The Experts below are selected from a list of 87606 Experts worldwide ranked by ideXlab platform
Jinpeng Gao - One of the best experts on this subject based on the ideXlab platform.
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an shr scr module specifies legume Cortical Cell fate to enable nodulation
Nature, 2021Co-Authors: Wentao Dong, Yayun Zhu, Huizhong Chang, Chunhua Wang, Jun Yang, Jincai Shi, Jinpeng GaoAbstract:Legumes, unlike other plants, have the ability to establish symbiosis with nitrogen-fixing rhizobia. It has been theorized that a unique property of legume root Cortical Cells enabled the initial establishment of rhizobial symbiosis1-3. Here we show that a SHORTROOT-SCARECROW (SHR-SCR) stem Cell program in Cortical Cells of the legume Medicago truncatula specifies their distinct fate. Regulatory elements drive the Cortical expression of SCR, and stele-expressed SHR protein accumulates in Cortical Cells of M. truncatula but not Arabidopsis thaliana. The Cortical SHR-SCR network is conserved across legume species, responds to rhizobial signals, and initiates legume-specific Cortical Cell division for de novo nodule organogenesis and accommodation of rhizobia. Ectopic activation of SHR and SCR in legumes is sufficient to induce root Cortical Cell division. Our work suggests that acquisition of the Cortical SHR-SCR module enabled Cell division coupled to rhizobial infection in legumes. We propose that this event was central to the evolution of rhizobial endosymbiosis.
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an shr scr module specifies legume Cortical Cell fate to enable nodulation
Nature, 2021Co-Authors: Wentao Dong, Yayun Zhu, Huizhong Chang, Chunhua Wang, Jun Yang, Jinpeng Gao, J R ShiAbstract:Legumes, unlike other plants, have the ability to establish symbiosis with nitrogen-fixing rhizobia. It has been theorized that a unique property of legume root Cortical Cells enabled the initial establishment of rhizobial symbiosis1–3. Here we show that a SHORTROOT–SCARECROW (SHR–SCR) stem Cell program in Cortical Cells of the legume Medicago truncatula specifies their distinct fate. Regulatory elements drive the Cortical expression of SCR, and stele-expressed SHR protein accumulates in Cortical Cells of M. truncatula but not Arabidopsis thaliana. The Cortical SHR–SCR network is conserved across legume species, responds to rhizobial signals, and initiates legume-specific Cortical Cell division for de novo nodule organogenesis and accommodation of rhizobia. Ectopic activation of SHR and SCR in legumes is sufficient to induce root Cortical Cell division. Our work suggests that acquisition of the Cortical SHR–SCR module enabled Cell division coupled to rhizobial infection in legumes. We propose that this event was central to the evolution of rhizobial endosymbiosis. Repurposing of an SHR–SCR stem Cell program in the legume root cortex enables rhizobial symbiosis.
Yayun Zhu - One of the best experts on this subject based on the ideXlab platform.
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an shr scr module specifies legume Cortical Cell fate to enable nodulation
Nature, 2021Co-Authors: Wentao Dong, Yayun Zhu, Huizhong Chang, Chunhua Wang, Jun Yang, Jincai Shi, Jinpeng GaoAbstract:Legumes, unlike other plants, have the ability to establish symbiosis with nitrogen-fixing rhizobia. It has been theorized that a unique property of legume root Cortical Cells enabled the initial establishment of rhizobial symbiosis1-3. Here we show that a SHORTROOT-SCARECROW (SHR-SCR) stem Cell program in Cortical Cells of the legume Medicago truncatula specifies their distinct fate. Regulatory elements drive the Cortical expression of SCR, and stele-expressed SHR protein accumulates in Cortical Cells of M. truncatula but not Arabidopsis thaliana. The Cortical SHR-SCR network is conserved across legume species, responds to rhizobial signals, and initiates legume-specific Cortical Cell division for de novo nodule organogenesis and accommodation of rhizobia. Ectopic activation of SHR and SCR in legumes is sufficient to induce root Cortical Cell division. Our work suggests that acquisition of the Cortical SHR-SCR module enabled Cell division coupled to rhizobial infection in legumes. We propose that this event was central to the evolution of rhizobial endosymbiosis.
