Phytoplasma

Phytoplasma
Phyllody induced by phytoplasma infection on a coneflower (Echinacea purpurea).
Scientific classification
Domain: Bacteria
Phylum: Tenericutes
Class: Mollicutes
Order: Acholeplasmatales
Family: Acholeplasmataceae
Genus: "Candidatus Phytoplasma"
Species

"Ca. Phytoplasma allocasuarinae"
"Ca. Phytoplasma americanum"
"Ca. Phytoplasma asteris"
"Ca. Phytoplasma aurantifolia"
"Ca. Phytoplasma australiense"
"Ca. Phytoplasma balanitae"
"Ca. Phytoplasma brasiliense"
"Ca. Phytoplasma caricae"
"Ca. Phytoplasma castaneae"
"Ca. Phytoplasma cirsii"
"Ca. Phytoplasma cocosnigeriae"
"Ca. Phytoplasma cocostanzaniae"
"Ca. Phytoplasma convolvuli"
"Ca. Phytoplasma costaricanum"
"Ca. Phytoplasma cynodontis"
"Ca. Phytoplasma fragariae"
"Ca. Phytoplasma fraxini"
"Ca. Phytoplasma graminis"
"Ca. Phytoplasma hispanicum"
"Ca. Phytoplasma japonicum"
"Ca. Phytoplasma luffae"
"Ca. Phytoplasma lycopersici"
"Ca. Phytoplasma malasianum"
"Ca. Phytoplasma mali"
"Ca. Phytoplasma meliae"
"Ca. Phytoplasma omanense"
"Ca. Phytoplasma oryzae"
"Ca. Phytoplasma palmae"
"Ca. Phytoplasma palmicola"
"Ca. Phytoplasma phoenicium"
"Ca. Phytoplasma pini"
"Ca. Phytoplasma pruni"
"Ca. Phytoplasma prunorum"
"Ca. Phytoplasma pyri"
"Ca. Phytoplasma rhamni"
"Ca. Phytoplasma rubi"
"Ca. Phytoplasma solani"
"Ca. Phytoplasma spartii"
"Ca. Phytoplasma sudamericanum"
"Ca. Phytoplasma tamaricis"
"Ca. Phytoplasma trifolii"
"Ca. Phytoplasma ulmi"
"Ca. Phytoplasma vitis"
"Ca. Phytoplasma ziziphi"

(as of September 2016)

Phytoplasmas are specialised bacteria that are obligate parasites of plant phloem tissue and transmitting insects (vectors). They were discovered by scientists in 1967 and were named mycoplasma-like organisms or MLOs.[1] Since their discovery, phytoplasmas have resisted all attempts to be cultured in vitro in any cell free media, hence routine cultivation in artificial media is still to be established. Nevertheless, still under trial stage, phytoplasma growth in specific artificial media has recently been shown.[2] They are characterised by their lack of a cell wall, a pleiomorphic or filamentous shape, normally with a diameter less than 1 μm, and their very small genomes.

Phytoplasmas are pathogens of agriculturally important plants, including coconut, sugarcane, and sandalwood, causing a wide variety of symptoms that range from mild yellowing to death of infected plants. They are most prevalent in tropical and subtropical regions of the world. They require a vector to be transmitted from plant to plant, and this normally takes the form of sap-sucking insects such as leaf hoppers, in which they are also able to survive and replicate.

History

References to diseases now known to be caused by phytoplasmas occurred as far back as 1603 for mulberry dwarf disease in Japan.[3] Such diseases were originally thought to be caused by viruses, which, like phytoplasmas, require insect vectors, cannot be cultured, and have some symptom similarity.[4] In 1967, phytoplasmas were discovered in ultrathin sections of plant phloem tissue and named mycoplasma-like organisms (MLOs), because they physically resembled mycoplasmas[1] The organisms were renamed phytoplasmas in 1994, at the 10th Congress of The International Organization for Mycoplasmology.[4]

Morphology

Being Mollicutes, a phytoplasma lacks a cell wall and instead is bound by a triple-layered membrane.[5] The cell membranes of all phytoplasmas studied so far usually contain a single immunodominant protein (of unknown function) that makes up the majority of the protein content of the cell membrane.[6] The typical phytoplasma exhibits a pleiomorphic or filamentous shape and is less than 1 μm in diameter. As prokaryotes, phytoplasmas' DNA is found throughout the cytoplasm, rather than being concentrated in a nucleus.

