These authors contributed equally to this work.
Mutations in the SLAC1 anion channel slow stomatal opening and severely reduce K+ uptake channel activity via enhanced cytosolic [Ca2+] and increased Ca2+ sensitivity of K+ uptake channels
Article first published online: 5 NOV 2012
© 2012 The Authors. New Phytologist © 2012 New Phytologist Trust
Volume 197, Issue 1, pages 88–98, January 2013
How to Cite
Laanemets, K., Wang, Y.-F., Lindgren, O., Wu, J., Nishimura, N., Lee, S., Caddell, D., Merilo, E., Brosche, M., Kilk, K., Soomets, U., Kangasjärvi, J., Schroeder, J. I. and Kollist, H. (2013), Mutations in the SLAC1 anion channel slow stomatal opening and severely reduce K+ uptake channel activity via enhanced cytosolic [Ca2+] and increased Ca2+ sensitivity of K+ uptake channels. New Phytologist, 197: 88–98. doi: 10.1111/nph.12008
- Issue published online: 26 NOV 2012
- Article first published online: 5 NOV 2012
- Manuscript Accepted: 17 SEP 2012
- Manuscript Received: 27 JUL 2012
- the Estonian Science Foundation. Grant Numbers: 7763, 7361, 9208, SF0180071s07
- the European Regional Fund
- NIH. Grant Number: R01GM060396
- ) and NSF. Grant Number: MCB0918220
- US Department of Energy. Grant Number: DE-FG02-03ER15449
- the National Natural Science Foundation of China. Grant Number: 31170227
- National Basic Research Program of China. Grant Numbers: 2012CB114300, 973
- Academy of Finland Centre of Excellence program
- abscisic acid (ABA);
- anion channel;
- Ca2+ signaling;
- cytosolic Ca2+ concentration;
- guard cells;
- potassium uptake channel;
- stomatal opening
- The Arabidopsis guard cell anion channel SLAC1 is essential for stomatal closure in response to various endogenous and environmental stimuli. Interestingly, here we reveal an unexpected impairment of slac1 alleles on stomatal opening.
- We report that mutations in SLAC1 unexpectedly slow stomatal opening induced by light, low CO2 and elevated air humidity in intact plants and that this is caused by the severely reduced activity of inward K+ (K+in) channels in slac1 guard cells.
- Expression of channels and transporters involved in stomatal opening showed small but significant reductions in transcript levels in slac1 guard cells; however, this was deemed insufficient to explain the severely impaired K+in channel activity in slac1. We further examined resting cytosolic Ca2+ concentration ([Ca2+]cyt) and K+in channel sensitivity to [Ca2+]cyt in slac1. These experiments showed higher resting [Ca2+]cyt in slac1 guard cells and that reducing [Ca2+]cyt to < 10 nM rapidly restored the activity of K+in channels in slac1 closer to wild-type levels.
- These findings demonstrate an unanticipated compensatory feedback control in plant stomatal regulation, which counteracts the impaired stomatal closing response of slac1, by down-regulating stomatal opening mechanisms and implicates enhanced [Ca2+]cyt sensitivity priming as a mechanistic basis for the down-regulated K+in channel activity.