The tomato leucine-rich repeat receptor-like kinases SlSERK3A and SlSERK3B have overlapping functions in bacterial and nematode innate immunity.
The tomato leucine-rich repeat receptor-like kinases SlSERK3A and SlSERK3B have overlapping functions in bacterial and nematode innate immunity.
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DOI：
10.1371/journal.pone.0093302
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Kaloshian I
中科院分区：
文献类型：
--
作者：
Peng HC;Kaloshian I
体细胞胚胎发生受体激酶3（SERK 3）/类甾醇（BR）不敏感1-相关激酶1（BAK 1）是拟南芥和本氏烟草中模式触发免疫（PTI）所必需的。番茄（Solanum lycopersicum）具有三个SlSERK成员。其中两个与AtSERK 3具有特别高的序列相似性，因此被命名为SlSERK 3A和SlSERK 3B。为了表征SlSERK 3A和SlSERK 3B在防御中的作用，我们在番茄品种中使用病毒诱导的基因沉默（VIGS）单独抑制每个基因或共沉默两者。摇钱树。共沉默SlSERK 3A和SlSERK 3B导致自发性坏死病变并降低对外源性BR治疗的敏感性。沉默SlSERK 3A或SlSERK 3B导致对根结线虫和非致病性假单胞菌pv.番茄（Pst）DC 3000 hrcC，表明两个SlSERK 3都是防御的正调节子。有趣的是，沉默SlSERK 3B而不是SlSERK 3A导致对致病菌株Pst DC 3000的易感性增强，表明这两种SlSERK 3旁系同源物的不同作用。SlSERK 3A和SlSERK 3B是定位于质膜的活性激酶，并且以flg 22依赖性方式在体内与鞭毛蛋白传感2受体相互作用。Atserk 3/bak 1 -4突变体与SlSERK 3A或SlSERK 3B的互补部分挽救了突变体表型。因此，SlSERK 3A和SlSERK 3B可能构成BAK 1的番茄直系同源物。
The Somatic Embryogenesis Receptor Kinase 3 (SERK3)/Brassinosteroid (BR) Insensitive 1-Associated Kinase 1 (BAK1) is required for pattern-triggered immunity (PTI) in Arabidopsis thaliana and Nicotiana benthamiana. Tomato (Solanum lycopersicum) has three SlSERK members. Two of them exhibit particularly high levels of sequence similarity to AtSERK3 and, therefore, were named SlSERK3A and SlSERK3B. To characterize a role for SlSERK3A and SlSERK3B in defense, we suppressed each gene individually or co-silenced both using virus-induced gene silencing (VIGS) in the tomato cv. Moneymaker. Co-silencing SlSERK3A and SlSERK3B resulted in spontaneous necrotic lesions and reduced sensitivity to exogenous BR treatment. Silencing either SlSERK3A or SlSERK3B resulted in enhanced susceptibility to root knot-nematode and to non-pathogenic Pseudomonas syringae pv. tomato (Pst) DC3000 hrcC indicating that both SlSERK3s are positive regulators of defense. Interestingly, silencing SlSERK3B, but not SlSERK3A, resulted in enhanced susceptibility to the pathogenic strain Pst DC3000 indicating distinct roles for these two SlSERK3 paralogs. SlSERK3A and SlSERK3B are active kinases, localized to the plasma membrane, and interact in vivo with the Flagellin Sensing 2 receptor in a flg22-dependent manner. Complementation of the Atserk3/bak1-4 mutant with either SlSERK3A or SlSERK3B partially rescued the mutant phenotype. Thus, SlSERK3A and SlSERK3B are likely to constitute tomato orthologs of BAK1.
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