Symptoms

A common symptom caused by phytoplasma infection is phyllody, the production of leaf-like structures in place of flowers. Evidence suggests the phytoplasma downregulates a gene involved in petal formation (AP3 and its orthologues) and genes involved in the maintenance of the apical meristem (Wus and CLV1).[7] Other symptoms, such as the yellowing of leaves, are thought to be caused by the phytoplasma's presence in the phloem, affecting its function and changing the transport of carbohydrates.[8]

Phytoplasma-infected plants may also suffer from virescence, the development of green flowers due to the loss of pigment in the petal cells.[9] Phytoplasma-harboring plants which are able to flower may nevertheless be sterile. A phytoplasma effector protein (SAP54) has been identified as inducing symptoms of virescence and phyllody when expressed in plants.

Many plants infected by phytoplasmas gain a bushy or "witches' broom" appearance due to changes in their normal growth patterns. Most plants show apical dominance, but phytoplasma infection can cause the proliferation of auxiliary (side) shoots and an increase in size of the internodes.[9] Such symptoms are actually useful in the commercial production of poinsettias. The infection produces more axillary shoots, which enables production of poinsettia plants that have more than one flower.[10]

Phytoplasmas may cause many other symptoms that are induced because of the stress placed on the plant by infection rather than specific pathogenicity of the phytoplasma. Photosynthesis, especially photosystem II, is inhibited in many phytoplasma-infected plants.[5] Phytoplasma-infected plants often show yellowing which is caused by the breakdown of chlorophyll, the biosynthesis of which is also inhibited.[5]

Effector (virulence) proteins

Many plant pathogens produce virulence factors (or effectors) that modulate or interfere with normal host processes in a way that is beneficial to the pathogen. [11] TCP transcription factors normally regulate plant development and control the expression of lipoxygenase (LOX) genes that are required for the biosynthesis of jasmonate. In infected Arabidopsis plants (and plants that express SAP11 transgenically), jasmonate levels are decreased. The downregulation of jasmonate production is beneficial to the phytoplasma because jasmonate is involved in plant defence against herbivorous insects such as leafhoppers, and leafhoppers have been shown to lay more eggs on AY-WB-infected plants at least in part because of SAP11. For example, the leafhopper Macrosteles quadrilineatus lays 30% more eggs on plants that express SAP11 transgenically, and 60% more eggs on plants infected with AY-WB.[11] Phytoplasmas cannot survive in the external environment and are dependent upon insects such as leafhoppers for transmission to new (healthy) plants. Thus, by interfering with jasmonate production, SAP11 'encourages' leafhoppers to lay more eggs on phytoplasma-infected plants, thereby ensuring that newly hatching leafhopper nymphs feed upon infected plants and become vectors for the bacteria.


Transmission

Movement between plants

Phytoplasmas are mainly spread by insects of the families Cicadellidea (leafhoppers), Fulgoridea (planthoppers), and Psyllidae (jumping plant lice) ,[12] which feed on the phloem tissues of infected plants, picking up the phytoplasmas and transmitting them to the next plant on which they feed. So, the host range of phytoplasmas is strongly dependent upon its insect vector. Phytoplasmas contain a major antigenic protein that makes up the majority of their cell surface proteins. This protein has been shown to interact with insect microfilament complexes and is believed to be the determining factor in insect-phytoplasma interaction.[13] Phytoplasmas may overwinter in insect vectors or perennial plants. Phytoplasmas can have varying effects on their insect hosts; examples of both reduced and increased fitness have been seen.[14]

Phytoplasmas enter the insect's body through the stylet, move through the intestine, and are then absorbed into the haemolymph.[14] From there they proceed to colonise the salivary glands, a process that can take up to three weeks.[14] Once established, phytoplasmas are found in most major organs of an infected insect host. The time between being taken up by the insect and reaching an infectious titre in the salivary glands is called the latency period.[14]

Phytoplasmas can also be spread via dodders (Cuscuta)[15] or vegetative propagation such as the grafting of a piece of infected plant onto a healthy plant.

