State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China.
State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
Mol Plant. 2018 Jan 8;11(1):163-174. doi: 10.1016/j.molp.2017.11.004. Epub 2017 Nov 22.
Secondary walls, which represent the bulk of biomass, have a large impact on plant growth and adaptation to environments. Secondary wall synthesis is switched and regulated by a sophisticated signaling transduction network. However, there is limited understanding of these regulatory pathways. Here, we report that ILA1-interacting protein 4 (IIP4) can repress secondary wall synthesis. IIP4 is a phosphorylation substrate of an Raf-like MAPKKK, but its function is unknown. By generating iip4 mutants and relevant transgenic plants, we found that lesions in IIP4 enhance secondary wall formation. Gene expression and transactivation activity assays revealed that IIP4 negatively regulates the expression of MYB61 and CESAs but does not bind their promoters. IIP4 interacts with NAC29/NAC31, the upstream regulators of secondary wall synthesis, and suppresses the downstream regulatory pathways in plants. Mutagenesis analyses showed that phosphomimic IIP4 proteins translocate from the nucleus to the cytoplasm, which releases interacting NACs and attenuates its repression function. Moreover, we revealed that IIPs are evolutionarily conserved and share unreported CCCH motifs, referred to as uncanonical CCCH-tandem zinc-finger proteins. Collectively, our study provides mechanistic insights into the control of secondary wall synthesis and presents an opportunity for improving relevant agronomic traits in crops.
次生壁，作为生物量的主要组成部分，对植物的生长和环境适应具有重要影响。次生壁的合成是由一个复杂的信号转导网络调控和切换的。然而，对于这些调控途径的了解还很有限。在这里，我们报告了 ILA1 相互作用蛋白 4（IIP4）可以抑制次生壁的合成。IIP4 是一种 Raf 样 MAPKKK 的磷酸化底物，但它的功能未知。通过生成 iip4 突变体和相关的转基因植物，我们发现 IIP4 的缺失会增强次生壁的形成。基因表达和转录激活活性分析表明，IIP4 负调控 MYB61 和 CESAs 的表达，但不结合它们的启动子。IIP4 与 NAC29/NAC31 相互作用，NAC29/NAC31 是次生壁合成的上游调控因子，抑制植物中的下游调控途径。突变分析表明，磷酸化模拟的 IIP4 蛋白从细胞核转移到细胞质，从而释放出相互作用的 NAC 并减弱其抑制功能。此外，我们揭示了 IIPs 在进化上是保守的，并具有未被报道的 CCCH 基序，被称为非典型的 CCCH 串联锌指蛋白。总的来说，我们的研究为次生壁合成的调控提供了机制上的见解，并为提高作物的相关农艺性状提供了机会。
