GhTIE1 Regulates Branching Through Modulating the Transcriptional Activity of TCPs in Cotton and Arabidopsis

Abstract

Transcription factors (TFs) and transcriptional regulators are important switches in transcriptional networks. In recent years, the transcriptional regulator TIE1 (TCP interactor containing EAR motif protein 1) was identified as a nuclear transcriptional repressor which regulates leaf development and controls branch development. However, the function and regulatory network of GhTIE1 has not been studied in cotton. Here, we demonstrated that GhTIE1 is functionally conserved in controlling shoot branching in cotton and Arabidopsis. Overexpression of GhTIE1 in Arabidopsis leads to higher bud vigor and more branches, while silencing GhTIE1 in cotton reduced bud activity and increased branching inhibition. Yeast two-hybrid (Y2H) and bimolecular fluorescence complementation (BiFC) assays showed that GhTIE1 directly interacted with subclass II TCPs (GhBRC1, GhBRC2, and GhTCP13) in vivo and in vitro. Overexpression of GhBRC1, GhBRC2, and GhTCP13 in mutant brc1-2 partially rescued the mutant phenotype and decreased the number of branches, showing that these TCPs are functionally redundant in controlling branching. A transient dual-luciferase reporter assay indicated that GhTIE1 repressed the protein activity of GhBRC1 and GhTCP13, and thereby decreased the expression of their target gene GhHB21. Gene expression level analysis in GhTIE1-overexpressed and silenced plants also proved that GhTIE1 regulated shoot branching via repressing the activity of BRC1, HB21, HB40, and HB53. Our data reveals that shoot branching can be controlled via modulation of the activity of the TIE1 and TCP proteins and provides a theoretical basis for cultivating cotton varieties with ideal plant types.

The Regulation of CIN-like TCP Transcription Factors

“…TIE1 had overlapping expression pattern with BRC1 in young axillary buds and overexpression of TIE1 resulted in excessive branches, indicating that TIE1 also represses the activity of BRC1 during shoot branching [ 40 ]. The function of TIE1 is conserved in controlling shoot branching in cotton ( Gossypium hirsutum ) [ 117 ]. GhTIE1 interacted with CYC subclade proteins GhBRC1, GhBRC2, and GhTCP13 in vivo.…”

“…GhTIE1 interacted with CYC subclade proteins GhBRC1, GhBRC2, and GhTCP13 in vivo. Silencing of GhTIE1 in cotton seriously decreased shoot branching [ 117 ]. A similar mechanism in suppression of CIN-like TCP activity is mediated by SPOROCYTELESS/NOZZLE (SPL/NZZ) during ovule development [ 118 ].…”

The miR164‐GhCUC2‐GhBRC1 module regulates plant architecture through abscisic acid in cotton

“…In rice, the moc1 mutant failed to develop tillers due to defects in axillary meristem formation, which is similar to the ls mutant tomato phenotype (Li et al., 2003 ; Schumacher et al., 1999 ). TIE1 promoted cotton branching via repressing the transcription activity of TCPs (Diao et al., 2019 ). Mutation of SP homologs promoted short‐branching architecture in cotton, and dynamic changes in GhSFT and GhSP expression level regulated cotton monopodial and sympodial branching architecture (McGarry et al., 2016 ; Si et al., 2018 ).…”

“…Here, we show that GhCUC2 is cleaved by gh‐miR164, and that GhCUC2 with mutated target sequence could not be cleaved by miR164. GhCUC2 physically interacts with a previously known lateral branch development‐related protein GhBRC1 and activates its transcriptional activity to regulate lateral branch development (Diao et al., 2019 ). In addition, genetic analysis demonstrated that GhCUC2 and GhBRC1 negatively regulate branching, exerting the opposite effect of miR164.…”

The miR319-Targeted GhTCP4 Promotes the Transition from Cell Elongation to Wall Thickening in Cotton Fiber

“…Another class I TCP, GbTCP of G. barbadense, affects fiber elongation through a complex interplay involving jasmonic acid biosynthesis and ethylene signaling (Hao et al, 2012). GhTCP13 and two other class II TCPs are functionally redundant in modulating plant architecture (Diao et al, 2019).…”