Movement within plants

Phytoplasmas are able to move within the phloem from source to sink, and they are able to pass through sieve tube elements. But since they spread more slowly than solutes, for this and other reasons, movement by passive translocation is not supported.[16]

Detection and diagnosis

Before molecular techniques were developed, the diagnosis of phytoplasma diseases was difficult because they could not be cultured. Thus, classical diagnostic techniques, such as observation of symptoms, were used. Ultrathin sections of the phloem tissue from suspected phytoplasma-infected plants would also be examined for their presence.[1] Treating infected plants with antibiotics such as tetracycline to see if this cured the plant was another diagnostic technique employed.

Molecular diagnostic techniques for the detection of phytoplasma began to emerge in the 1980s and included ELISA-based methods. In the early 1990s, polymerase chain reaction-based methods were developed that were far more sensitive than those that used ELISA, and RFLP analysis allowed the accurate identification of different strains and species of phytoplasma.[17]

More recently, techniques have been developed that allow for assessment of the level of infection. Both quantitative PCR and bioimaging have been shown to be effective methods of quantifying the titre of phytoplasmas within the plant.[16]

Control

Phytoplasmas are normally controlled by the breeding and planting of disease resistant varieties of crops (believed to the most economically viable option) and by the control of the insect vector.[9]

Tissue culture can be used to produce clones of phytoplasma-infected plants that are healthy. The chances of gaining healthy plants in this manner can be enhanced by the use of cryotherapy, freezing the plant samples in liquid nitrogen, before using them for tissue culture.[18]

Work has also been carried out investigating the effectiveness of plantibodies targeted against phytoplasmas.[19]

Tetracyclines are bacteriostatic to phytoplasmas.[20] However, without continuous use of the antibiotic, disease symptoms reappear. Thus, tetracycline is not a viable control agent in agriculture, but it is used to protect ornamental coconut trees.[21]

Genetics

The genomes of three phytoplasmas have been sequenced: aster yellows witches broom,[22] onion yellows (Ca. Phytoplasma asteris)[23] and Ca. Phytoplasma australiense[24] Phytoplasmas have very small genomes, which also have extremely low levels of the nucleotides G and C, sometimes as little as 23%, which is thought to be the threshold for a viable genome.[25] In fact Bermuda grass white leaf phytoplasma has a genome size of just 530 kb, one of the smallest known genomes of living organisms.[26] Larger phytoplasma genomes are around 1350 kb. The small genome size associated with phytoplasmas is due to their being the product of reductive evolution from Bacillus/Clostridium ancestors. They have lost 75% or more of their original genes, so can no longer survive outside of insects or plant phloem. Some phytoplasmas contain extrachromosomal DNA such as plasmids.[27]

Despite their very small genomes, many predicted genes are present in multiple copies. Phytoplasmas lack many genes for standard metabolic functions and have no functioning homologous recombination pathways, but do have a sec transport pathway.[22] Many phytoplasmas contain two rRNA operons. Unlike the rest of the Mollicutes, the triplet code of UGA is used as a stop codon in phytoplasmas.[28]

Phytoplasma genomes contain large numbers of transposon genes and insertion sequences. They also contain a unique family of repetitive extragenic palindromes called PhREPS whose role is unknown though it is theorised that the stem loop structures the PhREPS are capable of forming may play a role in transcription termination or genome stability.[29]

