towards it. However, the exact mechanisms are still unknown, but it appears to be through a gene CRP1. Interestingly, they also found little to no defensive response in the plant cells, indicating that it may not recognize the fungus’s presence. However, another group working with different Travor 5 systems, namely, cereal mildew and rust, found some other intriguing results. Research done in barley by (Prats et al., 2007) found that in these systems, when the R-avr gene interaction causes the hypersensitive response permanent, drastic stomatal dysfunction results: stomata become locked open in response to powdery mildew attack, and locked shut after rust attack. This would of course be a negative cost of conferring disease resistance on these crops. Consequently, this would be an issue in fields that are being treated with new R genes in order to confer better disease resistance. As stated in their article, more research needs to be done on this topic to further understand the mechanisms involved and other potential risks of genetically altering plants. Proper stomatal function is essential to the life of a photosynthesizing plant. Pathogens have evolved various ways to take advantage of these openings in the surface of a leaf as opportunities for endophytic infection. Consequently, plants have in turn developed various methods to prevent pathogens from gaining access. The evolutionary “arms race” then favored pathogenic evolution to develop a mechanism to induce stomatal reopening. This back and forth is a much more active relationship than previously thought, and is a prime example of the pressures of natural selection. Applications of research on how plants regulate their stomata in response to pathogens include agriculture, conservation efforts, and even animal biology. For example, agriculture is a vastly important part of the global economy, and of course it feeds the seven billion people on our planet. Anything that sheds light on how plants respond to pathogens and suggests mechanisms for overcoming virulence will be helpful. This is the focus of many of the genetic engineering efforts Travor 6 currently underway. As for conservation efforts, this research may be of use to some endangered species of plants. Applications to animal biology are less obvious, but if we can shed light on how pathogens infect plants, there will almost certainly be things we learn that can be applied to animals. For these reasons, among many others, stomatal responses to pathogenic invasion is an area of research that merits widespread interest, and funding, so that we may continue to feed a growing, changing world, and cure its diseases. Travor 7 References Anderson J.P., Gleason C.A., Foley R.C., Thrall P.H., Burdon J.B., Singh K.B. (2010) Plants versus pathogens: an evolutionary arms race. Functional Plant Biology 37, 499–512. Chisholm S.T., Coaker G., Day B., Staskawicz B.J. Host-microbe interactions: shaping the evolution of the plant immune response. Cell. 2006 Feb 24;124(4):803-14. Review. PubMed PMID: 16497589. Dangl J.L., Jones J.D. Plant pathogens and integrated defence responses to infection. Nature. 2001 Jun 14;411(6839):826-33. Review. PubMed PMID: 11459065. Freeman B.C., and Beattie G.A. (2009) Bacterial Growth Restriction During Host Resistance to Pseudomonas syringae Is Associated with Leaf Water Loss and Localized Cessation of Vascular Activity in Arabidopsis thaliana. Molecular Plant-Microbe Interactions, 22: 857-867. Gudesblat G.E., Torres P.S., Vojnov A.A. Stomata and pathogens: Warfare at the gates. Plant Signal Behav. 2009 Dec;4(12):1114-6. Review. PubMed PMID: 20514224; PubMed Central PMCID: PMC2819434. Kim H., Ridenour J.B., Dunkle L.D., Bluhm B.H. (2011) Regulation of Stomatal Tropism and Infection by Light in Cercospora zeaemaydis: Evidence for Coordinated Host/Pathogen Responses to Photoperiod? PLoS Pathog 7(7): e1002113. doi:10.1371/journal.ppat.1002113 Liu J., Elmore J.M., Fuglsang A.T., Palmgren M.G., Staskawicz B.J., et al. (2009) RIN4 Functions with Plasma Membrane H+-ATPases to Regulate Stomatal Apertures during Pathogen Attack. PLoS Biol 7(6): e1000139. doi:10.1371/journal.pbio.1000139 Melotto M., Underwood W., He S.Y. Role of stomata in plant innate immunity and foliar bacterial diseases. Annu Rev Phytopathol. 2008;46:101-22. doi: 10.1146/annurev.phyto.121107.104959. Review. PubMed PMID: 18422426; PubMedCentral PMCID: PMC2613263. Melotto M., Underwood W., Koczan J., Nomura K., He S.Y. Plant stomata function in innate immunity against bacterial invasion. Cell. 2006 Sep 8;126(5):969-80. PubMed PMID: 16959575. Prats E., Carver T.L., Gay A.P., Mur L.A. Enemy at the gates: interaction-specific stomatal responses to pathogenic challenge. Plant Signal Behav. 2007 Jul;2(4):275-7. PubMed PMID: 19704679; PubMed Central PMCID: PMC2634148. Travor 8 Reece, Jane B., Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, and Robert B. Jackson. Campbell Biology. 9th ed. San Francisco: Pearson Benjamin Cummings, 2011. Print. pp. 822-824. Underwood W, Melotto M, He S.Y. Role of plant stomata in bacterial invasion. Cell Microbiol. 2007 Jul;9(7):1621-9. Epub 2007 Apr 5. Review. PubMed PMID: 17419713. 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