|QI, MINGSHENG - Iowa State University|
|LINK, TOBIAS - University Of Hohenheim|
|MULLER, MANUEL - University Of Hohenheim|
|HIRSCHBURGER, DANIELLA - University Of Hohenheim|
|BRAUN, EDWARD - Iowa State University|
|VOEGELE, RALF - University Of Hohenheim|
|BAUM, THOMAS - Iowa State University|
|WHITHAM, STEVEN - Iowa State University|
Submitted to: PLoS Pathogens
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/15/2016
Publication Date: 9/27/2016
Publication URL: http://handle.nal.usda.gov/10113/5510077
Citation: Qi, M., Link, T.I., Muller, M., Hirschburger, D., Pedley, K.F., Braun, E., Voegele, R.T., Baum, T., Whitham, S.A. 2016. A small cysteine-rich protein from the Asian soybean rust fungus, Phakopsora pachyrhizi, suppresses plant immunity. PLoS Pathogens. 12(9):e1005827. doi: 10.1371/journal.ppat.1005827.
Interpretive Summary: The Asian soybean rust fungus, Phakopsora pachyrhizi, is an obligate pathogen capable of causing explosive disease epidemics that drastically reduce the yield of soybean. Currently, the mechanisms by which P. pachyrhizi and other related fungi cause disease are poorly understood. The genome sequences and other data obtained from these fungi indicate that a variety of small proteins play essential roles that enable them to cause disease. These proteins, called effectors, are released by the pathogen and interfere with a plant’s ability to fight the disease. Here, we identify an effector protein produced by P. pachyrhizi and demonstrate that it is capable of suppressing plant defense mechanisms. We also show that it physically interacts with a soybean protein that is involved in regulating the expression of soybean genes. Together, these data shed light on a mechanism employed by P. pachyrhizi to overcome soybean defense. Ultimately, these findings may enable the development of new strategies to mitigate losses caused by Asian soybean rust.
Technical Abstract: The Asian soybean rust fungus, Phakopsora pachyrhizi, is an obligate pathogen capable of causing explosive disease epidemics that drastically reduce the yield of soybean (Glycine max). Currently, the molecular mechanisms by which P. pachyrhizi and other rust fungi cause disease are poorly understood. The genomes and transcriptomes of rust fungi encode a variety of predicted small, secreted cysteine-rich (SSCR) proteins, which are proposed to have functions within host cells such as suppressing immunity. Here, we identify P. pachyrhizi effector candidate 23 (PpEC23), a SSCR protein, that can suppress effector- and pattern-triggered immunity (ETI and PTI) when delivered into plant cells via bacterial expression systems or transgene expression. PpEC23 interacts with GmSPL12l, a soybean transcription factor that is a member of the SQUAMOSA promoter-binding-like (SPL) family. Soybean plants in which GmSPL12l is silenced have constitutively activated immune responses demonstrating that PpEC23 targets a transcription factor that negatively regulates soybean immune responses.