Taxonomy

Phytoplasmas belong to the monophyletic order Acholeplasmatales.[9] In 1992, the Subcommittee on the Taxonomy of Mollicutes proposed the use of the name Phytoplasma in place of the use of the term MLO (mycoplasma-like organism) "for reference to the phytopathogenic mollicutes".[30] In 2004, the genus name Phytoplasma was adopted and is currently at Candidatus status[31] which is used for bacteria that cannot be cultured.[32] Its taxonomy is complicated because it can not be cultured, thus methods normally used for classification of prokaryotes are not possible.[9] Phytoplasma taxonomic groups are based on differences in the fragment sizes produced by the restriction digest of the 16S rRNA gene sequence (RFLP) or by comparison of DNA sequences from the 16s/23s spacer regions.[33] There is some disagreement over how many taxonomic groups the phytoplasmas fall into, recent work involving computer simulated restriction digests of the 16Sr gene suggest there may be up to 28 groups[34] whereas other papers argue for less groups, but more subgroups. Each group includes at least one Ca. Phytoplasma species, characterized by distinctive biological, phytopathological, and genetic properties.

See also

References

  1. 1 2 3 Doi Y, Teranaka M, Yora K, Asuyama H (1967). "Mycoplasma or PLT-group-like organisms found in the phloem elements of plants infected with mulberry dwarf, potato witches' broom, aster yellows or paulownia witches' broom". Annals of the Phytopathological Society of Japan. 33 (4): 259–266. doi:10.3186/jjphytopath.33.259.
  2. ↑ Contaldo, N.; Bertaccini, A.; Paltrinieri, S.; Windsor, H.M.; Windsor, G.D. (2012). "Axenic culture of a plant pathogenic Phytoplasma". Phytopathologia Mediterranea. 244: 607–117. doi:10.14601/Phytopathol_Mediterr-11773.
  3. ↑ Okuda, S (1972). "Occurrence of diseases caused by mycoplasma-like organisms in Japan". Plant Protection. 26: 180–183.
  4. 1 2 Hogenhout, SA; Oshima K; Ammar E-D; Kakizawa S; Kingdom HN; Namba S (2008). "Phytoplasmas: bacteria that manipulate plants and insects". Molecular Plant Pathology. 9 (4): 403–423. doi:10.1111/j.1364-3703.2008.00472.x. PMID 18705857. Retrieved 2008-07-04.
  5. 1 2 3 Bertamini, M; Grando M. S; Nedunchezhian N (2004). "Effects of Phytoplasma Infection on Pigments, Chlorophyll-Protein Complex and Photosynthetic Activities in Field Grown Apple Leaves". Biologia Plantarum. Springer Netherlands. 47 (2): 237–242. doi:10.1006/pmpp.2003.0450.
  6. ↑ Berg, M; Davis DL; Clark MF; Vetten HJ; Maier G; Marcone C; Seemuller E (1999). "Isolation of the gene encoding an immunodominant membrane protein of the apple proliferation phytoplasma, and expression and characterization of the gene product". Microbiology. Society for General Microbiology. 145: 1939–1943. doi:10.1099/13500872-145-8-1937. PMID 10463160.
  7. ↑ Pracros, P; Renaudin J; Eveillard S; Mouras A; Hernould M (2006). "Tomato Flower Abnormalities Induced by Stolbur Phytoplasma Infection Are Associated with Changes of Expression of Floral Development Genes". Molecular Plant Microbe Interactions. APS Press. 19 (1): 62–68. doi:10.1094/MPMI-19-0062. PMID 16404954.
  8. ↑ Muast BE, Espadas F, Talavera C, Aguilar M, Santamaría JM, Oropeza C (2003). "Changes in carbohydrate metabolism in coconut palms infected with the lethal yellowing phytoplasma". Phytopathology. 93 (8): 976–981. doi:10.1094/PHYTO.2003.93.8.976. PMID 18943864.
