SPOC domain-containing protein Leaf inclination3 interacts with LIP1 to regulate rice leaf inclination through auxin signaling.
SPOC domain-containing protein Leaf inclination3 interacts with LIP1 to regulate rice leaf inclination through auxin signaling.
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DOI：
10.1371/journal.pgen.1007829
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发表时间：
2018-11
期刊：
影响因子：
4.5
通讯作者：
Xue HW
中科院分区：
文献类型：
--
作者：
Chen SH;Zhou LJ;Xu P;Xue HW
叶角是影响作物结构和产量的重要农艺性状。研究已经证明了植物激素，特别是生长素和油菜素类固醇，以及各种因素在控制叶片倾斜中的作用。然而，其基本机制，特别是上游监管网络仍需澄清。在这里，我们报告的功能特性的水稻叶片倾斜3（LC 3），一个SPOC结构域的转录抑制因子，在调节叶片倾斜通过LIP 1（LC 3相互作用蛋白1），一个HIT锌指结构域的蛋白质。LC 3缺乏导致叶片倾斜度增加，OsIAA 12和OsGH3.2的表达增强。一致的是，具有0 sIAA 12过表达或缺乏与0 sIAA 12相互作用的0 sARF 17的转基因植物确实呈现增大的叶片倾斜度。LIPl直接结合OsIAA 12和OsGH3.2的启动子区，并与LC 3相互作用以协同抑制生长素信号传导。本研究揭示了IAA 12-ARF 17互作在叶片倾斜度调控中的独特作用，为阐明含SPOC结构域的转录抑制子通过LC 3调控生长素稳态和生长素信号转导调控叶片发育的精细调控网络的功能机制提供了有益的线索。叶角是作物理想构型的一个重要性状，与光合效率和产量密切相关。对这一机理的研究将有助于提高作物产量。植物激素特别是生长素和油菜素内酯在调节叶片倾斜度中起着重要作用，但其上游调控网络尚不清楚。在这里，我们功能上的特点，一个新的SPOC结构域包含蛋白LC 3（叶倾角3）在叶片联合发展通过调节生长素信号。LC 3缺乏导致叶片接合处近轴侧细胞过度伸长，从而导致叶角增大。LC 3通过与LIP 1（LC 3-interacting protein 1，一种含有HIT锌指结构域的转录因子）相互作用而发挥转录抑制因子的作用，LIP 1直接与生长素信号和稳态相关基因的启动子结合。我们的研究为SPOC结构域蛋白的功能机制提供了新的见解，并有助于阐明生长素信号在叶片联合发育过程中的调节。
Leaf angle is an important agronomic trait and influences crop architecture and yield. Studies have demonstrated the roles of phytohormones, particularly auxin and brassinosteroids, and various factors in controlling leaf inclination. However, the underlying mechanism especially the upstream regulatory networks still need being clarified. Here we report the functional characterization of rice leaf inclination3 (LC3), a SPOC domain-containing transcription suppressor, in regulating leaf inclination through interacting with LIP1 (LC3-interacting protein 1), a HIT zinc finger domain-containing protein. LC3 deficiency results in increased leaf inclination and enhanced expressions of OsIAA12 and OsGH3.2. Being consistent, transgenic plants with OsIAA12 overexpression or deficiency of OsARF17 which interacts with OsIAA12 do present enlarged leaf inclination. LIP1 directly binds to promoter regions of OsIAA12 and OsGH3.2, and interacts with LC3 to synergistically suppress auxin signaling. Our study demonstrate the distinct effects of IAA12-ARF17 interactions in leaf inclination regulation, and provide informative clues to elucidate the functional mechanism of SPOC domain-containing transcription suppressor and fine-controlled network of lamina joint development by LC3-regulated auxin homeostasis and auxin signaling through. Leaf angle is a major trait of ideal architecture of crops that associates with photosynthetic efficiency and yields. Studies of the underlying mechanism will greatly help to improve the crop yield. Phytohormones especially auxin and brassinosteroids play crucial roles in regulating the leaf inclination, however, the upstream regulatory network is still unknown. Here, we functionally characterize a novel SPOC domain-containing protein LC3 (leaf inclination3) in lamina joint development through regulating auxin signaling. LC3 deficiency results in the excessive cell elongation at lamina joint adaxial side and hence the enlarged leaf angle. LC3 acts as a transcription suppressor through interacting with LIP1 (LC3-interacting protein 1, a HIT zinc finger domain-containing transcription factor), which directly binds to the promoters of auxin signaling and homeostasis related genes. Our studies provide new insights in the functional mechanism of SPOC domain-containing proteins and help to elucidate how auxin signaling is regulated during lamina joint development.
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