Abstract

Stipa purpurea (S. purpurea) is the dominant plant species in the alpine steppe of the Qinghai-Tibet Plateau, China. It is highly resistant to cold and drought conditions. However, the underlying mechanisms regulating the stress tolerance are unknown. In this study, a CIPK gene from S. purpurea (SpCIPK26) was isolated. The SpCIPK26 coding region consisted of 1392 bp that encoded 464 amino acids. The protein has a highly conserved catalytic structure and regulatory domain. The expression of SpCIPK26 was induced by drought and salt stress. SpCIPK26 overexpression in Arabidopsis thaliana (A. thaliana) plants provided increased tolerance to drought and salt stress in an abscisic acid (ABA)-dependent manner. Compared with wild-type A. thaliana plants, SpCIPK26-overexpressing plants had higher survival rates, water potentials, and photosynthetic efficiency (Fv/Fm), as well as lower levels of reactive oxygen species (ROS) following exposure to drought and salt stress. Gene expression analyses indicated stress-inducible genes (RD29A, RD29B, and ABF2) and a ROS-scavenger gene (CAT1) were upregulated in SpCIPK26-overexpressing plants after stress treatments. All of these marker genes are associated with ABA-responsive cis-acting elements. Additionally, the similarities in the gene expression patterns following ABA, mannitol, and NaCl treatments suggest SpCIPK26 has an important role during plant responses to drought and salt stress and in regulating ABA signaling.

Highlights

  • Drought and salinity are two major abiotic stresses that inhibit plant growth and development [1,2,3]

  • SpCIPK26 was responsive to drought gradient in our transcriptome analysis, potentially contributing to drought adaptation of S. purpurea

  • SpCIPK26 mainly expressed in S. purpurea aboveground parts (Figure 2B), indicating its intricate regulation at whole-plant level

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Summary

Introduction

Drought and salinity are two major abiotic stresses that inhibit plant growth and development [1,2,3]. Plants are protected by the expression of various stress-related genes to synthesize hormones (e.g., abscisic acid (ABA)) and regulatory proteins to cope with drought and salt stress [5]. The CaMs and CBLs merely act as sensor relays because they do not have an intrinsic catalytic function [9]. Unlike CaMs, which interact with various target proteins to relay Ca2+ signals [10], CBLs interact with a specific group of sucrose non-fermenting-related kinases called CBL-interacting protein kinases (CIPKs) to transmit signals to downstream targets [11]. In the absence of stress, the FISL/NAF motif plays an auto-inhibitory role by inactivating the kinase domain of CIPKs. the perception of certain stress signals can induce CBLs to bind to the FISL/NAF motif and prevent it from inhibiting CIPK activity [14]

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