  9. 1 2 3 4 5 Lee, IM; Davis RE; Gundersen-Rindal DE (2000). "Phytoplasma: Phytopathogenic Mollicutes". Annual Review of Microbiology. 54: 221–255. doi:10.1146/annurev.micro.54.1.221. PMID 11018129.
  10. ↑ Lee, IM; Klopmeyer M; Bartoszyk IM; Gundersen-Rindal DE; Chou TS; Thomson KL; Eisenreich R (1997). "Phytoplasma induced free-branching in commercial poinsettia cultivars". Nature Biotechnology. Nature Publishing Group. 15 (2): 178–182. doi:10.1038/nbt0297-178. PMID 9035146.
  11. 1 2 Sugio, Akiko; Kingdom, H. N.; MacLean, A. M.; Grieve, V. M.; Hogenhout, S. A. (2011). "Phytoplasma protein effector SAP11 enhances insect vector reproduction by manipulating plant development and defense hormone biosynthesis". Proceedings of the National Academy of Sciences. 108 (48): E1254–E1263. doi:10.1073/pnas.1105664108.
  12. ↑ Weintraub, Phyllis G.; Beanland, LeAnn (2006). "Insect vectors of phytoplasmas". Annual Review of Entomology. 51: 91–111. doi:10.1146/annurev.ento.51.110104.151039. PMID 16332205.
  13. ↑ Suzuki, S.; Oshima, K.; Kakizawa, S.; Arashida, R.; Jung, H.-Y.; Yamaji, Y.; Nishigawa, H.; Ugaki, M.; Namba, S. (2006). "Interactions between a membrane protein of a pathogen and insect microfilament complex determines insect vector specificity". Proceedings of the National Academy of Sciences. 103 (11): 4252–4257. doi:10.1073/pnas.0508668103.
  14. 1 2 3 4 Christensen N, Axelsen K, Nicolaisen M, Schulz A (2005). "Phytoplasmas and their interactions with their hosts". Trends in Plant Sciences. 10 (11): 526–535. doi:10.1016/j.tplants.2005.09.008.
  15. ↑ Carraro, L.; Loi, N.; Favali, M. A.; Favali, M. A. (1991). "Transmission characteristics of the clover phyllody agent by dodder". J. Phytopathol. 133: 15–22. doi:10.1111/j.1439-0434.1991.tb00132.x.
  16. 1 2 Christensen NM, Nicolaisen M, Hansen M, Schulz A (2004). "Distribution of phytoplasmas in infected plants as revealed by real time PCR and bioimaging". Molecular Plant Microbe Interactions. 17 (11): 1175–1184. doi:10.1094/MPMI.2004.17.11.1175. PMID 15553243.
  17. ↑ Chen; et al. (1992). "Detection and identification of plant and insect mollicutes". The Mycoplasmas. 5: 393–424.
  18. ↑ Wang et al. (2007) Effective elimination of sweet potato little lead by cryotherapy of shoot tips. Plant Pathology online early edition.
  19. ↑ Chen, Y. D.; Chen, T. A. (1998). "Expression of engineered antibodies in plants: A possible tool for spiroplasma and phytoplasma disease control". Phytopathology. 88 (12): 1367–1371. doi:10.1094/PHYTO.1998.88.12.1367. PMID 18944841.
  20. ↑ Davies, R. E.; Whitcomb, R. F.; Steere, R. L. (1968). "Remission of aster yellows disease by antibiotics". Science. 161 (3843): 793–794. doi:10.1126/science.161.3843.793.
  21. ↑ Drug for Humans Checks Palm Trees Disease. New York Times, July 19 1983
  22. 1 2 Bai X, Zhang J, Ewing A, Miller SA, Jancso Radek A, Shevchenko DV, Tsukerman K, Walunas T, et al. (2006). "Living with Genome Instability: the Adaptation of Phytoplasmas to Diverse Environments of Their Insect and Plant Hosts". Journal of Bacteriology. 188 (10): 3682–3696. doi:10.1128/JB.188.10.3682-3696.2006. PMC 1482866Freely accessible. PMID 16672622.
