The remodeling of root architecture is a major developmental response of plants to phosphate （Pi） deficiency and is thought to enhance a plant＇s ability to forage for the available Pi in topsoil. The underlying mec...The remodeling of root architecture is a major developmental response of plants to phosphate （Pi） deficiency and is thought to enhance a plant＇s ability to forage for the available Pi in topsoil. The underlying mechanism controlling this response, however, is poorly understood. In this study, we identified an Arabidopsis mutant, hps 10 （hypersensitive to Pi starvation 10）, which is morphologically normal under Pi sufficient condition but shows increased inhibition of primary root growth and enhanced production of lateral roots under Pi defi- ciency, hpslO is a previously identified allele （als3-3） of the ALUMINUM SENSITIVE3 （ALS3） gene, which is involved in plant tolerance to aluminum toxicity. Our results show that ALS3 and its interacting protein AtSTAR1 form an ABC transporter complex in the tonoplast. This protein complex mediates a highly electro- genic transport in Xenopus oocytes. Under Pi deficiency, als3 accumulates higher levels of Fe3＋ in its roots than the wild type does. In Arabidopsis, LPR1 （LOW PHOSPHATE ROOT1） and LPR2 encode ferroxidases, which when mutated, reduce Fe3＋ accumulation in roots and cause root growth to be insensitive to Pi defi- ciency. Here, we provide compelling evidence showing that ALS3 cooperates with LPR1/2 to regulate Pi deficiency-induced remodeling of root architecture by modulating Fe homeostasis in roots.展开更多
Phosphatidylcholine-hydrolyzing phospholipase C （PC-PLC） catalyzes the hydrolysis of phosphatidylcholine （PC） to generate phosphocholine and diacylglycerol （DAG）. PC-PLC has a long tradition in animal signal tra...Phosphatidylcholine-hydrolyzing phospholipase C （PC-PLC） catalyzes the hydrolysis of phosphatidylcholine （PC） to generate phosphocholine and diacylglycerol （DAG）. PC-PLC has a long tradition in animal signal transduction to generate DAG as a second messenger besides the classical phosphatidylinositol splitting phospholipase C （PI-PLC）. Based on amino acid sequence similarity to bacterial PC-PLC, six putative PC-PLC genes （NPC1 to NPC6） were identified in the Arabidopsis genome. RT-PCR analysis revealed overlapping expression pattern of NPC genes in root, stem, leaf, flower, and silique. In auxin-treated PNPc3：GUS and PNPc4：GUS seedlings, strong increase of GUS activity was visible in roots, leaves, and shoots and, to a weaker extent, in brassinolide-treated （BL） seedlings. PNPc4：GUS seedlings also responded to cytokinin with increased GUS activity in young leaves. Compared to wild-type, T-DNA insertional knockouts npc3 and npc4 showed shorter primary roots and lower lateral root density at low BL concentrations but increased lateral root densities in response to exogenous 0.05-1.0 I^M BL BL-induced expression of TCH4 and LRX2, which are involved in cell expansion, was impaired but not impaired in repression of CPD, a BL biosynthesis gene, in BL-treated npc3 and npc4. These observations suggest NPC3 and NPC4 are important in BL-mediated signaling in root growth. When treated with 0.1 I^M BL, DAG accumulation was observed in tobacco BY-2 cell cultures labeled with fluorescent PC as early as 15 min after application. We hypothesize that at least one PC-PLC is a plant signaling enzyme in BL signal transduction and, as shown earlier, in elicitor signal transduction.展开更多