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an shr scr module specifies legume Cortical Cell fate to enable nodulation
Nature, 2021Co-Authors: Wentao Dong, Yayun Zhu, Huizhong Chang, Chunhua Wang, Jun Yang, Jinpeng Gao, J R ShiAbstract:Legumes, unlike other plants, have the ability to establish symbiosis with nitrogen-fixing rhizobia. It has been theorized that a unique property of legume root Cortical Cells enabled the initial establishment of rhizobial symbiosis1–3. Here we show that a SHORTROOT–SCARECROW (SHR–SCR) stem Cell program in Cortical Cells of the legume Medicago truncatula specifies their distinct fate. Regulatory elements drive the Cortical expression of SCR, and stele-expressed SHR protein accumulates in Cortical Cells of M. truncatula but not Arabidopsis thaliana. The Cortical SHR–SCR network is conserved across legume species, responds to rhizobial signals, and initiates legume-specific Cortical Cell division for de novo nodule organogenesis and accommodation of rhizobia. Ectopic activation of SHR and SCR in legumes is sufficient to induce root Cortical Cell division. Our work suggests that acquisition of the Cortical SHR–SCR module enabled Cell division coupled to rhizobial infection in legumes. We propose that this event was central to the evolution of rhizobial endosymbiosis. Repurposing of an SHR–SCR stem Cell program in the legume root cortex enables rhizobial symbiosis.
Huizhong Chang - One of the best experts on this subject based on the ideXlab platform.
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an shr scr module specifies legume Cortical Cell fate to enable nodulation
Nature, 2021Co-Authors: Wentao Dong, Yayun Zhu, Huizhong Chang, Chunhua Wang, Jun Yang, Jincai Shi, Jinpeng GaoAbstract:Legumes, unlike other plants, have the ability to establish symbiosis with nitrogen-fixing rhizobia. It has been theorized that a unique property of legume root Cortical Cells enabled the initial establishment of rhizobial symbiosis1-3. Here we show that a SHORTROOT-SCARECROW (SHR-SCR) stem Cell program in Cortical Cells of the legume Medicago truncatula specifies their distinct fate. Regulatory elements drive the Cortical expression of SCR, and stele-expressed SHR protein accumulates in Cortical Cells of M. truncatula but not Arabidopsis thaliana. The Cortical SHR-SCR network is conserved across legume species, responds to rhizobial signals, and initiates legume-specific Cortical Cell division for de novo nodule organogenesis and accommodation of rhizobia. Ectopic activation of SHR and SCR in legumes is sufficient to induce root Cortical Cell division. Our work suggests that acquisition of the Cortical SHR-SCR module enabled Cell division coupled to rhizobial infection in legumes. We propose that this event was central to the evolution of rhizobial endosymbiosis.
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an shr scr module specifies legume Cortical Cell fate to enable nodulation
Nature, 2021Co-Authors: Wentao Dong, Yayun Zhu, Huizhong Chang, Chunhua Wang, Jun Yang, Jinpeng Gao, J R ShiAbstract:Legumes, unlike other plants, have the ability to establish symbiosis with nitrogen-fixing rhizobia. It has been theorized that a unique property of legume root Cortical Cells enabled the initial establishment of rhizobial symbiosis1–3. Here we show that a SHORTROOT–SCARECROW (SHR–SCR) stem Cell program in Cortical Cells of the legume Medicago truncatula specifies their distinct fate. Regulatory elements drive the Cortical expression of SCR, and stele-expressed SHR protein accumulates in Cortical Cells of M. truncatula but not Arabidopsis thaliana. The Cortical SHR–SCR network is conserved across legume species, responds to rhizobial signals, and initiates legume-specific Cortical Cell division for de novo nodule organogenesis and accommodation of rhizobia. Ectopic activation of SHR and SCR in legumes is sufficient to induce root Cortical Cell division. Our work suggests that acquisition of the Cortical SHR–SCR module enabled Cell division coupled to rhizobial infection in legumes. We propose that this event was central to the evolution of rhizobial endosymbiosis. Repurposing of an SHR–SCR stem Cell program in the legume root cortex enables rhizobial symbiosis.
Sandra J Hewett - One of the best experts on this subject based on the ideXlab platform.
