Biology of SLAC1-type anion channels - from nutrient uptake to stomatal closure
© 2017 The Authors. New Phytologist © 2017 New Phytologist Trust.
| Publié dans: | The New phytologist. - 1990. - 216(2017), 1 vom: 15. Okt., Seite 46-61 |
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| Format: | Article en ligne |
| Langue: | English |
| Publié: |
2017
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| Accès à la collection: | The New phytologist |
| Sujets: | Journal Article Review S-type anion channel SLAC1 abscisic acid (ABA) signalling guard cell stomata Anions Ion Channels Phosphorus plus... |
| Résumé: | © 2017 The Authors. New Phytologist © 2017 New Phytologist Trust. Contents 46 I. 46 II. 47 III. 50 IV. 53 V. 56 VI. 57 58 58 References 58 SUMMARY: Stomatal guard cells control leaf CO2 intake and concomitant water loss to the atmosphere. When photosynthetic CO2 assimilation is limited and the ratio of CO2 intake to transpiration becomes suboptimal, guard cells, sensing the rise in CO2 concentration in the substomatal cavity, deflate and the stomata close. Screens for mutants that do not close in response to experimentally imposed high CO2 atmospheres identified the guard cell-expressed Slowly activating anion channel, SLAC1, as the key player in the regulation of stomatal closure. SLAC1 evolved, though, before the emergence of guard cells. In Arabidopsis, SLAC1 is the founder member of a family of anion channels, which comprises four homologues. SLAC1 and SLAH3 mediate chloride and nitrate transport in guard cells, while SLAH1, SLAH2 and SLAH3 are engaged in root nitrate and chloride acquisition, and anion translocation to the shoot. The signal transduction pathways involved in CO2 , water stress and nutrient-sensing activate SLAC/SLAH via distinct protein kinase/phosphatase pairs. In this review, we discuss the role that SLAC/SLAH channels play in guard cell closure, on the one hand, and in the root-shoot continuum on the other, along with the molecular basis of the channels' anion selectivity and gating |
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| Description: | Date Completed 15.05.2018 Date Revised 30.03.2022 published: Print-Electronic GENBANK: OEL21301.1, OQU82188.1, ONM14749.1, CAD41673.1, OAY64547.1, XP_008780343.1, XP_009384523.1, LN794219, LN794222, APA28903.1, APA28905.1, ANV22160.1, ANV22161.1, AT1G12480, XP_009148588.1, XP_002275215.1, XP_008448932.1, XP_005847542.1, Pp1s28_347V6.1, Pp1s22_399V6.1 Citation Status MEDLINE |
| ISSN: | 1469-8137 |
| DOI: | 10.1111/nph.14685 |