A mutant isolated from a screen of EMS-mutagenized Arabidopsis lines, per1, showed normal root hair development under control conditions but displayed an inhibited root hair elongation phenotype upon Pi deficiency. Ad...A mutant isolated from a screen of EMS-mutagenized Arabidopsis lines, per1, showed normal root hair development under control conditions but displayed an inhibited root hair elongation phenotype upon Pi deficiency. Additionally, the per1 mutant exhibited a pleiotropic phenotype under control conditions, resembling Pi-deficient plants in several aspects. Inhibition of root hair elongation upon growth on low Pi media was reverted by treatment with the Pi analog phosphite, suggesting that the mutant phenotype is not caused by a lack of Pi. Reciprocal grafting experiments revealed that the mutant rootstock is sufficient to cause the phenotype. Complementation analyses showed that the PER1 gene encodes an ubiquitin-specific protease, UBP14. The mutation caused a synonymous substitution in the 12th exon of this gene, resulting in a lower abundance of the UBP14 protein, probably as a consequence of reduced translation efficiency. Transcriptional profiling of per1 and wild-type plants subjected to short-term Pi starvation revealed genes that may be important for the signaling of Pi deficiency. We conclude that UBP14 function is crucial for adapting root development to the prevailing local availability of phosphate.展开更多
Phosphate （Pi） deficiency causes dramatic root system architecture （RSA） changes in higher plants. Here we report that overexpression of HRS1 leads to enhanced sensitivity to low Pi-elicited inhibition of primary ...Phosphate （Pi） deficiency causes dramatic root system architecture （RSA） changes in higher plants. Here we report that overexpression of HRS1 leads to enhanced sensitivity to low Pi-elicited inhibition of primary root growth in Arabidopsis thaliana seedlings. Bioinformatic investigations uncovered that HRS1 and its six homologs encode putative G2-like transcription factors in Arabidopsis. Analysis of promoter：：GUS reporter lines revealed that HRS1 transcripts were present mainly in the root hair region and root hair cells under Pi-sufficient conditions. Pi deprivation increased HRS1 expression level and expanded its expression domain. Although HRS1 knockout mutant did not differ from wild type （WT） control irrespective of Pi status, its overexpression lines were significantly more susceptible to low Pi-elicited primary root shortening. In both WT and HRS1 overexpression seedlings, low Pi-induced primary root shortening was accompanied by enhanced root hair cell differentiation, but this enhancement occurred to a greater extent in the latter genotype. Collectively, our data suggest that HRS1 may be involved in the modulation of primary root and root hair growth in Pi-deprived Arabidopsis seedlings, and provide useful clues for further research into the function of HRS1 and its homologs and the mechanisms behind RSA changes under Pi-deficient conditions.展开更多
文摘The remodeling of root architecture is a major developmental response of plants to phosphate （Pi） deficiency and is thought to enhance a plant＇s ability to forage for the available Pi in topsoil. The underlying mechanism controlling this response, however, is poorly understood. In this study, we identified an Arabidopsis mutant, hps 10 （hypersensitive to Pi starvation 10）, which is morphologically normal under Pi sufficient condition but shows increased inhibition of primary root growth and enhanced production of lateral roots under Pi defi- ciency, hpslO is a previously identified allele （als3-3） of the ALUMINUM SENSITIVE3 （ALS3） gene, which is involved in plant tolerance to aluminum toxicity. Our results show that ALS3 and its interacting protein AtSTAR1 form an ABC transporter complex in the tonoplast. This protein complex mediates a highly electro- genic transport in Xenopus oocytes. Under Pi deficiency, als3 accumulates higher levels of Fe3＋ in its roots than the wild type does. In Arabidopsis, LPR1 （LOW PHOSPHATE ROOT1） and LPR2 encode ferroxidases, which when mutated, reduce Fe3＋ accumulation in roots and cause root growth to be insensitive to Pi defi- ciency. Here, we provide compelling evidence showing that ALS3 cooperates with LPR1/2 to regulate Pi deficiency-induced remodeling of root architecture by modulating Fe homeostasis in roots.
