媒體：植物脅迫與抗逆研究  作者：內(nèi)詳

https://mp.weixin.qq.com/s/w6hZAKu90ytkGniXiopi6A

近日，由西農(nóng)馬鋒旺-李超團(tuán)隊(duì)在Plant J發(fā)表了題為《MdMYB54 reduces disease severity caused by Fusarium solani in apple by modulating cell wall cellulose and pectate lyase-dependent defense》的研究論文，揭示了蘋果中MYB54通過調(diào)節(jié)細(xì)胞壁纖維素和果膠裂解酶依賴的防御機(jī)制以減輕病害。

植物細(xì)胞壁是抵御病原體入侵的第一道屏障。Fusarium solani是導(dǎo)致蘋果再植病的主要病原菌。

在本研究中，作者鑒定了一種MYB蛋白MdMYB54，它與Fusarium solani抗性的正向調(diào)節(jié)因子MdERF114相互作用，并賦予蘋果對(duì)Fusarium solani的耐受性。通過DAP-seq篩選出纖維素合酶（CESA）基因MdCesA6和果膠裂解酶樣（PLL）基因MdPLL8和MdPLL12作為MdMYB54的三個(gè)潛在下游靶基因。

電泳遷移率變動(dòng)測定和酵母單雜交實(shí)驗(yàn)結(jié)果顯示，MdMYB54在體內(nèi)外直接結(jié)合到MdCesA6、MdPLL8和MdPLL12的啟動(dòng)子上。雙熒光素酶和β-葡萄糖苷酶實(shí)驗(yàn)顯示，MdMYB54激活了這些基因的表達(dá)。在Fusarium solani處理下，過表達(dá)MdMYB54的根系纖維素含量和果膠裂解酶活性顯著高于野生型植株，而在MdMYB54-RNAi根系中則相反。

纖維素的沉積增強(qiáng)了植物細(xì)胞壁的物理屏障，而果膠裂解酶的激活促進(jìn)了寡半乳糖醛酸的形成和活性氧物質(zhì)的產(chǎn)生。在根系中過表達(dá)MdCesA6、MdPLL8和MdPLL12增強(qiáng)了蘋果對(duì)Fusarium solani的耐受性。MdERF114與MdMYB54的直接互作增強(qiáng)了MdMYB54介導(dǎo)的細(xì)胞壁防御反應(yīng)。

這些結(jié)果表明，修改這些候選基因可能提供一種策略來提高蘋果對(duì)Fusarium solani的耐受性。

The plant cell wall is the first barrier against pathogen invasion. Fusarium solani is the primary pathogen responsible for apple replant disease. In this study, we identified an MYB protein, MdMYB54, which interacts with the positive regulator of F. solani resistance, MdERF114, and confers apple-increased tolerance against F. solani. The cellulose synthetase (CESA) gene MdCesA6 and pectin lyase-like (PLL) genes MdPLL8 and MdPLL12 were screened as three potential downstream target genes of MdMYB54 using DAP-seq. The results of electrophoretic mobility shift and yeast one-hybrid assays showed that MdMYB54 directly binds to the promoters of MdCesA6, MdPLL8, and MdPLL12 in vivo and in vitro. Dual-luciferase and β-glucuronidase assays showed that MdMYB54 activates the expression of these genes. The cellulose content and pectin lyase activity of MdMYB54-overexpressed roots were significantly higher than those of wild-type plants under F. solani treatment but were the opposite in MdMYB54-RNAi roots. The deposition of cellulose enhanced the physical barrier of the plant cell wall, whereas the activation of pectin lyase promoted the formation of oligogalacturonides and the production of reactive oxygen species. Overexpression of MdCesA6, MdPLL8, and MdPLL12 in the root system enhanced the tolerance of apple to F. solani. The direct interaction of MdERF114 with MdMYB54 enhanced MdMYB54-mediated cell wall defense response. These results suggest that modifying these candidate genes may provide a strategy for improving the resistance of apple to F. solani.

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