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sin 1 induced cytotoxicity in mixed Cortical Cell culture peroxynitrite dependent and independent induction of excitotoxic Cell death
Journal of Neurochemistry, 2008Co-Authors: Joseph L Trackey, Tracy F Uliasz, Sandra J HewettAbstract:3-Morpholinosyndnomine (SIN-1) has been reported to be a peroxynitrite (OONO−) donor because it produces both nitric oxide (NO) and superoxide ( O2−·) upon decomposition in aqueous solution. However, SIN-1 can decompose to primarily NO in the presence of electron acceptors, including those found in biological tissues, making it necessary to determine the release product(s) formed in any given biological system. In a mixed Cortical Cell culture system, SIN-1 caused a concentration-dependent increase in Cortical Cell injury with a parallel increase in the release of Cellular proteins containing 3-nitrotyrosine into the culture medium. The increase in 3-nitrotyrosine immunoreactivity, a footprint of OONO− production, was specific for SIN-1 as exposure to neurotoxic concentrations of an NO donor (Z)-1-[2-aminoethyl)-N-(2-ammonioethyl) aminodiazen-1-ium-1,2-diolate (DETA/NO), or NMDA did not result in the nitration of protein tyrosine residues. Both SIN-1-induced injury and 3-nitrotyrosine staining were prevented by the addition of either 5,10,15,20-Tetrakis (4-sulfonatophenyl) prophyrinato iron (III) [FeTPPS], an OONO− decomposition catalyst, or uric acid, an OONO− scavenger. Removal of NO alone was sufficient to inhibit the formation of OONO− from SIN-1 as well as its cytotoxicity. Removal of O2−· and the subsequently formed H2O2 by superoxide dismutase (SOD) plus catalase likewise prevented the nitration of protein-bound tyrosine but actually enhanced the cytotoxicity of SIN-1, indicating that Cortical Cells can cope with the oxidative but not the nitrosative stress generated. Finally, neural injury induced by SIN-1 in unadulterated Cortical Cells was prevented by antagonism of AMPA/kainate receptors, while blockade of the NMDA receptor was without effect. In contrast, activation of both NMDA and non-NMDA receptors contributed to the SIN-1-mediated neurotoxicity when cultures were exposed in the presence of SOD plus catalase. Thus, whether SIN-1 initiates neural Cell death in an OONO−-dependent or -independent manner is determined by the antioxidant status of the Cells. Further, the mode of excitotoxicity by which injury progresses is determined by the NO-related species generated.
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analysis of the neuroprotective effects of various nitric oxide donor compounds in murine mixed Cortical Cell culture
Journal of Neurochemistry, 2008Co-Authors: Aniruddha S Vidwans, Deborah O Coffin, David A Wink, Sandra J HewettAbstract:Nitric oxide (NO) has been implicated in bot the pathogenesis of and protection from NMDA receptor mediated neuronal injury. This apparent paradox ha been attributed to alternate redox states of nitrogen mon oxide, whereby, depending on the redox milieu, nitrogen monoxide can be neuroprotective via nitrosation chem istry or react with superoxide to form secondary toxic species. In our murine mixed Cortical Cell culture system the NONOate-type NO donors diethylamine/NO complex sodium (Dea/NO), (Z)-[N-(3-ammoniopropyl)-N-(n-propyl)amino]diazen-1-ium-1,2-diolate (Papa/NO), and spermine/NO complex sodium (Sper/NO), as well as the S-nitrosothiols S-nitroso-L-glutathione (GSNO) and S-ni troso-N-acetyl-D,L-penicillamine (SNAP) (NO equiva lents), decreased NMDA-induced neuronal injury in a concentration-dependent manner. 8-Bromo-cyclic GMP did not mimic the inhibitory effects of the donors, suggesting that the neuroprotection was not the result o NO-stimulated neuronal cyclic GMP production. Further more, neuronal injury induced by exposure of cultures to H 2 O 2 was not altered by the presence of Dea/NO, indicating the absence of a direct antioxidant effect. NONOates did, however, reduce NMDA-stimulated uptake of 45 Ca 2+ , whereas high potassium-induced 45 Ca 2+ accumulation, a measurement of entry via voltage-gated calcium channels, was unaffected. The parallel reduction of 45 Ca 2+ accumulation and NMDA neurotoxicity by NONOates mimicked that seen with an NMDA receptor antagonist. Electrochemical measurements of NO via an NO-sensitive electrode demonstrated that neuroprotective concentrations of all donors produced appreciable amounts of NO over the 5-min time frame. Determination of the formation of NO + equivalents, as assessed by N-nitrosation of 2,3-diaminonaphthylene, revealed little or no observable N-nitrosation by Sper/NO, GSNO, and SNAP with significant N-nitrosation observed by Papa/NO and Dea/NO. However, addition of ascorbate (400 μM) effectively prevented the nitrosation of 2,3-diaminonaphthylene produced by Dea/NO and Papa/NO without altering their neuroprotective properties or their effects on 45 Ca 2+ accumulation. Present results indicate that the intrinsic NO/NO + characteristics of NO donor compounds may not be a good predictor of their ability to inhibit NMDA receptor-mediated neurotoxicity at the Cellular level.
