A PIIB-type Ca2+-ATPase is essential for stress adaptation in Physcomitrella patens

被引:86
作者
Qudeimat, Enas [1 ]
Faltusz, Alexander M. C. [1 ]
Wheeler, Glen [4 ]
Lang, Daniel [1 ]
Brownlee, Colin [4 ]
Reski, Ralf [1 ,2 ,3 ]
Frank, Wolfgang [1 ,2 ]
机构
[1] Univ Freiburg, Fac Biol, Inst Biol 2, D-79104 Freiburg, Germany
[2] Univ Freiburg, Fac Biol, Freiburg Initiat Syst Biol, D-79104 Freiburg, Germany
[3] Univ Freiburg, Ctr Biol Signaling Studies, D-79104 Freiburg, Germany
[4] Marine Biol Assoc UK, Plymouth PL1 2PB, Devon, England
基金
英国生物技术与生命科学研究理事会;
关键词
abiotic stress; calcium; signaling; targeted knockout;
D O I
10.1073/pnas.0800864105
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Transient cytosolic Ca2+ ([Ca2+](cyt)) elevations are early events in plant signaling pathways including those related to abiotic stress. The restoration of [ Ca2+] cyt to prestimulus levels involves ATP-driven Ca2+ pumps, but direct evidence for an essential role of a plant Ca(2+)ATPase in abiotic stress adaptation is missing. Here, we report on a stress-responsive Ca2+-ATPase gene (PCA1) from the moss Physcomitrella patens. Functional analysis of PCA1 in a Ca2+ transport-deficient yeast mutant suggests that PCA1 encodes a P-IIB-type Ca2+-ATPase harboring an N-terminal autoinhibitory domain. In vivo localizations identified membranes of small vacuoles as the integration site for a PCA1:GFP fusion protein. PCA1 mRNA levels are up-regulated by dehydration, NaCl, and abscisic acid, and PCA1 loss-of-function mutants (Delta PCA1) exhibit an enhanced susceptibility to salt stress. The Delta PCA1 lines show sustained elevated [Ca2+](cyt) in response to salt treatment in contrast to WT that shows transient Ca2+ elevations, indicating a direct role for PCA1 in the restoration of prestimulus [Ca2+](cyt). The altered Ca2+ response of the Delta PCA1 mutant lines correlates with altered expression levels of stress-induced genes, suggesting disturbance of a stress-associated signaling pathway. We propose that PCA1 is an essential component for abiotic stress adaptation in Physcomitrella involved in the generation of a specific salt-induced Ca2+ signature.
引用
收藏
页码:19555 / 19560
页数:6
相关论文
共 53 条
[11]   Functional association of Arabidopsis CAX1 and CAX3 is required for normal growth and ion homeostasis [J].
Cheng, NH ;
Pittman, JK ;
Shigaki, T ;
Lachmansingh, J ;
LeClere, S ;
Lahner, B ;
Salt, DE ;
Hirschi, KD .
PLANT PHYSIOLOGY, 2005, 138 (04) :2048-2060
[12]  
CUNNINGHAM KW, 1994, J EXP BIOL, V196, P157
[13]   P-type calcium ATPases in higher plants - biochemical, molecular and functional properties [J].
Evans, DE ;
Williams, LE .
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON BIOMEMBRANES, 1998, 1376 (01) :1-25
[14]   Calcium oscillations in higher plants [J].
Evans, NH ;
McAinsh, MR ;
Hetherington, AM .
CURRENT OPINION IN PLANT BIOLOGY, 2001, 4 (05) :415-420
[15]   Activity of the hSPCA1 Golgi Ca2+ pump is essential for Ca2+-mediated Ca2+ response and cell viability in Darier disease [J].
Foggia, L ;
Aronchik, I ;
Aberg, K ;
Brown, B ;
Hovnanian, A ;
Mauro, TM .
JOURNAL OF CELL SCIENCE, 2006, 119 (04) :671-679
[16]   Molecular tools to study Physcomitrella patens [J].
Frank, W ;
Decker, EL ;
Reski, R .
PLANT BIOLOGY, 2005, 7 (03) :220-227
[17]   Physcomitrella patens is highly tolerant against drought, salt and osmotic stress [J].
Frank, W ;
Ratnadewi, D ;
Reski, R .
PLANTA, 2005, 220 (03) :384-394
[18]   Molecular aspects of higher plant P-type Ca2+-ATPases [J].
Geisler, M ;
Axelsen, KB ;
Harper, JF ;
Palmgren, MG .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES, 2000, 1465 (1-2) :52-78
[19]   The ACA4 gene of arabidopsis encodes a vacuolar membrane calcium pump that improves salt tolerance in yeast [J].
Geisler, M ;
Frangne, N ;
Gomès, E ;
Martinoia, E ;
Palmgren, MG .
PLANT PHYSIOLOGY, 2000, 124 (04) :1814-1827
[20]   The ACA10 Ca2+-ATPase regulates adult vegetative development and inflorescence architecture in Arabidopsis [J].
George, Lynn ;
Romanowsky, Shawn M. ;
Harper, Jeffrey F. ;
Sharrock, Robert A. .
PLANT PHYSIOLOGY, 2008, 146 (02) :716-728