4/29/2023 0 Comments Srdx rabidopsis![]() DET2 encodes a protein sharing sequence similarity with the mammalian steroid 5α-reductase ( Li et al., 1997). For example, de-etiolated2 ( det2) was identified as a deetiolated mutant from Arabidopsis ( Chory et al., 1991). Several genes encoding key BR biosynthetic enzymes have also been cloned using BR-deficient mutants identified from a number of plant species, such as Arabidopsis, pea ( Pisum sativum), tomato ( Solanum lycopersicum), and rice ( Orzya sativa Fujioka and Yokota, 2003). The entire BR biosynthetic pathway was initially elucidated using cultured Catharanthus roseus cells ( Fujioka and Yokota, 2003). As a consequence of these events, the plant is able to fine-tune its growth and development. Activated receptor/coreceptor complex initiates a phosphorylation/dephosphorylation cascade that can transduce the BR signal from the cell surface to the cytoplasm and eventually to the nucleus where gene expression patterns are altered through the action of two transcription factors BZR1 and BES1 ( Kim et al., 2009). A proposed pathway for BR signal transduction starts with the ligand (BR) binding to the extracellular domain of BRI1, which triggers a sequential phosphorylation between BRI1 and BAK1 ( Wang et al., 2008). Although a more detailed mechanistic understanding as to how the aforementioned proteins coordinate various steps in BR signaling is needed, evidence to date strongly indicates that they are key signaling components in BR signal transduction that relay information from the cell surface to nuclear transcription factors. Other important regulatory proteins, such as a secreted Ser carboxypeptidase designated as bri1 SUPPRESSOR1 ( Li et al., 2001a), a BRI1 inhibitory protein BKI1 ( Wang and Chory, 2006), several putative BRI1 substrates, including an Arabidopsis thaliana paralog of TGF-BETA RECEPTOR-INTERACTING PROTEIN-1 ( Jiang and Clouse, 2001 Ehsan et al., 2005), a TRANSTHYRETIN-LIKE protein ( Nam and Li, 2004), and three homologous BR SIGNALING KINASES ( Tang et al., 2008), a negative regulator called BRASSINOSTEROID INSENSITIVE2 ( Li et al., 2001b Li and Nam, 2002), a protein phosphatase (BSU1) ( Mora-Garcia et al., 2004), 14-3-3 proteins ( Bai et al., 2007 Gampala et al., 2007 Ryu et al., 2007), and two novel transcription factors, BZR1 ( Wang et al., 2002) and BES1 ( Yin et al., 2002), have also been identified using various approaches. A number of BR signaling regulators, such as the cell surface BR receptor BRASSINOSTEROID INSENSITIVE1 (BRI1) ( Li and Chory, 1997) and its coreceptor BRI1-ASSOCIATED PROTEIN KINASE1 (BAK1), were identified via genetic and biochemical methods ( Li et al., 2002 Nam and Li, 2002). Within the last two decades, detailed information regarding BR signal transduction and BR biosynthesis has been uncovered ( Kim and Wang, 2010). Mutant plants unable to biosynthesize or perceive BRs exhibit typical phenotypes, including extremely dwarfed statures, shortened leaf petioles, rounded and curled leaves, prolonged life spans, reduced male fertility, and deetiolated hypocotyls when grown in darkness. BRs play critical roles in multiple physiological processes during normal plant growth and development, from seed germination to leaf senescence. These studies demonstrate another level of regulation through which BRs mediate plant growth and development.īrassinosteroids (BRs) are a class of polyhydroxyl steroidal hormones naturally found in almost all plant species examined ( Clouse and Sasse, 1998). The expression of TCP1 appears to be regulated by BR levels. Confocal microscopy indicated that TCP1 is mainly confined to the nucleus. Real-time RT-PCR analysis further demonstrated that TCP1 regulates the transcription levels of DWF4, and chromatin immunoprecipitation experiments showed that TCP1 indeed interacts with the DWF4 promoter. BR profile assay (quantitative analysis of BR biosynthetic intermediates) strongly suggests that TCP1 expression level positively coordinates with the function of DWARF4 (DWF4), a key enzyme in BR biosynthesis. The defective phenotypes can be rescued by exogenously applied brassinolide but cannot be recovered by auxins, gibberellins, or cytokinins. Overexpression of a dominant-negative form of TCP1, TCP1-SRDX, with a 12–amino acid repressor sequence fused to TCP1 at its C terminus, results in dwarfed plants resembling BR-deficient or insensitive mutants. The dominant allele of TCP1, tcp1-1D, suppresses the defective phenotypes of bri1-5. TCP1 encodes a putative transcription factor possessing a basic helix-loop-helix domain. TCP1, a gene thought to be involved in floral organ symmetric control, was identified as a genetic suppressor of a weak BR receptor mutant, bri1-5, in an activation-tagging genetic screen. Brassinosteroids (BRs) are essential phytohormones regulating normal plant growth and development.
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