文摘Phosphatidylcholine-hydrolyzing phospholipase C （PC-PLC） catalyzes the hydrolysis of phosphatidylcholine （PC） to generate phosphocholine and diacylglycerol （DAG）. PC-PLC has a long tradition in animal signal transduction to generate DAG as a second messenger besides the classical phosphatidylinositol splitting phospholipase C （PI-PLC）. Based on amino acid sequence similarity to bacterial PC-PLC, six putative PC-PLC genes （NPC1 to NPC6） were identified in the Arabidopsis genome. RT-PCR analysis revealed overlapping expression pattern of NPC genes in root, stem, leaf, flower, and silique. In auxin-treated PNPc3：GUS and PNPc4：GUS seedlings, strong increase of GUS activity was visible in roots, leaves, and shoots and, to a weaker extent, in brassinolide-treated （BL） seedlings. PNPc4：GUS seedlings also responded to cytokinin with increased GUS activity in young leaves. Compared to wild-type, T-DNA insertional knockouts npc3 and npc4 showed shorter primary roots and lower lateral root density at low BL concentrations but increased lateral root densities in response to exogenous 0.05-1.0 I^M BL BL-induced expression of TCH4 and LRX2, which are involved in cell expansion, was impaired but not impaired in repression of CPD, a BL biosynthesis gene, in BL-treated npc3 and npc4. These observations suggest NPC3 and NPC4 are important in BL-mediated signaling in root growth. When treated with 0.1 I^M BL, DAG accumulation was observed in tobacco BY-2 cell cultures labeled with fluorescent PC as early as 15 min after application. We hypothesize that at least one PC-PLC is a plant signaling enzyme in BL signal transduction and, as shown earlier, in elicitor signal transduction.
文摘A mutant isolated from a screen of EMS-mutagenized Arabidopsis lines, per1, showed normal root hair development under control conditions but displayed an inhibited root hair elongation phenotype upon Pi deficiency. Additionally, the per1 mutant exhibited a pleiotropic phenotype under control conditions, resembling Pi-deficient plants in several aspects. Inhibition of root hair elongation upon growth on low Pi media was reverted by treatment with the Pi analog phosphite, suggesting that the mutant phenotype is not caused by a lack of Pi. Reciprocal grafting experiments revealed that the mutant rootstock is sufficient to cause the phenotype. Complementation analyses showed that the PER1 gene encodes an ubiquitin-specific protease, UBP14. The mutation caused a synonymous substitution in the 12th exon of this gene, resulting in a lower abundance of the UBP14 protein, probably as a consequence of reduced translation efficiency. Transcriptional profiling of per1 and wild-type plants subjected to short-term Pi starvation revealed genes that may be important for the signaling of Pi deficiency. We conclude that UBP14 function is crucial for adapting root development to the prevailing local availability of phosphate.
基金Supported by the National Natural Science Foundation of China(30521001)the Ministry of Science and Technology of China(2005CB120904).
文摘Phosphate （Pi） deficiency causes dramatic root system architecture （RSA） changes in higher plants. Here we report that overexpression of HRS1 leads to enhanced sensitivity to low Pi-elicited inhibition of primary root growth in Arabidopsis thaliana seedlings. Bioinformatic investigations uncovered that HRS1 and its six homologs encode putative G2-like transcription factors in Arabidopsis. Analysis of promoter：：GUS reporter lines revealed that HRS1 transcripts were present mainly in the root hair region and root hair cells under Pi-sufficient conditions. Pi deprivation increased HRS1 expression level and expanded its expression domain. Although HRS1 knockout mutant did not differ from wild type （WT） control irrespective of Pi status, its overexpression lines were significantly more susceptible to low Pi-elicited primary root shortening. In both WT and HRS1 overexpression seedlings, low Pi-induced primary root shortening was accompanied by enhanced root hair cell differentiation, but this enhancement occurred to a greater extent in the latter genotype. Collectively, our data suggest that HRS1 may be involved in the modulation of primary root and root hair growth in Pi-deprived Arabidopsis seedlings, and provide useful clues for further research into the function of HRS1 and its homologs and the mechanisms behind RSA changes under Pi-deficient conditions.