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cyclooxygenase 2 contributes to n methyl d aspartate mediated neuronal Cell death in primary Cortical Cell culture
Journal of Pharmacology and Experimental Therapeutics, 2000Co-Authors: Sandra J Hewett, Tracy F Uliasz, Aniruddha S Vidwans, James A HewettAbstract:Cyclooxygenase isozymes (COX-1 and COX-2) are found to be constitutively expressed in brain, with neuronal expression of COX-2 being rapidly induced after numerous insults, including cerebral ischemia. Because overactivation of N -methyl-d-aspartate (NMDA) receptors has been implicated in the Cell loss associated with ischemia, we characterized the expression of the COX isozymes in murine mixed Cortical Cell cultures and used isozyme-selective inhibitors to determine their relative contribution to NMDA receptor-stimulated prostaglandin (PG) production and excitotoxic neuronal Cell death. Immunocytochemical analysis of mixed Cortical Cell cultures revealed that COX-2 expression was restricted to neurons, whereas COX-1 was expressed in both neurons and astrocytes. Brief exposure to NMDA (5 min; 100 μM) elicited a time-dependent accumulation of PGs in the culture medium that preceded neuronal Cell death and correlated with the induction of COX-2 mRNA. COX-1 expression remained unchanged. Flurbiprofen, a nonselective COX-1/COX-2 inhibitor, blocked NMDA-stimulated PG production and attenuated neuronal death in a concentration-dependent manner. Similar results were obtained with the specific COX-2 inhibitor NS-398 (10–30 μM) but not with the selective COX-1 inhibitor valeryl salicylate (10–300 μM). Inhibition of total constitutive COX activity with aspirin (100 μM, 1.5 h) before NMDA exposure did not prevent subsequent NMDA-mediated neuronal Cell death. However, neuronal injury in aspirin-pretreated cultures was attenuated by flurbiprofen administration after NMDA exposure. Finally, the protection afforded by COX-2 inhibition was specific for NMDA because neither flurbiprofen nor NS-398 protected neurons against kainate-mediated neurotoxicity. Together, these results support the conclusion that newly synthesized COX-2 protein contributes to NMDA-induced neuronal injury.
Wentao Dong - One of the best experts on this subject based on the ideXlab platform.
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an shr scr module specifies legume Cortical Cell fate to enable nodulation
Nature, 2021Co-Authors: Wentao Dong, Yayun Zhu, Huizhong Chang, Chunhua Wang, Jun Yang, Jincai Shi, Jinpeng GaoAbstract:Legumes, unlike other plants, have the ability to establish symbiosis with nitrogen-fixing rhizobia. It has been theorized that a unique property of legume root Cortical Cells enabled the initial establishment of rhizobial symbiosis1-3. Here we show that a SHORTROOT-SCARECROW (SHR-SCR) stem Cell program in Cortical Cells of the legume Medicago truncatula specifies their distinct fate. Regulatory elements drive the Cortical expression of SCR, and stele-expressed SHR protein accumulates in Cortical Cells of M. truncatula but not Arabidopsis thaliana. The Cortical SHR-SCR network is conserved across legume species, responds to rhizobial signals, and initiates legume-specific Cortical Cell division for de novo nodule organogenesis and accommodation of rhizobia. Ectopic activation of SHR and SCR in legumes is sufficient to induce root Cortical Cell division. Our work suggests that acquisition of the Cortical SHR-SCR module enabled Cell division coupled to rhizobial infection in legumes. We propose that this event was central to the evolution of rhizobial endosymbiosis.
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an shr scr module specifies legume Cortical Cell fate to enable nodulation
Nature, 2021Co-Authors: Wentao Dong, Yayun Zhu, Huizhong Chang, Chunhua Wang, Jun Yang, Jinpeng Gao, J R ShiAbstract:Legumes, unlike other plants, have the ability to establish symbiosis with nitrogen-fixing rhizobia. It has been theorized that a unique property of legume root Cortical Cells enabled the initial establishment of rhizobial symbiosis1–3. Here we show that a SHORTROOT–SCARECROW (SHR–SCR) stem Cell program in Cortical Cells of the legume Medicago truncatula specifies their distinct fate. Regulatory elements drive the Cortical expression of SCR, and stele-expressed SHR protein accumulates in Cortical Cells of M. truncatula but not Arabidopsis thaliana. The Cortical SHR–SCR network is conserved across legume species, responds to rhizobial signals, and initiates legume-specific Cortical Cell division for de novo nodule organogenesis and accommodation of rhizobia. Ectopic activation of SHR and SCR in legumes is sufficient to induce root Cortical Cell division. Our work suggests that acquisition of the Cortical SHR–SCR module enabled Cell division coupled to rhizobial infection in legumes. We propose that this event was central to the evolution of rhizobial endosymbiosis. Repurposing of an SHR–SCR stem Cell program in the legume root cortex enables rhizobial symbiosis.
