Phytoplasmas are obligate intracellular parasites of plant phloem tissue and of the insect vectors that are involved in their plant-to-plant transmission.
Phytoplasmas are characterized by the lack of a cell wall, a pleiomorphic or filamentous shape, a diameter normally less than 1 μm, and a very small genome.
Phytoplasmas are pathogens of agriculturally important plants, including coconut, sugarcane, sandalwood, and cannabis, as well as horticultural crops like sweet cherry, peaches, and nectarines.
They cause a wide variety of symptoms ranging from mild yellowing, small fruit, and reduced sugar content to death.
[4] Such diseases were originally thought to be caused by viruses, which, like phytoplasmas, require insect vectors and cannot be cultured.
[5] In 1967, phytoplasmas were discovered in ultrathin sections of plant phloem tissue and were termed mycoplasma-like organisms due to their physiological resemblance.
One characteristic symptom is abnormal floral organ development, including phyllody (the production of leaf-like structures in place of flowers), virescence (the development of green flowers attributable to a loss of pigment by petal cells),[8] and fasciation (abnormal change in the apical meristem structure).
[citation needed] Many phytoplasma-infected plants develop a bushy or "witches' broom" appearance due to changes in their normal growth patterns.
Most plants exhibit apical dominance, but infection can trigger the proliferation of axillary (side) shoots and a reduction in internode size.
An infection triggers more axillary shoot production; the poinsettia plants thus produce more than a single flower.
The first phytoplasmal virulence factor, a secreted protein termed “tengu-su inducer” (TENGU; C0H5W6), was identified in 2009 from a phytoplasma causing yellowing of onions.
[14] Transgenic expression of TENGU in Arabidopsis plants induced sterility in male and female flowers.
[14] TENGU was suggested to inhibit both auxin- and jasmonic acid-related pathways, thereby affecting plant development.
[14][15] Surprisingly, the N-terminal 11 amino acid region of the mature protein triggers symptom development in Nicotiana benthamiana plants.
[16] TENGU undergoes proteolytic processing by a plant serine protease in vivo, suggesting that the N-terminal peptide alone induces the observed symptoms.
[18] In addition, it was demonstrated that SAP11 interacts with and destabilizes plant class II TCP protein domain transcription factors that lead to shoot proliferation and leaf shape changes.
[23] Phytoplasmas cannot survive in the external environment and are dependent upon insects such as leafhoppers for transmission to new (healthy) plants.
[31] MADS-box transcription factors (MTFs) of the ABCE model play critical roles in floral organ development in Arabidopsis.
RAD23 proteins are also required for promoting leafhopper vector egg laying on plants that express SAP54 and are infected with AY-WB phytoplasma.
Phytoplasmas can have varying effects on their insect hosts; examples of both reduced and increased fitness have been noted.
[39] Phytoplasmas enter the insect body through the stylet, pass through the intestine, and then move to the hemolymph and colonize the salivary glands.
The time between ingestion by the insect and attainment of an infectious titer in the salivary glands is termed the latency period.
[citation needed] Molecular diagnostic techniques for phytoplasma detection began to emerge in the 1980s and included enzyme-linked immunosorbent assay (ELISA)-based methods.
These are far more sensitive than ELISAs, and restriction fragment length polymorphism (RFLP) analysis allowed the accurate identification of various phytoplasma strains and species.
[41] In addition, loop-mediated isothermal amplification (LAMP) is now available as a commercial kit, allowing all known phytoplasma species to be detected in about 1 h, including the DNA extraction step.
The small genome size of phytoplasma is attributable to reductive evolution from Bacillus/Clostridium[dubious – discuss] ancestors.
[55] Phytoplasma genomes contain large numbers of transposons and insertion sequences, as well as a unique family of repetitive extragenic palindromes termed PhREPS, for which no role is known.