Abstract: Phytoplasmas are pathogenic microorganism belonging to the class Mollicutes. The phytoplasmas parasitize the phloem tissues of infected plant hosts and are transmitted by insect vectors. To date，the complete genome sequence of six phytoplasmas，and draft genome of nineteen phytoplasmas have been published. The phytoplasmas genomes are featured with low G + C content（19.3%–28.6%），lack of genes for numerous biosynthetic pathways，such as amino acid synthesis，fatty acid synthesis，the tricarboxylic acid cycle，oxidative phosphorylation，and pentose phosphate pathway. A large portion of phytoplasmas genome encodes potential mobile units，consisting of repeats that resemble composite transposable elements. Phytoplasmas have functional Sec（Signal sequences）-dependent pathway，secrete effector proteins into the cytoplasm of phloem sieve cells of the host plants. The most studied phytoplasma virulence effectors are SAP11，Tengu and Phyllogen. SAP11 and Tengu induce stem proliferation，dwarf，while Phyllogen induces the development of leaf-like flowers. The developmental symptoms of the host plant promoted the insect vectors colonization and reproduction，thus contribute to the phytoplasma transmission. The SAP11 interacts with TCP transcription factors to destabilize their functions. The SAP11 also antagonistically regulates the jasmine acid and auxin signaling pathway，leading to the proliferation of axillary meristems. Phyllogen interacts and degrades A and E class MADS-box transcription factors，which were involved in flower development. In the future，we will be able to sequence more and more phytoplasma genome by mega-genomic methods，and analyze the host selection mechanism. The combination of phenomics，metabonomics，proteomics，and transcriptomics techniques can be applied on the screening and identification of the phytoplasma virulence effectors，for a more comprehensive understanding of the phytoplasma pathogenic mechanism to provide valuable information for phytoplasma disease control.

Key words: phytoplasma, genome sequencing, virulence effector, pathogenic mechanism