Jiangsu Key Laboratory for the Research and Utilization of Plant Resources, Institute of Botany, Jiangsu Province and Chinese Academy of Sciences, Nanjing 210014, China.
Int J Mol Sci. 2024 Feb 5;25(3):1930. doi: 10.3390/ijms25031930.
Kiwifruit bacterial canker caused by pv. (Psa) is the most serious disease threatening kiwifruit production. Our previous study found genes encoding the U-box containing proteins were significantly regulated by Psa infection. Here, we report a U-box type E3 ubiquitin ligase PUB23 in kiwifruit which acts as a negative regulator of immune responses against Psa. PUB23 was found to physically interact with GT1, a trihelix transcription factor, in vitro and in vivo. The expression of was up-regulated in -silenced plants, indicating that interacting with PUB23 may directly or indirectly suppress expression. The silencing of led to enhanced immune responses of PAMP-triggered immunity (PTI), including a higher expression level of defense marker genes and , and increased accumulation of hydrogen peroxide and superoxide anion. Our results reveal a negative role PUB23 plays in kiwifruit immune responses against Psa and may regulate gene expression by interacting with GT1.
猕猴桃溃疡病菌（Psa）引起的猕猴桃溃疡病是威胁猕猴桃生产的最严重病害。我们之前的研究发现，编码 U-box 蛋白的基因受 Psa 感染的显著调控。在这里，我们报道了猕猴桃中的一种 U-box 型 E3 泛素连接酶 PUB23，它作为一种对 Psa 免疫反应的负调控因子。PUB23 被发现能够在体外和体内与 GT1（一种三螺旋转录因子）发生物理相互作用。在沉默植株中 的表达上调，表明与 PUB23 的相互作用可能直接或间接抑制 的表达。 的沉默导致了 PAMP 触发免疫（PTI）的增强的免疫反应，包括防御标记基因 和 的更高表达水平，以及过氧化氢和超氧阴离子的积累增加。我们的结果揭示了 PUB23 在猕猴桃对 Psa 免疫反应中所起的负作用，并可能通过与 GT1 的相互作用来调节基因表达。