  23. ↑ Oshima K, Kakizawa S, Nishigawa H, Jung HY, Wei W, Suzuki S, Arashida R, Nakata D, et al. (2004). "Reductive evolution suggested from the complete genome sequence of a plant-pathogenic phytoplasma". Nature Genetics. 36 (1): 27–29. doi:10.1038/ng1277. PMID 14661021.
  24. ↑ Tran-Nguyen, LT; Kube, M; Schneider, B; Reinhardt, R; Gibb, KS (2008). "Comparative Genome Analysis of "Candidatus Phytoplasma australiense" (Subgroup tuf-Australia I; rp-A) and "Ca. Phytoplasma asteris" Strains OY-M and AY-WB". Journal of Bacteriology. 190 (11): 3979–91. doi:10.1128/JB.01301-07. PMC 2395047Freely accessible. PMID 18359806.
  25. ↑ Dikinson, M. Molecular Plant Pathology (2003) BIOS Scientific Publishers
  26. ↑ Marcone, C; Neimark H; Ragozzino A; Lauer U; Seemüller E (1999). "Chromosome Sizes of Phytoplasmas Composing Major Phylogenetic Groups and Subgroups". Phytopathology. APS Press. 89 (9): 805–810. doi:10.1094/PHYTO.1999.89.9.805. PMID 18944709.
  27. ↑ Nishigawa; et al. (2003). "Complete set of extrachromosomal DNAs from three pathogenic lines of onion yellows phytoplasma and use of PCR to differentiate each line". Journal of General Plant Pathology. 69: 194–198.
  28. ↑ Razin S, Yogev D, Naot Y (1998). "Molecular Biology and Pathogenicity of Mycoplasmas". Microbiology Molecular Biology Review. 62 (4): 1094–1156. PMC 98941Freely accessible. PMID 9841667.
  29. ↑ Jomantiene R, Davis RE (2006). "Clusters of diverse genes existing as multiple, sequence variable mosaics in a phytoplasma genomes". FEMS Microbiology Letters. 255 (1): 59–65. doi:10.1111/j.1574-6968.2005.00057.x. PMID 16436062.
  30. ↑ Subcommittee on the Taxonomy of Mollicutes. Minutes of the Interim Meetings, 1 and 2 August, 1992, Ames, Iowa Int. J. of Syst. Bact. April 1993, p. 394-397; Vol. 43, No. 2 (see minutes 10 and 25)
  31. ↑ The IRPCM Phytoplasma/Spiroplasma Working Team - Phytoplasma taxonomy group: Candidatus Phytoplasma, a taxon for the wall-less, non-helical prokaryotes that colonize plant phloem and insects. Int. J. Syst. Evol. Microbiol., 2004, 54, 1243-1255.
  32. ↑ Murry; Syst, Bacteriol; et al. (1995). 45: 186–187. Missing or empty |title= (help)
  33. ↑ Hodgetts, J.; Ball, T.; Boonham, N.; Mumford, R.; Dickinson, M. (2007). "Taxonomic groupings based on the analysis on the 16s/23s spacer regions which shows greater variation than the normally used 16srRNA gene results in classification similar to that derived from 16s rRNA data but with more detailed subdivisions". Plant Pathology. 56: 357–365. doi:10.1111/j.1365-3059.2006.01561.x.
  34. ↑ Wei W, Davis RE, Lee IM, Zhao Y (2007). "Computer-simulated RFLP analysis of 16S rRNA genes: identification of ten new phytoplasma groups". International Journal of Systematic and Evolutionary Microbiology. 57 (Pt 8): 1855–1867. doi:10.1099/ijs.0.65000-0. PMID 17684271.
  35. ↑ Yadav, A.; Bhale, U.; Thorat, V.; Shouche, Y. (2014). "First Report of new subgroup 16SrII- M 'Candidatus Phytoplasma aurantifolia' associated with 'Witches Broom' disease of Tephrosia purpurea in India". Plant Disease. 98: 990. doi:10.1094/PDIS-11-13-1183-PDN.
  36. ↑ Nasare, K.; Yadav, Amit; Singh, A. K.; Shivasharanappa, K. B.; Nerkar, Y. S.; Reddy, V. S. (2007). "Molecular and symptom analysis reveal the presence of new phytoplasmas associated with sugarcane grassy shoot disease in India". Plant Disease. 91 (11): 1413–1418. doi:10.1094/PDIS-91-11-1413.
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