The Arabidopsis (Arabidopsis thaliana) calmodulin-binding transcription activator3 (CAMTA3) is a repressor of immunity-related genes but an activator of cold-induced or general stress-responsive genes in plants. Post-transcriptional or posttranslational mechanisms have been proposed to control CAMTA3 functions in different stress responses. Here, we show that treatment with the bacterial flg22 elicitor induces CAMTA3 phosphorylation, which is accompanied by its destabilization and nuclear export. Two flg22-responsive mitogen-activated protein kinases (MAPKs), MPK3 and MPK6, directly phosphorylate CAMTA3, with the phospho-sites contributing to CAMTA3 degradation and suppression of downstream target gene expression. However, the flg22-induced nuclear export and phospho-mobility shift can still be observed for the CAMTA3 phospho-null variant of the MAPK-modified sites, suggesting additional flg22-responsive kinases might be involved. Taken together, we propose that flg22-induced CAMTA3 depletion facilitates de-repression of downstream defense target genes, which involves phosphorylation, increased protein turnover, and nucleo-cytoplasmic trafficking.

拟南芥 ( Arabidopsis thaliana ) 钙调蛋白结合转录激活子 3 (CAMTA3) 是植物中免疫相关基因的抑制子，但也是冷诱导或一般应激响应基因的激活子。转录后或翻译后机制已被提出来控制不同应激反应中的 CAMTA3 功能。在这里，我们证明用细菌 flg22 激发子处理会诱导 CAMTA3 磷酸化，并伴有其不稳定和核输出。两种 flg22 响应的丝裂原激活蛋白激酶 (MAPK) MPK3 和 MPK6 直接磷酸化 CAMTA3，磷酸位点有助于 CAMTA3 降解并抑制下游靶基因表达。然而，对于 MAPK 修饰位点的 CAMTA3 磷酸无效变体，仍然可以观察到 flg22 诱导的核输出和磷酸迁移率变化，这表明可能涉及其他 flg22 响应激酶。综上所述，我们认为 flg22 诱导的 CAMTA3 耗竭有助于下游防御靶基因的去抑制，其中涉及磷酸化、蛋白质周转增加和核质运输。