Os03g0203200
HTD2 gene could negatively regulate tiller bud outgrowth by the strigolactone pathway
Contents
Annotated Information
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Function
The function of Dwarf 88 was confirmed by complementation test and antisense analysis. D88, thus, represents a new category of genes that regulates cell growth and organ development and consequently plant architecture. The potential relationship between the tiller formation associated genes and D88 is discussed and future identification of the substrate for D88 may lead to the characterization of new pathways regulating plant development [1].
We propose that D14 functions downstream of strigolactone synthesis, as a component of hormone signaling or as an enzyme that participates in the conversion of strigolactones to the bioactive form [2]. The d14 mutant exhibits increased shoot branching with reduced plant height like the previously characterized strigolactone-defi cient and -insensitive mutants d10 and d3 , respectively [2].
The results suggest that the HTD2 gene could negatively regulate tiller bud outgrowth by the strigolactone pathway [3]. which is characterized by a high tillering and dwarf phenotype. Phenotypic analysis of the mutant showed that the mutation did not aVect formation of tiller bud, but promoted the subsequent outgrowth of tiller bud [3].
Expression
The gene Dwarf 88 was expressed in most rice organs, with especially high levels in the vascular tissues [1]. The mutant had excessive shorter tillers and smaller panicles and seeds compared to the wild-type. A reduction in number and size of parenchyma cells around stem marrow cavity as well as a delay in the elongation of parenchyma cells caused slender tillers and dwarfism in the d88 mutant [1].
The d14 branching phenotype could not be rescued by exogenous strigolactones. In addition, the d14 mutant contained a higher level of 2 ′ - epi -5-deoxystrigol than the wild type. Positional cloning revealed that D14 encodes a protein of the α / β -fold hydrolase superfamily, some members of which play a role in metabolism or signaling of plant hormones [2].
Leaves, inflorescences, internodes, nodes, roots and lateral buds (about 2 cm in length) were excised from 100-day-old wild-type plants. The mRNA expression of HTD2 in different tissues was analyzed by real-time PCR (Fig.6). The results showed that the highest expression levels were observed in leaves, followed by internodes, nodes, roots,lateral buds and inXorescences. The HTD2 expression levels in leaves were signiWcantly higher than that in other tissues [3].
Evolution
The strigolactone signal regulates bud outgrowth by controlling auxin transport capacity in the stem in Arabidopsis .In max mutants, there is an increase in auxin transport capacity. The elevated capacity of auxin transport causes bud outgrowth,since increased expression of PIN auxin eZux carrier was observed in maxmutants and the pin1mutation suppressed the max phenotype. In htd2 mutant, the biosynthesis of strigolactone is likely to be arrested as a result of the htd2 mutation. The absence of strigolactone could result in increased auxin transport, further promoting bud outgrowth in the htd2 mutant. Four high tillering and dwarf genes, including D10,HTD1, D3and TB1, have been cloned in rice .Their orthologous genes have similar functions in Arabidopsis, pea and petunia .These findings indicate that monocot and eudicot plants share a conserved mechanism controlling shoot branching. In the present study, we identified a new high tillering and dwarf gene HTD2, which encodes an esterase/lipase/thioesterase. Although orthologous genes for HTD2 widely exist in other plants (Fig.Phylogenetic tree of HTD2 and its homologous proteins), none has been characterized so far. Characterization of the HTD2gene and study on its interaction with other tillering-related genes will be helpful to further understand the regulation mechanism of outgrowth of tiller buds in plants.[3].
Knowledge Extension
Strigolactones (SLs) are a group of newly identified plant hormones that control plant shoot branching[4]. SL signaling requires the hormone-dependent interaction of DWARF14 (D14) which is regulated by the interaction of OsMADS57 with OsTB1[5]. In this study[4], they have identified theD53gene that encodes a substrate of the SCF(D3) ubiquitination complex, and revealed that D53 functions as a repressor ofSL signalling. These results allow to establish a model of SL signalling that is centred around a D14–D3–D53 signalling axis . In the presence of SLs, perception of SL by D14 and the SCF(D3) complex leads to ubiquitination of D53 and its subsequent degradation by the ubiquitin proteasome system, which in turn releases the repression of downstream target genes . In the d53 plant, the mutated D53 protein is resistant to ubiquitination and degradation, leading to the accumulation of d53, which blocks SL signalling and results in dwarf and high tillering phenotypes. The signalling paradigm of SLs is still emerging as SLs are a relatively new class of plant hormone for which many knowledge gaps still exist. Identification of D53 as a repressor of SL signalling adds a critical piece of information that helps to paint the whole picture of the SL signalling pathways. Moreover, the work has also provided an important paradigm for understanding signalling pathways of other plant hormones, for example, karrikins, a class of plant growth regulators found in the smoke of burning plants. Karrikin signalling involves MAX2 and KAI2, a D14-like α / β-hydrolase. It is probable that a similar protein to D53 could serve as the repressor of karrikin signalling. Indeed, multiple D53-like proteins are found in rice and inArabidopsis. We propose that these proteins could serve as repressors of signalling by karrikin and other plant hormones, in a similar way to D53 in SL signalling.[4]
Labs working on this gene
- National Center for Gene Research/Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 500 Caobao Road, 200233 Shanghai, China
- State Key Laboratory of Rice Biology, China National Rice Research Institute, Chinese Academy of Agricultural Sciences, 310006 Hangzhou, China
- Ishikawa Prefectural University, Nonoichi, Ishikawa, 921-8836 Japan
- RIKEN Plant Science Center, Tsurumi, Yokohama, 230-0045 Japan
- Graduate School of Agriculture and Life Sciences, University of Tokyo, Yayoi, Bunkyo, Tokyo, 113-8657 Japan
- Research Institute for Bioresources, Okayama University, Kurashiki, Okayama, 710-0046 Japan
- State Key Laboratory of Rice Biology, China National Rice Research Institute, 359 Tiyuchang Road, 310006 Hangzhou, Zhejiang, China
- Biotechnology Research Center, China Three Gorges University, 443002 Yichang, Hubei, China
References
- ↑ 1.0 1.1 1.2 Gao Z, Qian Q, Liu X, et al. Dwarf 88, a novel putative esterase gene affecting architecture of rice plant[J]. Plant molecular biology, 2009, 71(3): 265-276.
- ↑ 2.0 2.1 2.2 Arite T, Umehara M, Ishikawa S, et al. d14, a strigolactone-insensitive mutant of rice, shows an accelerated outgrowth of tillers[J]. Plant and cell physiology, 2009, 50(8): 1416-1424.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Liu W, Wu C, Fu Y, et al. Identification and characterization of HTD2: a novel gene negatively regulating tiller bud outgrowth in rice[J]. Planta, 2009, 230(4): 649-658.
- ↑ 4.0 4.1 4.2 4.3 Jiang L, Liu X, Xiong G, et al. DWARF 53 acts as a repressor of strigolactone signalling in rice[J]. Nature 2013.
- ↑ Guo S, Xu Y, Liu H, et al. The interaction between OsMADS57 and OsTB1 modulates rice tillering via DWARF14[J]. Nature communications 2013; 4: 1566.
