Lysophosphatidylcholine enhances susceptibility in signaling pathway against pathogen infection through biphasic production of reactive oxygen species and ethylene in tobacco plants.
It was previously reported that the amounts of lysophosphatidylcholines (lysoPCs), which are naturally occurring bioactive lipid molecules, significantly increase following pathogen inoculation, as determined using ultraperformance liquid chromatography-quadrupole-time of flight/mass spectrometry analyses. Here, real-time quantitative RT-PCR was performed for the phospholipase A2 (PLA2) genes, Nt1PLA2 and Nt2PLA2, which are responsible for LysoPCs generation. The transcription level of Nt2PLA2 in pathogen-infected tobacco plants transiently peaked at 1h and 36 h, whereas induction of Nt1PLA2 transcription peaked at 36 h. A prominent biphasic ROS accumulation in lysoPC (C18:1(9Z))-treated tobacco leaves was also observed. Transcription of NtRbohD, a gene member of NADPH oxidase, showed biphasic kinetics upon lysoPC 18:1 treatment, as evidenced by an early transient peak in phase I at 1h and a massive peak in phase II at 12h. Each increase in NtACS2 and NtACS4 transcription, gene members of the ACC synthase family, was followed by biphasic peaks of ethylene production after lysoPC 18:1 treatment. This suggested that lysoPC (C18:1)-induced ethylene production was regulated at the transcriptional level of time-dependent gene members. LysoPC 18:1 treatment also rapidly induced cell damage. LysoPC 18:1-induced cell death was almost completely abrogated in ROS generation-impaired transgenic plants (rbohD-as and rbohF-as), ethylene production-impaired transgenic plants (CAS-AS and CAO-AS), and ethylene signaling-impaired transgenic plants (Ein3-AS), respectively. Taken together, pathogen-induced lysoPCs enhance pathogen susceptibility accompanied by ROS and ethylene biosynthesis, resulting in chlorophyll degradation and cell death. Expression of PR genes (PR1-a, PR-3, and PR-4b) and LOX3 was strongly induced in lysoPC 18:1-treated leaves, indicating the involvement of lysoPC 18:1 in the defense response. However, lysoPC 18:1 treatment eventually resulted in cell death, as evidenced by metacaspase gene expression. Therefore, a hypothesis is proposed that the antipathogenic potential of lysoPC 18:1 is dependent on how quickly it is removed from cells for avoidance of lysoPC toxicity.
Department of Biology, Sunchon National University, Sunchon, Chonnam 540-742, Republic of Korea.
Soo Jin
SJ
Wi
Department of Biology, Sunchon National University, Sunchon, Chonnam 540-742, Republic of Korea.
So yeon
Sy
Seo
Seoul Center, Korea Basic Science Institute (KBSI), Seoul 136-713, Republic of Korea.
Kyoungwon
K
Cho
Seoul Center, Korea Basic Science Institute (KBSI), Seoul 136-713, Republic of Korea.
Myung Hee
MH
Nam
Department of Biology, Sunchon National University, Sunchon, Chonnam 540-742, Republic of Korea. Electronic address: plpm@sunchon.ac.kr.
Ky Young
KY
Park
D002734:Chlorophyll / Q000378:metabolism; D005030:Ethylenes / Q000378:metabolism; D015971:Gene Expression Regulation, Enzymologic; D018506:Gene Expression Regulation, Plant / Q000187:drug effects*; D007527:Isoenzymes; D008244:Lysophosphatidylcholines / Q000737:chemistry / Q000494:pharmacology*; D054467:Phospholipases A2 / Q000235:genetics* / Q000378:metabolism; D010838:Phytophthora / Q000502:physiology; D010935:Plant Diseases / Q000276:immunology*; D010937:Plant Growth Regulators / Q000378:metabolism; D057865:Plant Immunity / Q000187:drug effects; D018515:Plant Leaves / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism; D030821:Plants, Genetically Modified; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013997:Time Factors; D014026:Nicotiana / Q000187:drug effects* / Q000235:genetics / Q000502:physiology
D005030:Ethylenes; D007527:Isoenzymes; D008244:Lysophosphatidylcholines; D010937:Plant Growth Regulators; D010940:Plant Proteins; D017382:Reactive Oxygen Species; D002734:Chlorophyll; C036216:ethylene; D054467:Phospholipases A2
Ethylene; Lysophosphatidylcholine; Nicotiana tabacum L. Wisconsin 38; Pathogenesis-related genes; Phospholipase A(2); Reactive oxygen species; Solanaceae; Tobacco