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Plant Cell. 2018 May;30(5):1132-1146. doi: 10.1105/tpc.17.00701. Epub 2018 Apr 30.

Danger-Associated Peptides Close Stomata by OST1-Independent Activation of Anion Channels in Guard Cells.

Author information

1
Nanjing University-Nanjing Forestry University Joint Institute for Plant Molecular Biology, College of Life Sciences, Nanjing University, Nanjing 210093, China.
2
Department of Plant and Microbial Biology, University of California, Berkeley, California 94720.
3
College of Life Sciences, Northwest University, Xi'an 710069, China.
4
Center for Cognition and Sociality, Institute for Basic Science, KAIST, Yuseong-gu, Daejeon 34141, Republic of Korea.
5
College of Life Sciences, Capital Normal University, Beijing 100048, China.
6
State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
7
Department of Plant Science and Landscape Architecture, Agricultural Biotechnology Laboratory, University of Connecticut, Storrs, Connecticut 06269-4163.
8
Nanjing University-Nanjing Forestry University Joint Institute for Plant Molecular Biology, Key Laboratory of Forest Genetics and Biotechnology, Nanjing Forestry University, Nanjing 210037, China.
9
Nanjing University-Nanjing Forestry University Joint Institute for Plant Molecular Biology, College of Life Sciences, Nanjing University, Nanjing 210093, China fgzhao@nju.edu.cn sluan@berkeley.edu.
10
Department of Plant and Microbial Biology, University of California, Berkeley, California 94720 fgzhao@nju.edu.cn sluan@berkeley.edu.

Abstract

The plant elicitor peptides (Peps), a family of damage/danger-associated molecular patterns (DAMPs), are perceived by two receptors, PEPR1 and PEPR2, and contribute to plant defense against pathogen attack and abiotic stress. Here, we show that the Peps-PEPR signaling pathway functions in stomatal immunity by activating guard cell anion channels in Arabidopsis thaliana The mutant plants lacking both PEPR1 and PEPR2 (pepr1 pepr2) displayed enhanced bacterial growth after being sprayed with Pseudomonas syringae pv tomato (Pst) DC3000, but not after pathogen infiltration into leaves, implicating PEPR function in stomatal immunity. Indeed, synthetic Arabidopsis Peps (AtPeps) effectively induced stomatal closure in wild-type but not pepr1 pepr2 mutant leaves, suggesting that the AtPeps-PEPR signaling pathway triggers stomatal closure. Consistent with this finding, patch-clamp recording revealed AtPep1-induced activation of anion channels in the guard cells of wild-type but not pepr1 pepr2 mutant plants. We further identified two guard cell-expressed anion channels, SLOW ANION CHANNEL1 (SLAC1) and its homolog SLAH3, as functionally overlapping components responsible for AtPep1-induced stomatal closure. The slac1 slah3 double mutant, but not slac1 or slah3 single mutants, failed to respond to AtPep1 in stomatal closure assays. Interestingly, disruption of OPEN STOMATA1 (OST1), an essential gene for abscisic acid-triggered stomatal closure, did not affect the AtPep1-induced anion channel activity and stomatal response. Together, these results illustrate a DAMP-triggered signaling pathway that, unlike the flagellin22-FLAGELLIN-SENSITIVE2 pathway, triggers stomata immunity through an OST1-independent mechanism.

PMID:
29716993
PMCID:
PMC6002199
DOI:
10.1105/tpc.17.00701
[Indexed for MEDLINE]
Free PMC Article

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