Arabidopsis det2 Is Defective in the Conversion of (24R)-24-Methylcholest-4-En-3-One to (24R)-24-Methyl-5α-Cholestan-3-One in Brassinosteroid Biosynthesis1

Noguchi, Takahiro; Fujioka, Shozo; Takatsuto, Suguru; Sakurai, Akira; Yoshida, Shigeo; Li, Jianming; Chory, Joanne

doi:10.1104/pp.120.3.833

Cited by 157 publications

(97 citation statements)

References 34 publications

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“…Mutants det2 presented only 8-15% of the campestanol levels found in the wild type and less than 10% of the wild type levels of other BRs. Mutants det2 were also unable to convert H 2 -campesterol into H 2 -campestanol, demonstrating that det2 mutantes were deficient in brassinoesteroids (reviewed in Li and Chory, 1999). Additional support to this finding came from rescue experiments in which all intermediates of the BRs biosynthetic pathway after the reaction catalyzed by det2 were able to rescue det2 mutant phenotypes (Li et al, 1996;Li and Chory, 1999).…”

Section: Cpdsupporting

confidence: 59%

“…The genetic approach used to identify the components of the BR biosynthetic and signal transduction pathways have relied on the isolation and characterization of mutants deficient in BRs biosynthesis or response. The availability of these mutants has played a major role in the increase in the knowledge concerning BRs Li and Chory, 1999;Bishop and Yokota, 2001;Clouse, 2002). BR-deficient mutants usually result from lesions in genes encoding for BR biosynthetic enzymes and are rescued to the wild type phenotype by exogenously supplied BRs Choe et al, 1998Choe et al, , 2000.…”

Section: Introductionmentioning

confidence: 99%

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Genes involved in brassinosteroids's metabolism and signal transduction pathways

Pereira-Netto

2007

Braz. arch. biol. technol.

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Brassinosteroids (BRs) are plant steroids essential for the normal growth and development, which carry an oxygen moiety at C-3 and additional ones at one or more of the C-2, C-6, C-22 and C-23 carbon atoms. In the past few years, application of molecular genetics allowed significant progress on the understanding of the BRs biosynthetic pathway regulation and on the identification of several components of their signal transduction pathway, as well. Search in eletronic databases show dozens of records for brassinosteroid-related genes for the last twelve months, demonstrating the big efforts being carried out in this field. This review highlights the recent advances on the characterization of genes and mutations that are helping to unravel the molecular mechanisms involved in the BRs

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Section: Cpdsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Genes involved in brassinosteroids's metabolism and signal transduction pathways

Pereira-Netto

2007

Braz. arch. biol. technol.

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“…7B). The phenotype of the rcd1-3; sro1-1 double mutant seedlings superficially resembles that of mutations in components of the brassinosteroid biosynthetic pathway, such as det2 mutants (Noguchi et al, 1999); however, the double mutant seedlings do expand their leaves, in a manner similar to the wild type, when exposed to exogenous brassinosteroid (Fig. 7D).…”

Section: Conditionsmentioning

confidence: 99%

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

2009

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RADICAL-INDUCED CELL DEATH1 (RCD1) and SIMILAR TO RCD ONE1 (SRO1) are the only two proteins encoded in the Arabidopsis (Arabidopsis thaliana) genome containing both a putative poly(ADP-ribose) polymerase catalytic domain and a WWE protein-protein interaction domain, although similar proteins have been found in other eukaryotes. Poly(ADP-ribose) polymerases mediate the attachment of ADP-ribose units from donor NAD + molecules to target proteins and have been implicated in a number of processes, including DNA repair, apoptosis, transcription, and chromatin remodeling. We have isolated mutants in both RCD1 and SRO1, rcd1-3 and sro1-1, respectively. rcd1-3 plants display phenotypic defects as reported for previously isolated alleles, most notably reduced stature. In addition, rcd1-3 mutants display a number of additional developmental defects in root architecture and maintenance of reproductive development. While single mutant sro1-1 plants are relatively normal, loss of a single dose of SRO1 in the rcd1-3 background increases the severity of several developmental defects, implying that these genes do share some functions. However, rcd1-3 and sro1-1 mutants behave differently in several developmental events and abiotic stress responses, suggesting that they also have distinct functions. Remarkably, rcd1-3; sro1-1 double mutants display severe defects in embryogenesis and postembryonic development. This study shows that RCD1 and SRO1 are at least partially redundant and that they are essential genes for plant development.

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“…DET2 encodes a steroid 5a-reductase that catalyzes a key step in BR biosynthesis (Noguchi et al, 1999). This close proximity raised the possibility that the large-leaf phenotype we attributed to a disruption of PHT4;2 was instead caused by an overexpression of DET2 via T-DNA activation (Weigel et al, 2000;Ren et al, 2004).…”

Section: Plant Size and Biomassmentioning

confidence: 99%

The Sink-Specific Plastidic Phosphate Transporter PHT4;2 Influences Starch Accumulation and Leaf Size in Arabidopsis

et al. 2011

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Nonphotosynthetic plastids are important sites for the biosynthesis of starch, fatty acids, and amino acids. The uptake and subsequent use of cytosolic ATP to fuel these and other anabolic processes would lead to the accumulation of inorganic phosphate (Pi) if not balanced by a Pi export activity. However, the identity of the transporter(s) responsible for Pi export is unclear. The plastid-localized Pi transporter PHT4;2 of Arabidopsis (Arabidopsis thaliana) is expressed in multiple sink organs but is nearly restricted to roots during vegetative growth. We identified and used pht4;2 null mutants to confirm that PHT4;2 contributes to Pi transport in isolated root plastids. Starch accumulation was limited in pht4;2 roots, which is consistent with the inhibition of starch synthesis by excess Pi as a result of a defect in Pi export. Reduced starch accumulation in leaves and altered expression patterns for starch synthesis genes and other plastid transporter genes suggest metabolic adaptation to the defect in roots. Moreover, pht4;2 rosettes, but not roots, were significantly larger than those of the wild type, with 40% greater leaf area and twice the biomass when plants were grown with a short (8-h) photoperiod. Increased cell proliferation accounted for the larger leaf size and biomass, as no changes were detected in mature cell size, specific leaf area, or relative photosynthetic electron transport activity. These data suggest novel signaling between roots and leaves that contributes to the regulation of leaf size.

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Arabidopsis det2 Is Defective in the Conversion of (24R)-24-Methylcholest-4-En-3-One to (24R)-24-Methyl-5α-Cholestan-3-One in Brassinosteroid Biosynthesis1

Cited by 157 publications

References 34 publications

Genes involved in brassinosteroids's metabolism and signal transduction pathways

Genes involved in brassinosteroids's metabolism and signal transduction pathways

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

The Sink-Specific Plastidic Phosphate Transporter PHT4;2 Influences Starch Accumulation and Leaf Size in Arabidopsis

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