Phytoplasma

Phytoplasmas are obligate intracellular parasites of plant phloem tissue and of the insect vectors that are involved in their plant-to-plant transmission. Phytoplasmas were discovered in 1967 by Japanese scientists who termed them mycoplasma-like organisms. Since their discovery, phytoplasmas have resisted all attempts at in vitro culture in any cell-free medium; routine cultivation in an artificial medium thus remains a major challenge. 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. Phytoplasmas are most prevalent in tropical and subtropical regions. They are transmitted from plant to plant by vectors (normally sap-sucking insects such as leafhoppers) in which they both survive and replicate.

References to diseases now known to be caused by phytoplasmas can be found as far back as 1603 (mulberry dwarf disease in Japan). Such diseases were originally thought to be caused by viruses, which, like phytoplasmas, require insect vectors and cannot be cultured. Viral and phytoplasmic infections share some symptoms. In 1967, phytoplasmas were discovered in ultrathin sections of plant phloem tissue and were termed mycoplasma-like organisms due to their physiological resemblance. The organisms were renamed phytoplasmas in 1994 at the 10th Congress of the International Organization for Mycoplasmology.

Phytoplasmas are Mollicutes that are bound by a triple-layered membrane rather than a cell wall. The phytoplasma cell membranes studied to date usually contain a single immunodominant protein of unknown function that constitutes most of the protein in the membrane. A typical phytoplasma is pleiomorphic or filamentous in shape and is less than 1 μm in diameter. Like other prokaryotes, phytoplasmic DNA is distributed throughout the cytoplasm instead of being concentrated in a nucleus.^{[citation needed]}

Phytoplasmas can infect and cause various symptoms in more than 700 plant species. 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), and fasciation (abnormal change in the apical meristem structure). Phytoplasma-harboring flowering plants may become sterile. The expression of genes involved in maintaining the apical meristem or in the development of floral organs is altered in the morphologically affected floral organs of phytoplasma-infected plants.

A phytoplasma infection often triggers leaf yellowing, probably due to the presence of phytoplasma cells in the phloem, which can affect phloem function and carbohydrate transport, inhibit chlorophyll biosynthesis, and trigger chlorophyll breakdown. These symptoms may be attributable to stress caused by the infection rather than a specific pathogenetic process.^{[citation needed]}

Many phytoplasma-infected plants develop a bushy or witch's 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. Such symptoms are actually useful in the commercial production of poinsettias. An infection triggers more axillary shoot production; the poinsettia plants thus produce more than a single flower.

Many plant pathogens produce virulence factors, or effectors, that modulate or interfere with normal host processes to the benefit of the pathogens. 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. TENGU induces characteristic symptoms, including witches' broom and dwarfism. Transgenic expression of TENGU in Arabidopsis plants induced sterility in male and female flowers. TENGU contains a signal peptide at its N-terminus. After cleavage, the mature protein is only 38 amino acids long. Although phytoplasmas are restricted to the phloem, TENGU is transported from the phloem to other cells, including those of the apical and axillary meristems. TENGU was suggested to inhibit both auxin- and jasmonic acid-related pathways, thereby affecting plant development. Surprisingly, the N-terminal 11 amino acid region of the mature protein triggers symptom development in Nicotiana benthamiana plants. TENGU undergoes proteolytic processing by a plant serine protease in vivo, suggesting that the N-terminal peptide alone induces the observed symptoms. TENGU homologs have been identified in AY-group phytoplasmas. All such homologs undergo processing and can induce symptoms, suggesting that the symptom-inducing mechanism is conserved among TENGU homologs.