SummaryAtHKT1 is a sodium (Na þ ) transporter that functions in mediating tolerance to salt stress. To investigate the membrane targeting of AtHKT1 and its expression at the translational level, antibodies were generated against peptides corresponding to the first pore of AtHKT1. Immunoelectron microscopy studies using anti-AtHKT1 antibodies demonstrate that AtHKT1 is targeted to the plasma membrane in xylem parenchyma cells in leaves. AtHKT1 expression in xylem parenchyma cells was also confirmed by AtHKT1 promoter-GUS reporter gene analyses. Interestingly, AtHKT1 disruption alleles caused large increases in the Na þ content of the xylem sap and conversely reduced the Na þ content of the phloem sap. The athkt1 mutant alleles had a smaller and inverse influence on the potassium (K þ ) content compared with the Na þ content of the xylem, suggesting that K þ transport may be indirectly affected. The expression of AtHKT1 was modulated not only by the concentrations of Na þ and K þ but also by the osmolality of non-ionic compounds. These findings show that AtHKT1 selectively unloads sodium directly from xylem vessels to xylem parenchyma cells. AtHKT1 mediates osmolality balance between xylem vessels and xylem parenchyma cells under saline conditions. Thus AtHKT1 reduces the sodium content in xylem vessels and leaves, thereby playing a central role in protecting plant leaves from salinity stress.
Sodium (Na + ) is toxic to most plants, but the molecular mechanisms of plant Na + uptake and distribution remain largely unknown. Here we analyze Arabidopsis lines disrupted in the Na + transporter AtHKT1. AtHKT1 is expressed in the root stele and leaf vasculature. athkt1 null plants exhibit lower root Na + levels and are more salt resistant than wild-type in short-term root growth assays. In shoot tissues, however, athkt1 disruption produces higher Na + levels, and athkt1 and athkt1/ sos3 shoots are Na + -hypersensitive in long-term growth assays. Thus wild-type AtHKT1 controls root/shoot Na + distribution and counteracts salt stress in leaves by reducing leaf Na + accumulation. ß 2002 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.
We pursue the possibility of the scenario in which the Higgs field is identified with the extra-space component of a bulk gauge field. The space-time we take is M 4 ⊗ S 1 /Z 2 . We show that a non-trivial Z 2 -parity assignment allows some of the extra-space component to have radiatively induced VEV, which strongly modifies the mass spectrum and gauge symmetry of the theory, realized by oribifolding. In particular we investigate the dynamical mass generation of zero-mode fermion and spontaneous gauge symmetry breaking due to the VEV. The gauge theories we adopt are a prototype model SU(2) and SU (3) model, of special interest as the realistic minimal scheme to incorporate the standard model SU(2) × U(1).
The effects of the vasoconstrictor angiotensin II (Ang II) on whole‐cell ATP‐sensitive K+currents (Ik,atp) of smooth muscle cells isolated enzymatically from rat mesenteric arteries were investigated using the patch clamp technique.
Ang II, at a physiological concentration (100 nm), reduced Ik,atp activated by 0.1 mm internal ATP and 10 μm levcromakalim by 36.4 ± 2.3%.
The protein kinase C (PKC) activator 1‐oleoyl‐2‐acetyl‐sn‐glycerol (OAG, 1 μm) reduced Ik,atp by 44.1 ± 2.7%. GDPβS (1 mm), included in the pipette solution, abolished the inhibition by Ang II, while that by OAG was unaffected.
Pretreatment with the PKC inhibitors staurosporine (100 nm) or calphostin C (500 nm) prevented the Ang II‐induced inhibition of Ik,atp.
Ang II inhibition was unaffected by cell dialysis with PKA inhibitor peptide (5 μm), and the PKA inhibitor Rp‐cAMPS (100 μ) did not reduce Ik,atp.
Our results suggest that Ang II modulates Katp channels through activation of PKC but not through inhibition of PKA.
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