CIPK11-Dependent Phosphorylation Modulates FIT Activity to Promote Arabidopsis Iron Acquisition in Response to Calcium Signaling
CIPK11-Dependent Phosphorylation Modulates FIT Activity to Promote Arabidopsis Iron Acquisition in Response to Calcium Signaling
复制标题
DOI：
10.1016/j.devcel.2019.01.006
复制
发表时间：
2019-03-11
影响因子：
11.8
通讯作者：
Brumbarova, Tzvetina
中科院分区：
文献类型：
--
作者：
Gratz, Regina;Manishankar, Prabha;Brumbarova, Tzvetina
养分获取与固着生物的生长和应激密切相关。 bHLH 转录因子 FIT 是拟南芥铁 (Fe) 获取的关键调节因子，并在低 Fe 时被翻译后激活。我们将 CBL 相互作用蛋白激酶 CIPK11 确定为 FIT 相互作用因子。 Fe 缺乏会诱导胞质 Ca2+ 浓度和 CIPK11 表达。 cipk11 突变植物表现出根部铁动员和种子铁含量受损。 Fe 的吸收取决于 CBL1/CBL9。 CIPK11 在 Ser272 位点磷酸化 FIT，该靶位点的突变可调节 FIT 核积累、同源二聚化、与 bHLH039 的相互作用以及转录活性，并影响植物的 Fe 吸收能力。我们提出 Ca2+ 触发 CBL1/9 介导的 CIPK11 激活以及随后的 FIT 磷酸化将非活性转变为活性 FIT，从而允许细胞核中的调节蛋白相互作用。 Fe 缺乏与细胞 Ca2+ 解码机制之间的这种生化联系代表了一种调节营养吸收的环境感知机制。
Nutrient acquisition is entangled with growth and stress in sessile organisms. The bHLH transcription factor FIT is a key regulator of Arabidopsis iron (Fe) acquisition and post-translationally activated upon low Fe. We identified CBL-INTERACTING PROTEIN KINASE CIPK11 as a FIT interactor. Cytosolic Ca2+ concentration and CIPK11 expression are induced by Fe deficiency. cipk11 mutant plants display compromised root Fe mobilization and seed Fe content. Fe uptake is dependent on CBL1/CBL9. CIPK11 phosphorylates FIT at Ser272, and mutation of this target site modulates FIT nuclear accumulation, homo-dimerization, interaction with bHLH039, and transcriptional activity and affects the plant's Fe-uptake ability. We propose that Ca2+-triggered CBL1/9-mediated activation of CIPK11 and subsequent phosphorylation of FIT shifts inactive into active FIT, allowing regulatory protein interactions in the nucleus. This biochemical link between Fe deficiency and the cellular Ca2+ decoding machinery represents an environment-sensing mechanism to adjust nutrient uptake.