Phytoplasmas are pathogens of important crops, including coconuts and sugarcane, causing a wide variety of symptoms that ranges from mild yellowing to death of infected plants. They are most prevalent in tropical and sub-tropical regions of the world. Phytoplasmas 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 replicate.
There are references to diseases now known to be caused by phytoplasmas as far back as 1603 for Mulberry dwarf disease in Japan. Such diseases were originally thought to be caused by viruses, which, like phytoplasmas, require insect vectors, cannot be cultured, and have some symptom similarity. In 1967 phytoplasmas were discovered in ultrathin sections of plant phloem tissue and named mycoplasma-like organisms due to the fact that they physically resembled mycoplasmas The organisms were renamed phytoplasmas in 1994 at the 10th congress of the International Organization of Mycoplasmology.
Being mollicutes, phytoplasmas lack cell walls and instead are bound by a triple layered membrane. 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. The typical phytoplasma exhibits a pleiomorphic or filamentous shape and is less than 1 micrometer in diameter. Like other prokaryotes, DNA is free in the cytoplasm. They are believed to reproduce through binary fission.
A common symptom caused by phytoplasma infection is phyllody, the production of leaf-like structures in place of flowers. Evidence suggests that 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). This causes sepals to form where petals should. 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.
Many phytoplasma infected plants gain a bushy or witch's broom appearance due to changes in normal growth patterns caused by the infection. Most plants show apical dominance, but phytoplasma infection can cause the proliferation of auxiliary (side) shoots and an increase in size of the internodes. Such symptoms are actually useful in the commercial production of poinsettia. The infection produces more axillary shoots, which enables production of poinsettia plants that have more than one flower.
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. Phytoplasma infected plants often show yellowing which is caused by the breakdown of chlorophyll, whose biosynthesis is also inhibited.
The phytoplasmas are mainly spread by insects of the families Cicadellidea (leafhoppers) and Fulgoridea (planthoppers) which feed on the phloem tissues of infected plants, picking up the phytoplasmas and transmitting them to the next plant they feed on. For this reason 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.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.
Phytoplasmas enter the insect's body through the stylet, move through the intestine, and are then absorbed into the haemolymph. From here they proceed to colonise the salivary glands, a process that can take up to three weeks. Once established, phytoplasmas will be 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.
Phytoplasmas can also be spread via vegetative propagation such as the grafting of a piece of infected plant onto a healthy plant.
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.
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. 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, PCR-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.
More recently, techniques have been developed that allow for assessment of the level of infection. Both QPCR and bioimaging have been shown to be effective methods of quantifying the titre of phytoplasmas within the plant.
Phytoplasmas are normally controlled by the breeding and planting of disease resistance varieties of crops (believed to the most economically viable option) and by the control of the insect vector.
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.
Tetracyclines are bacteriostatic to phytoplasmas, that is they inhibit their growth. However, without continuous use of the antibiotic, disease symptoms will reappear. Thus, tetracycline is not a viable control agent in agriculture, but it is used to protect ornamental coconut trees.
The genomes of three phytoplasmas have been sequenced: Aster Yellows Witches Broom, Onion Yellows (Ca. Phytoplasma asteris) and Ca. Phytoplasma australiense 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. In fact Bermuda grass white leaf phytoplasma has a genome size of just 530Kb, one of the smallest known genomes of living organisms. 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, and this is why they can no longer survive outside of insects or plant phloem. Some phytoplasmas contain extrachromosomal DNA such as plasmids.
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. Many phytoplasmas contain 2 rRNA operons. Unlike the rest of the Mollicutes, the triplet code of UGA is used as a stop codon in phytoplasmas, rather than to code for tryptophan.
Phytoplasma genomes contain large numbers of transposon genes and insertion sequences. They also contain a unique family of repetitive extragenic palindromes (REPs) 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.
|16Sr Group||Group Name||Species|
|16SrI||Aster yellows|| Ca. Phytoplasma asteris|
Ca. Phytoplasma japonicum
|16SrII||Peanut witch's broom||Ca. Phytoplasma aurantifolia|
|16SrIII||X-disease||Ca. Phytoplasma pruni|
|16SrIV||Coconut lethal yellowing|| Ca. Phytoplasma palmae|
Ca. Phytoplasma castaneae
Ca. Phytoplasma cocosnigeriae
|16SrV||Elm yellows|| Ca. Phytoplasma ziziphi|
Ca. Phytoplasma vitis
Ca. Phytoplasma ulmi
|16SrVI||Clover proliferation||Ca. Phytoplasma trifolii|
|16SrVII||Ash yellows||Ca. Phytoplasma fraxini|
|16SrVIII||Luffa witch's-broom||Ca. Phytoplasma luffae|
|16SrIX||Pidgeon pea witch's broom||Ca. Phytoplasma phoenicium|
|16SrX||Apple proliferation|| Ca. Phytopalsma Mali|
Ca. Phytoplasma pyri
Ca. Phytoplasma prunorum
Ca. Phytoplasma spartii
Ca. Phytoplasma rhamnii
Ca. Phytoplasma allocasuarinae
|16SrXI||Rice Yellow Dwarf||Ca. Phytopalsma oryzae|
|16SrXII||Stolbur|| Ca. Phytoplasma solani|
Ca. Phytoplasma australiense
|16SrXIII||Mexican periwinkle virescence||Undefined|
|16SrXIV||Bermuda white leaf||Ca. Phytoplasma cynodontis|
|16SrXV||Hibiscus witch's-broom||Ca. Phytoplasma brasiliense|