Abstract
Teosinte Branched1/Cycloidea/Proliferating cell factors (TCP) genes are key mediators of genetic innovations underlying morphological novelties, stress adaptation, and evolution of immune response in plants. They have a remarkable ability to integrate and translate diverse endogenous, and environmental signals with high fidelity. Compilation of studies, aimed at elucidating the mechanism of TCP functions, shows that it takes an amalgamation and interplay of several different factors, regulatory processes and pathways, instead of individual components, to achieve the incredible functional diversity and specificity, demonstrated by TCP proteins. Through this minireview, we provide a brief description of key structural features and molecular components, known so far, that operate this conglomerate, and highlight the important conceptual challenges and lacunae in TCP research.
Highlights
TCP (Teosinte Branched1/Cycloidea/Proliferating cell factors) is a plant-specific family of transcription factors (TFs), with the earliest members reported in fresh water charophyte algae (Cubas et al, 1999a; Navaud et al, 2007)
TCP proteins are characterized by a non-canonical beta helix-loop-helix domain, known as TCP domain
TCP proteins have little homology with beta helix-loop-helix (bHLH) TFs and bind to DNA elements distinct from those recognized by bHLH TFs; the DNA contacting residues and mechanism of binding seem to be conserved in both the families (Kosugi and Ohashi, 1997)
Summary
TCP (Teosinte Branched1/Cycloidea/Proliferating cell factors) is a plant-specific family of transcription factors (TFs), with the earliest members reported in fresh water charophyte algae (Cubas et al, 1999a; Navaud et al, 2007). Only CYC/TB1 genes have been implicating in branching, a recent study in Physcomitrella patens revealed a role of CIN gene PpTCP5 in determining sporangia architecture by negatively regulating branching (Ortiz-Ramírez et al, 2016). These results indicate regulation of branching as an ancient role of class II TCPs. These results indicate regulation of branching as an ancient role of class II TCPs Members of both the classes are targeted by pathogens to manipulate host defense. TCP14-regulated subset of JA response genes are de-repressed thereby, promoting pathogen virulence (Yang et al, 2017)
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