乙烯和水杨酸在大豆胞囊线虫与大豆间亲和性反应中的相互作用

Crosstalk between ethylene and salicylic acid in a compatible soybean-Heterodera glycines interaction

  • 摘要: 乙烯(Ethylene,ET)和水杨酸(Salicylic Acid,SA)不仅是重要的植物生长调节物质,而且在调控植物与病原线虫互作中起着重要作用,但两者在感病大豆与大豆胞囊线虫(Soybean cyst nematode,SCN)间亲和性反应中的相互作用关系尚不清楚。转录组分析表明,SCN侵染24 h后明显激活ET合成途径,但SA途径变化不显著。0.5 mM乙烯利(Ethephon,ET供体)外源处理能显著增加感病大豆William 82对SCN的敏感性,喷施2 mM SA则明显降低SCN在大豆上的繁殖能力,但是该诱导作用能被乙烯利处理消除。qRT-PCR分析表明,乙烯利能抑制SA合成途径关键酶基因GmICS2表达,暗示ET和SA可能存在拮抗作用。进一步研究发现,SA的诱导抗性与上调下游防御基因GmPR1GmPR2表达密切相关,而乙烯利处理进一步加剧了线虫对GmPR2GmPR5表达的抑制作用。以上研究结果表明,ET在感病大豆与SCN间亲和性反应中起正调控作用,而ET与SA信号途径间可能存在的部分负向调节影响了寄主对SCN侵染的响应。

     

    Abstract: Ethylene (ET) and Salicylic Acid (SA) are important modulators of plant growth,and also play a key role in regulating interactions between plant and plant-parasitic nematodes.However,their crucial cross-talks are unclear in a compatible susceptible soybean-Heterodera glycines (soybean cyst nematode,SCN) interaction.RNA-Seq analysis revealed that ET but not SA metabolism was activated in soybean roots infected with SCN for 24 h.Exogenous ethephon (ETH,ET donor) supply at 0.5 mM induced SCN susceptibility in the roots of William 82,and application of 2 mM SA markedly decreased the reproduction of SCN.However,the immune inducible effect of SA was at least partly compromised by ETH treatments.Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) confirmed that ETH supply led to reduce the expression of GmICS2,a gene of SA biosynthesis,suggesting the ET and SA pathway might be antagonistic in soybean roots.In addition,we found that the SA-induced resistance was associated with up-regulation of SA-responsive genes GmPR1 and GmPR2,whereas ETH treatment exhibited an inhibitory effect on the expression levels of GmPR2 and GmPR3 in SCN-infected roots.Collectively,these results indicate that ET plays a positive role in a compatible interaction between susceptible soybean and SCN,and the negative cross-talk between the ET and SA pathway may involve in modulating the outcome of soybean-SCN interaction.

     

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