Os05g0213500
The cytosolic ABA receptor OsPYL/RCAR5 (PYL5) functions as a positive regulator of abiotic stress-responsive gene expression[1][2].
Contents
Annotated Information
Function
- Although exogenous expression of OsPYL/RCAR5 is able to improve abiotic stress tolerance in rice, fine regulation of its expression will be required to avoid deleterious effects on agricultural traits[1].
- A rice ABA signalling unit composed of OsPYL/RCAR5, OsPP2C30, SAPK2, and OREB1 for ABA-dependent gene regulation was further identified, via interaction assays and a transient gene expression assay. Thus, a core signalling unit for ABA-responsive gene expression modulating seed germination and early seedling growth in rice has been unravelled[2].
- OsPYL/RCAR5 might function as an ABA receptor, implying that the ABA-sensing mechanism is conserved in both rice and Arabidopsis. OsPYL/RCAR5 is a positive regulator in ABA signalling. These imply that the induction of the ABA-dependent reporter gene by OREB1 occurs in the context of ABA signalling via OsPYL/RCAR5, OsPP2C30, SAPK2, and OREB1[2].
Mutation
- OsPYL/RCAR5-OE plants[1]:
- All three independent lines displayed OsPYL/RCAR5 expression levels at least 50-fold higher than the control line, which also confirmed by agarose gel electrophoresis of RT-PCR products.
- Ectopic expression of OsPYL/RCAR5 in transgenic rice leads to drought and salt tolerance in the vegetative growth stage.
- For the drought tolerance assay, 3-week-old plants were rewatered after 5 d of drying. More leaves survived in the OsPYL/RCAR5-OE plants than in control plants, and the freshweights of the OsPYL/RCAR5-OE plants were almost 2-fold higher than those of control plants. The three independent transgenic lines showed similar phenotypes, which indicating that overexpression of the ABA receptor OsPYL/RCAR5 can increase drought tolerance in rice at the vegetative stage.
- Growth of transgenic plants overexpressing OsPYL/RCAR5 is retarded under osmotic stress and ABA treatment.
- Transgenic plants overexpressing OsPYL/RCAR5 have dwarf phenotypes and show reduced yield.
- Transgenic rice plants expressing OsPYL/RCAR5 were found to be hypersensitive to ABA during seed germination and early seedling growth[2].
Expression
- The constitutive expression of OsPYL/ RCAR5 in rice driven by the Zea mays ubiquitin promoter induced the expression of many stress-responsive genes even under normal growth conditions and resulted in improved drought and salt stress tolerance in rice. However, it slightly reduced plant height under paddy field conditions and severely reduced total seed yield[1].
- It was expressed in all tissues examined and was the most abundant in the leaf blade, followed by the leaf sheath, and was the lowest in root tissue. Strong GUS staining was detected in the leaf blades of the young seedlings, but did not observe staining in the roots of young seedlings. Microscopic analysis of leaf blades stained using X-Glu showed that the OsPYL/ RCAR5 promoter drove GUS expression throughout the surface of the leaf blade, including guard cells[1].
- The expression of OsPYL/RCAR5 was repressed under ABA or PEG treatment and was changed marginally under NaCl treatment. Thus, OsPYL/RCAR5 is not induced and is actually slightly suppressed by certain abiotic stresses[1].
- Expression of abiotic stress-responsive genes is altered in transgenic rice overexpressing OsPYL/RCAR5. 61 genes were commonly upregulated by both drought and overexpression of OsPYL/RCAR5, and 12 genes showed opposite differential expression with a change more than 2-fold. Of the latter, 69 genes were commonly downregulated and three genes inversely upregulated with respect to drought[1].
- Constitutive expression of OsPYL/RCAR5 increases expression of the ABA-responsive genes under ABA treatment. OsPYL/RCAR5 interacts with clade A rice PP2Cs in an ABA-dependent manner[2].
Subcellular localization
The OsPYL/RCAR5–OsPP2C30 complex is localized to the nucleus[2].
Evolution
OsPYL/RCAR5 is a PYL/RCAR orthologue of rice. OsPYR/RCARs have high similarity to Arabidopsis PYR/RCARs[2].
Knowledge Extension
- The default state of the SnRK2 kinases is an autophosphorylated, active state and that the SnRK2 kinases are kept inactive by the PP2Cs through physical interaction and dephosphorylation. Fujii et al. found that in the presence of ABA, the PYR/PYL (pyrabactin resistance 1/PYR1-like) receptor proteins can disrupt the interaction between the SnRK2s and PP2Cs, thus preventing the PP2C-mediated dephosphorylation of the SnRK2s and resulting in the activation of the SnRK2 kinases[3].
- The PYR/PYL family consists of 14 members. Although genetic studies suggested redundancy in their function12, it is not known whether all members can act as ABA receptors and transduce the ABA signal to induce gene expression[3].
Labs working on this gene
- Molecular Breeding Division, National Academy of Agricultural Science, RDA, Suwon 441-707, Republic of Korea
- Department of Plant Molecular Systems Biotechnology and Crop Biotech Institute, Kyung Hee University, Yongin 446-701, Republic of Korea
- Graduate School of Biotechnology, Kyung Hee University, Yongin 446-701, Republic of Korea
- Department of Plant Bioscience, Pusan National University, Miryang, 627-706, Republic of Korea
- Department of Biological Sciences, Sungkyunkwan University, Suwon, 440-746 Korea
- Department of Genetic Engineering, Sungkyunkwan University, Suwon, 440-746 Korea
- School of Biological Sciences (BK21 program), Chung-Ang University, Seoul, 156-756 Korea
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Kim H, Lee K, Hwang H, et al. Overexpression of PYL5 in rice enhances drought tolerance, inhibits growth, and modulates gene expression[J]. Journal of experimental botany, 2014, 65(2): 453-464.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Kim H, Hwang H, Hong J W, et al. A rice orthologue of the ABA receptor, OsPYL/RCAR5, is a positive regulator of the ABA signal transduction pathway in seed germination and early seedling growth[J]. Journal of experimental botany, 2012, 63(2): 1013-1024.
- ↑ 3.0 3.1 Fujii H, Chinnusamy V, Rodrigues A, et al. In vitro reconstitution of an abscisic acid signalling pathway[J]. Nature, 2009, 462(7273): 660-664.
